Acute tubular necrosis
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Slide Content
Acute Tubular NecrosisAcute Tubular Necrosis
Resident’s conference
Presented by Dr Gagandeep K Heer, MD
(PGY-2)
Resident’s conference
Presented by Dr Gagandeep K Heer, MD
(PGY-2)
BackgroundBackground
DefinitionDefinition:: ARF is defined as an abrupt or ARF is defined as an abrupt or
rapid decline in the renal function.rapid decline in the renal function.
A rise in serum BUN or creatinine A rise in serum BUN or creatinine
concentration, with or without decrease in concentration, with or without decrease in
urine output, usually is evidence of ARF.urine output, usually is evidence of ARF.
ARF is often transient and completely ARF is often transient and completely
reversible.reversible.
DefinitionDefinition:: ARF is defined as an abrupt or ARF is defined as an abrupt or
rapid decline in the renal function.rapid decline in the renal function.
A rise in serum BUN or creatinine A rise in serum BUN or creatinine
concentration, with or without decrease in concentration, with or without decrease in
urine output, usually is evidence of ARF.urine output, usually is evidence of ARF.
ARF is often transient and completely ARF is often transient and completely
reversible.reversible.
Background Background
The causes of ARF are divided into 3 categories: The causes of ARF are divided into 3 categories:
PPrerenalrerenal
Renal Renal
PostrenalPostrenal
ATNATN is the most common cause of ARF in the is the most common cause of ARF in the renalrenal category.category.
ATN is the 2ATN is the 2
ndnd
most common cause of all categories of ARF in most common cause of all categories of ARF in
hospitalizedhospitalized patients, with only prerenal azotemia occurring patients, with only prerenal azotemia occurring
more frequently.more frequently.
In outpatients, obstruction (ureteric, bladder neck or urethral) In outpatients, obstruction (ureteric, bladder neck or urethral)
is the 2is the 2
ndnd
most common cause of ARF after prerenal azotemia. most common cause of ARF after prerenal azotemia.
Other causes of ARF include acute interstitial nephritis, acute Other causes of ARF include acute interstitial nephritis, acute
glumerulonephtitis, vasculitis, HUS, TTP, DIC, accelerated HTN, glumerulonephtitis, vasculitis, HUS, TTP, DIC, accelerated HTN,
radiation nephritis, acute on chronic renal failure, renovascular radiation nephritis, acute on chronic renal failure, renovascular
obstruction (bilateral or unilateral in the setting of single obstruction (bilateral or unilateral in the setting of single
functioning kidney), renal allograft rejection, intratubular functioning kidney), renal allograft rejection, intratubular
deposition and obstruction (myeloma proteins, urate, oxalate deposition and obstruction (myeloma proteins, urate, oxalate
crystals, etc.)crystals, etc.)
The causes of ARF are divided into 3 categories: The causes of ARF are divided into 3 categories:
PPrerenalrerenal
Renal Renal
PostrenalPostrenal
ATNATN is the most common cause of ARF in the is the most common cause of ARF in the renalrenal category.category.
ATN is the 2ATN is the 2
ndnd
most common cause of all categories of ARF in most common cause of all categories of ARF in
hospitalizedhospitalized patients, with only prerenal azotemia occurring patients, with only prerenal azotemia occurring
more frequently.more frequently.
In outpatients, obstruction (ureteric, bladder neck or urethral) In outpatients, obstruction (ureteric, bladder neck or urethral)
is the 2is the 2
ndnd
most common cause of ARF after prerenal azotemia. most common cause of ARF after prerenal azotemia.
Other causes of ARF include acute interstitial nephritis, acute Other causes of ARF include acute interstitial nephritis, acute
glumerulonephtitis, vasculitis, HUS, TTP, DIC, accelerated HTN, glumerulonephtitis, vasculitis, HUS, TTP, DIC, accelerated HTN,
radiation nephritis, acute on chronic renal failure, renovascular radiation nephritis, acute on chronic renal failure, renovascular
obstruction (bilateral or unilateral in the setting of single obstruction (bilateral or unilateral in the setting of single
functioning kidney), renal allograft rejection, intratubular functioning kidney), renal allograft rejection, intratubular
deposition and obstruction (myeloma proteins, urate, oxalate deposition and obstruction (myeloma proteins, urate, oxalate
crystals, etc.)crystals, etc.)
PathophysiologyPathophysiology
ATN usually occurs after an acute ischemic or ATN usually occurs after an acute ischemic or
toxic event, and it has a well-defined sequence of toxic event, and it has a well-defined sequence of
events. events.
Initiation phaseInitiation phase characterized by acute decrease characterized by acute decrease
in GFR to very low levels, with a sudden increase in GFR to very low levels, with a sudden increase
in serum Cr and BUN concentrations. in serum Cr and BUN concentrations.
Maintenance phaseMaintenance phase is characterized by sustained is characterized by sustained
severe reduction in GFR and the BUN and Cr severe reduction in GFR and the BUN and Cr
continue to rise.continue to rise.
Recovery phaseRecovery phase, in which the tubular function is , in which the tubular function is
restored, is characterized by an increase in urine restored, is characterized by an increase in urine
volume (if oliguria was present) and gradual volume (if oliguria was present) and gradual
decrease in Cr and BUN to their pre-injury level.decrease in Cr and BUN to their pre-injury level.
ATN usually occurs after an acute ischemic or ATN usually occurs after an acute ischemic or
toxic event, and it has a well-defined sequence of toxic event, and it has a well-defined sequence of
events. events.
Initiation phaseInitiation phase characterized by acute decrease characterized by acute decrease
in GFR to very low levels, with a sudden increase in GFR to very low levels, with a sudden increase
in serum Cr and BUN concentrations. in serum Cr and BUN concentrations.
Maintenance phaseMaintenance phase is characterized by sustained is characterized by sustained
severe reduction in GFR and the BUN and Cr severe reduction in GFR and the BUN and Cr
continue to rise.continue to rise.
Recovery phaseRecovery phase, in which the tubular function is , in which the tubular function is
restored, is characterized by an increase in urine restored, is characterized by an increase in urine
volume (if oliguria was present) and gradual volume (if oliguria was present) and gradual
decrease in Cr and BUN to their pre-injury level.decrease in Cr and BUN to their pre-injury level.
Ischemic ATNIschemic ATN
Ischemic ATN is often described as a continuum of prerenal Ischemic ATN is often described as a continuum of prerenal
azotemia. Response to fluid repletion can help distinguish azotemia. Response to fluid repletion can help distinguish
between the two: return of renal function within 24-72 between the two: return of renal function within 24-72
hours usually indicate prerenal disease although short-lived hours usually indicate prerenal disease although short-lived
ATN can recover within similar timeframe (e.g. self limited ATN can recover within similar timeframe (e.g. self limited
insult such as transient aortic clamping during suprarenal insult such as transient aortic clamping during suprarenal
aortic aneurysm surgery).aortic aneurysm surgery).
Initiation phaseInitiation phase:: Hypoperfusion initiates cell injury that Hypoperfusion initiates cell injury that
often leads to cell death. It is most prominent in straight often leads to cell death. It is most prominent in straight
portion of the proximal tubules and thick ascending limb of portion of the proximal tubules and thick ascending limb of
loop of Henle. The reduction in the GFR occurs not only loop of Henle. The reduction in the GFR occurs not only
from from reduced filtrationreduced filtration due to hypoperfusion but also from due to hypoperfusion but also from
casts and debris casts and debris obstructingobstructing the lumen, causing back leak the lumen, causing back leak
of filtrate through the damaged epithelium (of filtrate through the damaged epithelium (ineffective ineffective
filtrationfiltration). In addition, ischemia leads to decreased ). In addition, ischemia leads to decreased
production of vasodilators (i.e. nitric oxide, prostacyclin) by production of vasodilators (i.e. nitric oxide, prostacyclin) by
tubular epithelial cells, leading to further vasoconstriction tubular epithelial cells, leading to further vasoconstriction
and hypoperfusion.and hypoperfusion.
Ischemic ATN is often described as a continuum of prerenal Ischemic ATN is often described as a continuum of prerenal
azotemia. Response to fluid repletion can help distinguish azotemia. Response to fluid repletion can help distinguish
between the two: return of renal function within 24-72 between the two: return of renal function within 24-72
hours usually indicate prerenal disease although short-lived hours usually indicate prerenal disease although short-lived
ATN can recover within similar timeframe (e.g. self limited ATN can recover within similar timeframe (e.g. self limited
insult such as transient aortic clamping during suprarenal insult such as transient aortic clamping during suprarenal
aortic aneurysm surgery).aortic aneurysm surgery).
Initiation phaseInitiation phase:: Hypoperfusion initiates cell injury that Hypoperfusion initiates cell injury that
often leads to cell death. It is most prominent in straight often leads to cell death. It is most prominent in straight
portion of the proximal tubules and thick ascending limb of portion of the proximal tubules and thick ascending limb of
loop of Henle. The reduction in the GFR occurs not only loop of Henle. The reduction in the GFR occurs not only
from from reduced filtrationreduced filtration due to hypoperfusion but also from due to hypoperfusion but also from
casts and debris casts and debris obstructingobstructing the lumen, causing back leak the lumen, causing back leak
of filtrate through the damaged epithelium (of filtrate through the damaged epithelium (ineffective ineffective
filtrationfiltration). In addition, ischemia leads to decreased ). In addition, ischemia leads to decreased
production of vasodilators (i.e. nitric oxide, prostacyclin) by production of vasodilators (i.e. nitric oxide, prostacyclin) by
tubular epithelial cells, leading to further vasoconstriction tubular epithelial cells, leading to further vasoconstriction
and hypoperfusion.and hypoperfusion.
Ischemic ATNIschemic ATN
Maintenance phaseMaintenance phase is characterized by stabilization of is characterized by stabilization of
GFR at a very low level, and it typically lasts 1-2 weeks. GFR at a very low level, and it typically lasts 1-2 weeks.
Uremic complications typically develop during this phase. Uremic complications typically develop during this phase.
In addition to the above mentioned mechanism of injury, In addition to the above mentioned mechanism of injury,
tubulo-glomerular feedback also plays a role by causing tubulo-glomerular feedback also plays a role by causing
constriction of afferent arterioles by the macula densa constriction of afferent arterioles by the macula densa
cells, which detect and increased salt load in the distal cells, which detect and increased salt load in the distal
tubules.tubules.
During During Recovery phaseRecovery phase, there is regeneration of tubular , there is regeneration of tubular
epithelial cells. An abnormal diuresis sometimes occurs, epithelial cells. An abnormal diuresis sometimes occurs,
causing salt and water loss and volume depletion. The causing salt and water loss and volume depletion. The
mechanism of the diuresis is not completely understood, mechanism of the diuresis is not completely understood,
but it may in part be due to delayed recovery of tubular but it may in part be due to delayed recovery of tubular
cell function in the setting of increased glomerular cell function in the setting of increased glomerular
filtration. In addition, continued use of diuretics (often filtration. In addition, continued use of diuretics (often
administered during initiation and maintenance phases) administered during initiation and maintenance phases)
may also add to the problem.may also add to the problem.
Maintenance phaseMaintenance phase is characterized by stabilization of is characterized by stabilization of
GFR at a very low level, and it typically lasts 1-2 weeks. GFR at a very low level, and it typically lasts 1-2 weeks.
Uremic complications typically develop during this phase. Uremic complications typically develop during this phase.
In addition to the above mentioned mechanism of injury, In addition to the above mentioned mechanism of injury,
tubulo-glomerular feedback also plays a role by causing tubulo-glomerular feedback also plays a role by causing
constriction of afferent arterioles by the macula densa constriction of afferent arterioles by the macula densa
cells, which detect and increased salt load in the distal cells, which detect and increased salt load in the distal
tubules.tubules.
During During Recovery phaseRecovery phase, there is regeneration of tubular , there is regeneration of tubular
epithelial cells. An abnormal diuresis sometimes occurs, epithelial cells. An abnormal diuresis sometimes occurs,
causing salt and water loss and volume depletion. The causing salt and water loss and volume depletion. The
mechanism of the diuresis is not completely understood, mechanism of the diuresis is not completely understood,
but it may in part be due to delayed recovery of tubular but it may in part be due to delayed recovery of tubular
cell function in the setting of increased glomerular cell function in the setting of increased glomerular
filtration. In addition, continued use of diuretics (often filtration. In addition, continued use of diuretics (often
administered during initiation and maintenance phases) administered during initiation and maintenance phases)
may also add to the problem.may also add to the problem.
Nephrotoxic ATNNephrotoxic ATN
Most of the pathophysiological features of Most of the pathophysiological features of
ischemic ATN are shared by the ischemic ATN are shared by the
nephrotoxic forms and it has the same nephrotoxic forms and it has the same
three phases.three phases.
Nephrotoxic injury to tubular cells occurs Nephrotoxic injury to tubular cells occurs
by multiple mechanisms including direct by multiple mechanisms including direct
toxicity, intrarenal vasoconstriction, and toxicity, intrarenal vasoconstriction, and
intratubular obstruction.intratubular obstruction.
Most of the pathophysiological features of Most of the pathophysiological features of
ischemic ATN are shared by the ischemic ATN are shared by the
nephrotoxic forms and it has the same nephrotoxic forms and it has the same
three phases.three phases.
Nephrotoxic injury to tubular cells occurs Nephrotoxic injury to tubular cells occurs
by multiple mechanisms including direct by multiple mechanisms including direct
toxicity, intrarenal vasoconstriction, and toxicity, intrarenal vasoconstriction, and
intratubular obstruction.intratubular obstruction.
At cellular level…At cellular level…
Ischemic ATNIschemic ATN::
Cellular ischemia results in series of alterations in energetics, Cellular ischemia results in series of alterations in energetics,
ion transport and membrane integrity that ultimately leads to cell ion transport and membrane integrity that ultimately leads to cell
injury or necrosis. These changes include depletion of ATP, injury or necrosis. These changes include depletion of ATP,
inhibition of active sodium transport and transport of other inhibition of active sodium transport and transport of other
solutes, impairment of cell volume regulation, cytoskeletal solutes, impairment of cell volume regulation, cytoskeletal
disruption and loss of cell polarity, cell-cell and cell-matrix disruption and loss of cell polarity, cell-cell and cell-matrix
attachment, accumulation of intracellular calcium, altered attachment, accumulation of intracellular calcium, altered
phospholipid metabolism, oxygen free radical formation and phospholipid metabolism, oxygen free radical formation and
peroxidation of membrane lipids. peroxidation of membrane lipids.
A characteristic feature of ischemic ATN is the absence of A characteristic feature of ischemic ATN is the absence of
widespread necrosis of tubular epithelial cells. Necrosis is more widespread necrosis of tubular epithelial cells. Necrosis is more
subtle and is reflected in individual necrotic cells within some subtle and is reflected in individual necrotic cells within some
proximal or distal tubules. These single cells shed into tubular proximal or distal tubules. These single cells shed into tubular
lumen, with resulting focal denudation of the tubular basement lumen, with resulting focal denudation of the tubular basement
membrane. Interstitial edema is common.membrane. Interstitial edema is common.
Ischemic ATNIschemic ATN::
Cellular ischemia results in series of alterations in energetics, Cellular ischemia results in series of alterations in energetics,
ion transport and membrane integrity that ultimately leads to cell ion transport and membrane integrity that ultimately leads to cell
injury or necrosis. These changes include depletion of ATP, injury or necrosis. These changes include depletion of ATP,
inhibition of active sodium transport and transport of other inhibition of active sodium transport and transport of other
solutes, impairment of cell volume regulation, cytoskeletal solutes, impairment of cell volume regulation, cytoskeletal
disruption and loss of cell polarity, cell-cell and cell-matrix disruption and loss of cell polarity, cell-cell and cell-matrix
attachment, accumulation of intracellular calcium, altered attachment, accumulation of intracellular calcium, altered
phospholipid metabolism, oxygen free radical formation and phospholipid metabolism, oxygen free radical formation and
peroxidation of membrane lipids. peroxidation of membrane lipids.
A characteristic feature of ischemic ATN is the absence of A characteristic feature of ischemic ATN is the absence of
widespread necrosis of tubular epithelial cells. Necrosis is more widespread necrosis of tubular epithelial cells. Necrosis is more
subtle and is reflected in individual necrotic cells within some subtle and is reflected in individual necrotic cells within some
proximal or distal tubules. These single cells shed into tubular proximal or distal tubules. These single cells shed into tubular
lumen, with resulting focal denudation of the tubular basement lumen, with resulting focal denudation of the tubular basement
membrane. Interstitial edema is common.membrane. Interstitial edema is common.
Ischemic ATNIschemic ATN
Histology (continued…)Histology (continued…)
Toxic ATNToxic ATN:: The morphology differs from ischemic The morphology differs from ischemic
ATN in that the former is characterized by more ATN in that the former is characterized by more
extensive necrosis of the tubular epithelium. In extensive necrosis of the tubular epithelium. In
most cases, however, the necrosis is limited to most cases, however, the necrosis is limited to
certain segments that are most sensitive to the certain segments that are most sensitive to the
toxin. ATN caused by hemoglobin or myoglobin toxin. ATN caused by hemoglobin or myoglobin
has added feature of numerous red-brown has added feature of numerous red-brown
tubular casts, colored by heme pigments.tubular casts, colored by heme pigments.
During the During the recovery phase recovery phase of ATN, the tubular of ATN, the tubular
epithelium regenerates, leading to the epithelium regenerates, leading to the
appearance of mitoses, increased size of cells and appearance of mitoses, increased size of cells and
nuclei, and cell crowding. Survivors eventually nuclei, and cell crowding. Survivors eventually
display complete restoration of normal renal display complete restoration of normal renal
architecture.architecture.
Toxic ATNToxic ATN:: The morphology differs from ischemic The morphology differs from ischemic
ATN in that the former is characterized by more ATN in that the former is characterized by more
extensive necrosis of the tubular epithelium. In extensive necrosis of the tubular epithelium. In
most cases, however, the necrosis is limited to most cases, however, the necrosis is limited to
certain segments that are most sensitive to the certain segments that are most sensitive to the
toxin. ATN caused by hemoglobin or myoglobin toxin. ATN caused by hemoglobin or myoglobin
has added feature of numerous red-brown has added feature of numerous red-brown
tubular casts, colored by heme pigments.tubular casts, colored by heme pigments.
During the During the recovery phase recovery phase of ATN, the tubular of ATN, the tubular
epithelium regenerates, leading to the epithelium regenerates, leading to the
appearance of mitoses, increased size of cells and appearance of mitoses, increased size of cells and
nuclei, and cell crowding. Survivors eventually nuclei, and cell crowding. Survivors eventually
display complete restoration of normal renal display complete restoration of normal renal
architecture.architecture.
Nephrotoxic ATNNephrotoxic ATN
FrequencyFrequency
In the US: ARF is seen in 5% of all In the US: ARF is seen in 5% of all
hospital admissions and upto 30% of hospital admissions and upto 30% of
patients admitted to the ICU. Prerenal patients admitted to the ICU. Prerenal
causes account for about half of all cases. causes account for about half of all cases.
ATN is most common cause out of the ATN is most common cause out of the
intrinsic renal diseases.intrinsic renal diseases.
In the US: ARF is seen in 5% of all In the US: ARF is seen in 5% of all
hospital admissions and upto 30% of hospital admissions and upto 30% of
patients admitted to the ICU. Prerenal patients admitted to the ICU. Prerenal
causes account for about half of all cases. causes account for about half of all cases.
ATN is most common cause out of the ATN is most common cause out of the
intrinsic renal diseases.intrinsic renal diseases.
HistoryHistory
A good history is very important in diagnosis of A good history is very important in diagnosis of
ATN. ATN.
Find out about: Find out about:
Recent hypotensionRecent hypotension
SepsisSepsis
Muscle necrosis (e.g. h/o seizure, cocaine use)Muscle necrosis (e.g. h/o seizure, cocaine use)
Exposure to contrast or nephrotoxic medicationsExposure to contrast or nephrotoxic medications
HypovolumiaHypovolumia
Other risk factors for development of ATN like Other risk factors for development of ATN like
underlying renal disease from DM, HTN, etc.underlying renal disease from DM, HTN, etc.
A good history is very important in diagnosis of A good history is very important in diagnosis of
ATN. ATN.
Find out about: Find out about:
Recent hypotensionRecent hypotension
SepsisSepsis
Muscle necrosis (e.g. h/o seizure, cocaine use)Muscle necrosis (e.g. h/o seizure, cocaine use)
Exposure to contrast or nephrotoxic medicationsExposure to contrast or nephrotoxic medications
HypovolumiaHypovolumia
Other risk factors for development of ATN like Other risk factors for development of ATN like
underlying renal disease from DM, HTN, etc.underlying renal disease from DM, HTN, etc.
Physical ExamPhysical Exam
Physical exam may be unremarkable because ARF Physical exam may be unremarkable because ARF
is often found incidentally during routine is often found incidentally during routine
laboratory studies (i.e. elevated BUN and Cr).laboratory studies (i.e. elevated BUN and Cr).
Look for pericardial friction rub (pt may have Look for pericardial friction rub (pt may have
pericarditis), asterixis and/or excoriation marks pericarditis), asterixis and/or excoriation marks
related to uremic pruritis.related to uremic pruritis.
Hypertension or edema may be noted.Hypertension or edema may be noted.
Physical findings related to the underlying Physical findings related to the underlying
disease.disease.
Physical exam may be unremarkable because ARF Physical exam may be unremarkable because ARF
is often found incidentally during routine is often found incidentally during routine
laboratory studies (i.e. elevated BUN and Cr).laboratory studies (i.e. elevated BUN and Cr).
Look for pericardial friction rub (pt may have Look for pericardial friction rub (pt may have
pericarditis), asterixis and/or excoriation marks pericarditis), asterixis and/or excoriation marks
related to uremic pruritis.related to uremic pruritis.
Hypertension or edema may be noted.Hypertension or edema may be noted.
Physical findings related to the underlying Physical findings related to the underlying
disease.disease.
Causes of ATNCauses of ATN
ATN is usually caused by an acute event, ATN is usually caused by an acute event,
either ischemic or toxic. either ischemic or toxic.
ATN is usually caused by an acute event, ATN is usually caused by an acute event,
either ischemic or toxic. either ischemic or toxic.
Causes of Ischemic ATNCauses of Ischemic ATN
It may be considered part of the spectrum It may be considered part of the spectrum
of prerenal azotemia and they have the of prerenal azotemia and they have the
same causes and risk factorssame causes and risk factors
•Hypovolumic states – hemorrhage, volume Hypovolumic states – hemorrhage, volume
depletion from GI or renal losses, burns, depletion from GI or renal losses, burns,
fluid sequestration.fluid sequestration.
•Low cardiac output states – CHF and other Low cardiac output states – CHF and other
diseases of the myocardium, valvulopathy, diseases of the myocardium, valvulopathy,
arrhythmia, pericardial diseases, arrhythmia, pericardial diseases,
tamponade.tamponade.
It may be considered part of the spectrum It may be considered part of the spectrum
of prerenal azotemia and they have the of prerenal azotemia and they have the
same causes and risk factorssame causes and risk factors
•Hypovolumic states – hemorrhage, volume Hypovolumic states – hemorrhage, volume
depletion from GI or renal losses, burns, depletion from GI or renal losses, burns,
fluid sequestration.fluid sequestration.
•Low cardiac output states – CHF and other Low cardiac output states – CHF and other
diseases of the myocardium, valvulopathy, diseases of the myocardium, valvulopathy,
arrhythmia, pericardial diseases, arrhythmia, pericardial diseases,
tamponade.tamponade.
Causes of Ischemic ATNCauses of Ischemic ATN
•Systemic vasodilation – sepsis, Systemic vasodilation – sepsis,
anaphylaxisanaphylaxis
•DICDIC
•Renal vasoconstriction – cyclosporine, Renal vasoconstriction – cyclosporine,
norepinephrine, epinephrine, amphotericin norepinephrine, epinephrine, amphotericin
B, etcB, etc
•Hyperviscosity syndromeHyperviscosity syndrome
•Impaired renal autoregulatory responses – Impaired renal autoregulatory responses –
cyclooxygenase inhibitorscyclooxygenase inhibitors
•Systemic vasodilation – sepsis, Systemic vasodilation – sepsis,
anaphylaxisanaphylaxis
•DICDIC
•Renal vasoconstriction – cyclosporine, Renal vasoconstriction – cyclosporine,
norepinephrine, epinephrine, amphotericin norepinephrine, epinephrine, amphotericin
B, etcB, etc
•Hyperviscosity syndromeHyperviscosity syndrome
•Impaired renal autoregulatory responses – Impaired renal autoregulatory responses –
cyclooxygenase inhibitorscyclooxygenase inhibitors
Causes of Nephrotoxic ATNCauses of Nephrotoxic ATN
The kidney is a good target for toxins. Not The kidney is a good target for toxins. Not
only does it have a rich blood supply, only does it have a rich blood supply,
receiving 25% of CO, but it also helps in receiving 25% of CO, but it also helps in
the excretion of these toxins by the excretion of these toxins by
glomerular filtration and tubular secretion.glomerular filtration and tubular secretion.
The kidney is a good target for toxins. Not The kidney is a good target for toxins. Not
only does it have a rich blood supply, only does it have a rich blood supply,
receiving 25% of CO, but it also helps in receiving 25% of CO, but it also helps in
the excretion of these toxins by the excretion of these toxins by
glomerular filtration and tubular secretion.glomerular filtration and tubular secretion.
Exogenous toxinsExogenous toxins
Aminoglycosides:Aminoglycosides:
•10-30% of patients getting aminoglycosides 10-30% of patients getting aminoglycosides
develop ATN. develop ATN.
•Risk factors include preexisting liver disease, Risk factors include preexisting liver disease,
renal disease, concomitant use of other renal disease, concomitant use of other
nephrotoxins, advanced age, shock, female sex nephrotoxins, advanced age, shock, female sex
and a higher level 1 hr after the dose.and a higher level 1 hr after the dose.
•Toxicity presumably more common with 3 Toxicity presumably more common with 3
doses/day than a single daily dose (as the drug doses/day than a single daily dose (as the drug
uptake by tubules is saturable phenomenon).uptake by tubules is saturable phenomenon).
Amphotericin B:Amphotericin B: The likelihood of toxicity is in direct The likelihood of toxicity is in direct
proportion to the total dose administered and is proportion to the total dose administered and is
more common if > 3 grams is administered.more common if > 3 grams is administered.
Aminoglycosides:Aminoglycosides:
•10-30% of patients getting aminoglycosides 10-30% of patients getting aminoglycosides
develop ATN. develop ATN.
•Risk factors include preexisting liver disease, Risk factors include preexisting liver disease,
renal disease, concomitant use of other renal disease, concomitant use of other
nephrotoxins, advanced age, shock, female sex nephrotoxins, advanced age, shock, female sex
and a higher level 1 hr after the dose.and a higher level 1 hr after the dose.
•Toxicity presumably more common with 3 Toxicity presumably more common with 3
doses/day than a single daily dose (as the drug doses/day than a single daily dose (as the drug
uptake by tubules is saturable phenomenon).uptake by tubules is saturable phenomenon).
Amphotericin B:Amphotericin B: The likelihood of toxicity is in direct The likelihood of toxicity is in direct
proportion to the total dose administered and is proportion to the total dose administered and is
more common if > 3 grams is administered.more common if > 3 grams is administered.
Exogenous ToxinsExogenous Toxins
Radiocontrast media:Radiocontrast media:
•Contrast-induced nephropathy has become a frequent Contrast-induced nephropathy has become a frequent
occurrence with increased number of studies requiring occurrence with increased number of studies requiring
contrast media like angiography, CT scan, etccontrast media like angiography, CT scan, etc
•Iodinated contrast media causes vasoconstriction as well as Iodinated contrast media causes vasoconstriction as well as
a direct toxic effects on tubular cells.a direct toxic effects on tubular cells.
•Patients at increased risk include diabetes, baseline renal Patients at increased risk include diabetes, baseline renal
insufficiency, large contrast load, history of HTN, older age insufficiency, large contrast load, history of HTN, older age
and presence of proteinuria.and presence of proteinuria.
Cyclosporine and tacrolimus:Cyclosporine and tacrolimus: Can cause ARF as well as chronic Can cause ARF as well as chronic
interstitial nephritis.interstitial nephritis.
Sulfa drugsSulfa drugs, , acycloviracyclovir and and indinavirindinavir cause ARF by tubular cause ARF by tubular
obstruction due to crystal formation in the tubular lumenobstruction due to crystal formation in the tubular lumen
Others:Others: Cisplatin, methotrexate and foscarnet, etc. Cisplatin, methotrexate and foscarnet, etc.
Radiocontrast media:Radiocontrast media:
•Contrast-induced nephropathy has become a frequent Contrast-induced nephropathy has become a frequent
occurrence with increased number of studies requiring occurrence with increased number of studies requiring
contrast media like angiography, CT scan, etccontrast media like angiography, CT scan, etc
•Iodinated contrast media causes vasoconstriction as well as Iodinated contrast media causes vasoconstriction as well as
a direct toxic effects on tubular cells.a direct toxic effects on tubular cells.
•Patients at increased risk include diabetes, baseline renal Patients at increased risk include diabetes, baseline renal
insufficiency, large contrast load, history of HTN, older age insufficiency, large contrast load, history of HTN, older age
and presence of proteinuria.and presence of proteinuria.
Cyclosporine and tacrolimus:Cyclosporine and tacrolimus: Can cause ARF as well as chronic Can cause ARF as well as chronic
interstitial nephritis.interstitial nephritis.
Sulfa drugsSulfa drugs, , acycloviracyclovir and and indinavirindinavir cause ARF by tubular cause ARF by tubular
obstruction due to crystal formation in the tubular lumenobstruction due to crystal formation in the tubular lumen
Others:Others: Cisplatin, methotrexate and foscarnet, etc. Cisplatin, methotrexate and foscarnet, etc.
Endogenous toxinsEndogenous toxins
MyoglobinuriaMyoglobinuria
•The breakdown of muscle (rhabdomyolysis), leading to The breakdown of muscle (rhabdomyolysis), leading to
myoglobinuria, occurs in many clinical settings like crush injuries, myoglobinuria, occurs in many clinical settings like crush injuries,
viral illness, cocaine, heavy exercise, alcoholism, seizures and viral illness, cocaine, heavy exercise, alcoholism, seizures and
certain medications. ATN can develop in small proportion of these certain medications. ATN can develop in small proportion of these
patients.patients.
•The exact mechanism of renal failure is not clearly understood, The exact mechanism of renal failure is not clearly understood,
but several theories include direct toxic injury, development of but several theories include direct toxic injury, development of
DIC, mechanical tubular obstruction by the pigment and intrarenal DIC, mechanical tubular obstruction by the pigment and intrarenal
ischemia from vasomediator release.ischemia from vasomediator release.
•Factors that increase the risk of ATN in this setting include Factors that increase the risk of ATN in this setting include
extracellular fluid volume depletion, liver dysfunction and extracellular fluid volume depletion, liver dysfunction and
hypotension.hypotension.
HemoglobinuriaHemoglobinuria
ARF is a rare complication of hemolysis and hemoglobinuria and is ARF is a rare complication of hemolysis and hemoglobinuria and is
most often associated with transfusion reactions. Hemoglobin has most often associated with transfusion reactions. Hemoglobin has
no apparent direct toxicity on the cells and the renal failure in this no apparent direct toxicity on the cells and the renal failure in this
setting is probably related to hypotension and decrease renal setting is probably related to hypotension and decrease renal
perfusion.perfusion.
MyoglobinuriaMyoglobinuria
•The breakdown of muscle (rhabdomyolysis), leading to The breakdown of muscle (rhabdomyolysis), leading to
myoglobinuria, occurs in many clinical settings like crush injuries, myoglobinuria, occurs in many clinical settings like crush injuries,
viral illness, cocaine, heavy exercise, alcoholism, seizures and viral illness, cocaine, heavy exercise, alcoholism, seizures and
certain medications. ATN can develop in small proportion of these certain medications. ATN can develop in small proportion of these
patients.patients.
•The exact mechanism of renal failure is not clearly understood, The exact mechanism of renal failure is not clearly understood,
but several theories include direct toxic injury, development of but several theories include direct toxic injury, development of
DIC, mechanical tubular obstruction by the pigment and intrarenal DIC, mechanical tubular obstruction by the pigment and intrarenal
ischemia from vasomediator release.ischemia from vasomediator release.
•Factors that increase the risk of ATN in this setting include Factors that increase the risk of ATN in this setting include
extracellular fluid volume depletion, liver dysfunction and extracellular fluid volume depletion, liver dysfunction and
hypotension.hypotension.
HemoglobinuriaHemoglobinuria
ARF is a rare complication of hemolysis and hemoglobinuria and is ARF is a rare complication of hemolysis and hemoglobinuria and is
most often associated with transfusion reactions. Hemoglobin has most often associated with transfusion reactions. Hemoglobin has
no apparent direct toxicity on the cells and the renal failure in this no apparent direct toxicity on the cells and the renal failure in this
setting is probably related to hypotension and decrease renal setting is probably related to hypotension and decrease renal
perfusion.perfusion.
Endogenous ToxinsEndogenous Toxins
Crystals: Crystals:
Acute crystal-induced nephropathy is encountered in Acute crystal-induced nephropathy is encountered in
conditions where crystals are produced endogenously due conditions where crystals are produced endogenously due
to high cellular turnover (i.e. uric acid, calcium phosphate), to high cellular turnover (i.e. uric acid, calcium phosphate),
as seen in certain malignancies or the treatment of these as seen in certain malignancies or the treatment of these
malignancies (tumor lysis syndrome). However, this malignancies (tumor lysis syndrome). However, this
condition is also associated with ingestion of certain toxic condition is also associated with ingestion of certain toxic
substances, such as ethylene glycol. substances, such as ethylene glycol.
Multiple myeloma:Multiple myeloma:
This condition causes renal failure by several mechanisms, This condition causes renal failure by several mechanisms,
such as prerenal azotemia due to volume contraction, cast such as prerenal azotemia due to volume contraction, cast
nephropathy due to increased light chain proteins nephropathy due to increased light chain proteins
precipitated into the tubular lumen, hypercalcemia and uric precipitated into the tubular lumen, hypercalcemia and uric
acid nephropathy.acid nephropathy.
Crystals: Crystals:
Acute crystal-induced nephropathy is encountered in Acute crystal-induced nephropathy is encountered in
conditions where crystals are produced endogenously due conditions where crystals are produced endogenously due
to high cellular turnover (i.e. uric acid, calcium phosphate), to high cellular turnover (i.e. uric acid, calcium phosphate),
as seen in certain malignancies or the treatment of these as seen in certain malignancies or the treatment of these
malignancies (tumor lysis syndrome). However, this malignancies (tumor lysis syndrome). However, this
condition is also associated with ingestion of certain toxic condition is also associated with ingestion of certain toxic
substances, such as ethylene glycol. substances, such as ethylene glycol.
Multiple myeloma:Multiple myeloma:
This condition causes renal failure by several mechanisms, This condition causes renal failure by several mechanisms,
such as prerenal azotemia due to volume contraction, cast such as prerenal azotemia due to volume contraction, cast
nephropathy due to increased light chain proteins nephropathy due to increased light chain proteins
precipitated into the tubular lumen, hypercalcemia and uric precipitated into the tubular lumen, hypercalcemia and uric
acid nephropathy.acid nephropathy.
WorkupWorkup
Lab studiesLab studies
•Serum chemistries: By definition, BUN and serum Cr Serum chemistries: By definition, BUN and serum Cr
concentrations are increased. In addition, hyponatremia, concentrations are increased. In addition, hyponatremia,
hyperkalemia, hypermagnesemia, hypocalcemia, hyperkalemia, hypermagnesemia, hypocalcemia,
hyperphosphatemia and metabolic acidosis may be present. hyperphosphatemia and metabolic acidosis may be present.
Remember that hypercalcemia and hyperuricemia may Remember that hypercalcemia and hyperuricemia may
suggest a malignant condition as a cause.suggest a malignant condition as a cause.
•CBC: Pt may be anemic. Not only is erythropoietin CBC: Pt may be anemic. Not only is erythropoietin
production decreased but platelet dysfunction from uremia production decreased but platelet dysfunction from uremia
also makes bleeding more likely.also makes bleeding more likely.
•Urinalysis: May reveal muddy brown, granular casts and Urinalysis: May reveal muddy brown, granular casts and
epithelial cell casts. In addition, checking urine lytes may epithelial cell casts. In addition, checking urine lytes may
also help differentiate ATN from prerenal azotemia. also help differentiate ATN from prerenal azotemia.
Lab studiesLab studies
•Serum chemistries: By definition, BUN and serum Cr Serum chemistries: By definition, BUN and serum Cr
concentrations are increased. In addition, hyponatremia, concentrations are increased. In addition, hyponatremia,
hyperkalemia, hypermagnesemia, hypocalcemia, hyperkalemia, hypermagnesemia, hypocalcemia,
hyperphosphatemia and metabolic acidosis may be present. hyperphosphatemia and metabolic acidosis may be present.
Remember that hypercalcemia and hyperuricemia may Remember that hypercalcemia and hyperuricemia may
suggest a malignant condition as a cause.suggest a malignant condition as a cause.
•CBC: Pt may be anemic. Not only is erythropoietin CBC: Pt may be anemic. Not only is erythropoietin
production decreased but platelet dysfunction from uremia production decreased but platelet dysfunction from uremia
also makes bleeding more likely.also makes bleeding more likely.
•Urinalysis: May reveal muddy brown, granular casts and Urinalysis: May reveal muddy brown, granular casts and
epithelial cell casts. In addition, checking urine lytes may epithelial cell casts. In addition, checking urine lytes may
also help differentiate ATN from prerenal azotemia. also help differentiate ATN from prerenal azotemia.
Laboratory Findings Used to Laboratory Findings Used to
Differentiate Prerenal Azotemia Differentiate Prerenal Azotemia
from ATNfrom ATN
Differentiate Prerenal Azotemia Differentiate Prerenal Azotemia
from ATNfrom ATN
FindingFinding Prerenal Prerenal
AzotemiaAzotemia
ATNATN
Urine osmolarity Urine osmolarity
(mOsm/kg)(mOsm/kg)
>500>500 <350 <350
Urine sodium Urine sodium
(mmol/d)(mmol/d)
<20<20 >40>40
Fraction excretion Fraction excretion
of sodium(%)of sodium(%)
<1<1 >2>2
Fraction excretion Fraction excretion
of Urea(%)of Urea(%)
<35<35 >50>50
Plasma BUN/Cr Plasma BUN/Cr
ratioratio
>20>20 <10-15<10-15
Urine Cr/Plasma Cr Urine Cr/Plasma Cr
ratioratio
>40>40 <20<20
Urine sedimentUrine sediment Bland and/or Bland and/or
nonspecificnonspecific
May show muddy May show muddy
brown granular brown granular
castscasts
AzotemiaAzotemia
ATNATN
Urine osmolarity Urine osmolarity
(mOsm/kg)(mOsm/kg)
>500>500 <350 <350
Urine sodium Urine sodium
(mmol/d)(mmol/d)
<20<20 >40>40
Fraction excretion Fraction excretion
of sodium(%)of sodium(%)
<1<1 >2>2
Fraction excretion Fraction excretion
of Urea(%)of Urea(%)
<35<35 >50>50
Plasma BUN/Cr Plasma BUN/Cr
ratioratio
>20>20 <10-15<10-15
Urine Cr/Plasma Cr Urine Cr/Plasma Cr
ratioratio
>40>40 <20<20
Urine sedimentUrine sediment Bland and/or Bland and/or
nonspecificnonspecific
May show muddy May show muddy
brown granular brown granular
castscasts
Lab (continued…)Lab (continued…)
Loss of concentrating ability is an early and Loss of concentrating ability is an early and
almost universal finding in ATN.almost universal finding in ATN.
None of the above criteria for the diagnosis of None of the above criteria for the diagnosis of
prerenal disease may be present in a patient with prerenal disease may be present in a patient with
underlying renal disease. Hence, a cautious trial underlying renal disease. Hence, a cautious trial
of fluids may be given.of fluids may be given.
Loss of concentrating ability is an early and Loss of concentrating ability is an early and
almost universal finding in ATN.almost universal finding in ATN.
None of the above criteria for the diagnosis of None of the above criteria for the diagnosis of
prerenal disease may be present in a patient with prerenal disease may be present in a patient with
underlying renal disease. Hence, a cautious trial underlying renal disease. Hence, a cautious trial
of fluids may be given.of fluids may be given.
Imaging StudiesImaging Studies
Abdominal radiograph is of limited benefit Abdominal radiograph is of limited benefit
in ARF except in diagnosing (or excluding) in ARF except in diagnosing (or excluding)
nephrolithiasis.nephrolithiasis.
UltrasoundUltrasound,, CT scan CT scan, or, or MRI MRI very useful, very useful,
both to exclude obstructive uropathy and both to exclude obstructive uropathy and
measure renal size and cortical thickness. measure renal size and cortical thickness.
Renal USRenal US is a simple, relatively is a simple, relatively
inexpensive and non-invasive imaging inexpensive and non-invasive imaging
modality and should be done in all patients modality and should be done in all patients
presenting with ARF.presenting with ARF.
Abdominal radiograph is of limited benefit Abdominal radiograph is of limited benefit
in ARF except in diagnosing (or excluding) in ARF except in diagnosing (or excluding)
nephrolithiasis.nephrolithiasis.
UltrasoundUltrasound,, CT scan CT scan, or, or MRI MRI very useful, very useful,
both to exclude obstructive uropathy and both to exclude obstructive uropathy and
measure renal size and cortical thickness. measure renal size and cortical thickness.
Renal USRenal US is a simple, relatively is a simple, relatively
inexpensive and non-invasive imaging inexpensive and non-invasive imaging
modality and should be done in all patients modality and should be done in all patients
presenting with ARF.presenting with ARF.
Renal biopsyRenal biopsy
Biopsy is rarely necessary. It should only be performed when the Biopsy is rarely necessary. It should only be performed when the
exact renal cause of ARF is unclear, the course is protracted and exact renal cause of ARF is unclear, the course is protracted and
knowing the exact cause is possibly knowing the exact cause is possibly going to change the going to change the
management.management.
Needless to say, prerenal and postrenal causes must be ruled out Needless to say, prerenal and postrenal causes must be ruled out
before subjecting a patient to this invasive procedure. The before subjecting a patient to this invasive procedure. The
diagnosis of ATN is made on a clinical basis, i.e. with the help of diagnosis of ATN is made on a clinical basis, i.e. with the help of
detailed and accurate history, thorough physical exam, and detailed and accurate history, thorough physical exam, and
pertinent lab tests and imaging studies. pertinent lab tests and imaging studies.
A more urgent indication for renal biopsy is in the setting of A more urgent indication for renal biopsy is in the setting of
clinical and urinary findings suggestive of clinical and urinary findings suggestive of renal vasculitisrenal vasculitis rather rather
than ATN and the diagnosis needs to be established quickly so than ATN and the diagnosis needs to be established quickly so
that appropriate immunomodulatory therapy can be initiated. that appropriate immunomodulatory therapy can be initiated.
Biopsy may also be more critically important in a Biopsy may also be more critically important in a renal transplant renal transplant
patient to rule out rejection.patient to rule out rejection.
Other indications for biopsy include suspected Other indications for biopsy include suspected glomerulonephritisglomerulonephritis, ,
HUSHUS, , TTPTTP and and acute interstitial nephritisacute interstitial nephritis..
The biopsy is performed under ultrasound or CT guidance after The biopsy is performed under ultrasound or CT guidance after
ascertaining the safety of the procedure.ascertaining the safety of the procedure.
Biopsy is rarely necessary. It should only be performed when the Biopsy is rarely necessary. It should only be performed when the
exact renal cause of ARF is unclear, the course is protracted and exact renal cause of ARF is unclear, the course is protracted and
knowing the exact cause is possibly knowing the exact cause is possibly going to change the going to change the
management.management.
Needless to say, prerenal and postrenal causes must be ruled out Needless to say, prerenal and postrenal causes must be ruled out
before subjecting a patient to this invasive procedure. The before subjecting a patient to this invasive procedure. The
diagnosis of ATN is made on a clinical basis, i.e. with the help of diagnosis of ATN is made on a clinical basis, i.e. with the help of
detailed and accurate history, thorough physical exam, and detailed and accurate history, thorough physical exam, and
pertinent lab tests and imaging studies. pertinent lab tests and imaging studies.
A more urgent indication for renal biopsy is in the setting of A more urgent indication for renal biopsy is in the setting of
clinical and urinary findings suggestive of clinical and urinary findings suggestive of renal vasculitisrenal vasculitis rather rather
than ATN and the diagnosis needs to be established quickly so than ATN and the diagnosis needs to be established quickly so
that appropriate immunomodulatory therapy can be initiated. that appropriate immunomodulatory therapy can be initiated.
Biopsy may also be more critically important in a Biopsy may also be more critically important in a renal transplant renal transplant
patient to rule out rejection.patient to rule out rejection.
Other indications for biopsy include suspected Other indications for biopsy include suspected glomerulonephritisglomerulonephritis, ,
HUSHUS, , TTPTTP and and acute interstitial nephritisacute interstitial nephritis..
The biopsy is performed under ultrasound or CT guidance after The biopsy is performed under ultrasound or CT guidance after
ascertaining the safety of the procedure.ascertaining the safety of the procedure.
ComplicationsComplications
Patients with ATN can have several complications.Patients with ATN can have several complications.
Electrolyte abnormalitiesElectrolyte abnormalities
•Hyperkalemia: Higher levels are associated with ECG Hyperkalemia: Higher levels are associated with ECG
abnormalities (e.g. peaked T waves, prolonged PR interval, P abnormalities (e.g. peaked T waves, prolonged PR interval, P
wave flattening, widened QRS) and risk of developing life-wave flattening, widened QRS) and risk of developing life-
threatening arrhythmias (e.g. ventricular tachycardia or threatening arrhythmias (e.g. ventricular tachycardia or
fibrillation, complete heart block, bradycardia, asystole). fibrillation, complete heart block, bradycardia, asystole).
Arrhythmias have been reported in up to 30% of patients. In Arrhythmias have been reported in up to 30% of patients. In
addition to these worrisome cardiac effects, hyperkalemia can addition to these worrisome cardiac effects, hyperkalemia can
also lead to neuromuscular dysfunction and, potentially, also lead to neuromuscular dysfunction and, potentially,
respiratory failure.respiratory failure.
•HyponatremiaHyponatremia
•HyperphosphatemiaHyperphosphatemia
•HypermagnesemiaHypermagnesemia
•Hypocalcemia: Hypocalcemia may be secondary to both Hypocalcemia: Hypocalcemia may be secondary to both
deposition of calcium phosphate and reduced levels of 1,25 deposition of calcium phosphate and reduced levels of 1,25
dihydroxyvitamin D. It is usually asymptomatic, but dihydroxyvitamin D. It is usually asymptomatic, but
hypocalcemia may result in nonspecific ECG changes, muscle hypocalcemia may result in nonspecific ECG changes, muscle
cramps, or seizures.cramps, or seizures.
•Metabolic acidosisMetabolic acidosis
Patients with ATN can have several complications.Patients with ATN can have several complications.
Electrolyte abnormalitiesElectrolyte abnormalities
•Hyperkalemia: Higher levels are associated with ECG Hyperkalemia: Higher levels are associated with ECG
abnormalities (e.g. peaked T waves, prolonged PR interval, P abnormalities (e.g. peaked T waves, prolonged PR interval, P
wave flattening, widened QRS) and risk of developing life-wave flattening, widened QRS) and risk of developing life-
threatening arrhythmias (e.g. ventricular tachycardia or threatening arrhythmias (e.g. ventricular tachycardia or
fibrillation, complete heart block, bradycardia, asystole). fibrillation, complete heart block, bradycardia, asystole).
Arrhythmias have been reported in up to 30% of patients. In Arrhythmias have been reported in up to 30% of patients. In
addition to these worrisome cardiac effects, hyperkalemia can addition to these worrisome cardiac effects, hyperkalemia can
also lead to neuromuscular dysfunction and, potentially, also lead to neuromuscular dysfunction and, potentially,
respiratory failure.respiratory failure.
•HyponatremiaHyponatremia
•HyperphosphatemiaHyperphosphatemia
•HypermagnesemiaHypermagnesemia
•Hypocalcemia: Hypocalcemia may be secondary to both Hypocalcemia: Hypocalcemia may be secondary to both
deposition of calcium phosphate and reduced levels of 1,25 deposition of calcium phosphate and reduced levels of 1,25
dihydroxyvitamin D. It is usually asymptomatic, but dihydroxyvitamin D. It is usually asymptomatic, but
hypocalcemia may result in nonspecific ECG changes, muscle hypocalcemia may result in nonspecific ECG changes, muscle
cramps, or seizures.cramps, or seizures.
•Metabolic acidosisMetabolic acidosis
Complications Complications
IntravascularIntravascular volume overload:volume overload: It is characterized by weight gain, It is characterized by weight gain,
raised jugular venous pressure and dependent edema. In its most raised jugular venous pressure and dependent edema. In its most
severe manifestation, this may lead to respiratory failure from severe manifestation, this may lead to respiratory failure from
pulmonary edema.pulmonary edema.
Hypertension:Hypertension: Hypertension is suspected to mainly be due to salt Hypertension is suspected to mainly be due to salt
and water retention. About 25% of patients with ARF develop and water retention. About 25% of patients with ARF develop
some hypertension. some hypertension.
Uremic syndrome/Uremia:Uremic syndrome/Uremia: Uremia results from the accumulation Uremia results from the accumulation
of nitrogenous waste. It is a potentially life-threatening of nitrogenous waste. It is a potentially life-threatening
complication associated with ARF. complication associated with ARF.
•Platelet dysfunction is common and can lead to life-threatening Platelet dysfunction is common and can lead to life-threatening
hemorrhage.hemorrhage.
•This may manifest as pericardial disease (uremic pericarditis…This may manifest as pericardial disease (uremic pericarditis…
listen for a rub on exam)listen for a rub on exam)
•GI symptoms (i.e. nausea, vomiting, cramping)GI symptoms (i.e. nausea, vomiting, cramping)
•Neurological symptoms (i.e. lethargy, confusion, asterixis, Neurological symptoms (i.e. lethargy, confusion, asterixis,
seizures). seizures).
Anemia:Anemia: Anemia may develop from many possible causes. Anemia may develop from many possible causes.
Erythropoiesis is reduced in ARF, but platelet dysfunction is also Erythropoiesis is reduced in ARF, but platelet dysfunction is also
observed in the setting of uremia, which may predispose to observed in the setting of uremia, which may predispose to
hemorrhage. In addition, volume overload may lead to hemorrhage. In addition, volume overload may lead to
hemodilution, and red cell survival time may be decreased. hemodilution, and red cell survival time may be decreased.
IntravascularIntravascular volume overload:volume overload: It is characterized by weight gain, It is characterized by weight gain,
raised jugular venous pressure and dependent edema. In its most raised jugular venous pressure and dependent edema. In its most
severe manifestation, this may lead to respiratory failure from severe manifestation, this may lead to respiratory failure from
pulmonary edema.pulmonary edema.
Hypertension:Hypertension: Hypertension is suspected to mainly be due to salt Hypertension is suspected to mainly be due to salt
and water retention. About 25% of patients with ARF develop and water retention. About 25% of patients with ARF develop
some hypertension. some hypertension.
Uremic syndrome/Uremia:Uremic syndrome/Uremia: Uremia results from the accumulation Uremia results from the accumulation
of nitrogenous waste. It is a potentially life-threatening of nitrogenous waste. It is a potentially life-threatening
complication associated with ARF. complication associated with ARF.
•Platelet dysfunction is common and can lead to life-threatening Platelet dysfunction is common and can lead to life-threatening
hemorrhage.hemorrhage.
•This may manifest as pericardial disease (uremic pericarditis…This may manifest as pericardial disease (uremic pericarditis…
listen for a rub on exam)listen for a rub on exam)
•GI symptoms (i.e. nausea, vomiting, cramping)GI symptoms (i.e. nausea, vomiting, cramping)
•Neurological symptoms (i.e. lethargy, confusion, asterixis, Neurological symptoms (i.e. lethargy, confusion, asterixis,
seizures). seizures).
Anemia:Anemia: Anemia may develop from many possible causes. Anemia may develop from many possible causes.
Erythropoiesis is reduced in ARF, but platelet dysfunction is also Erythropoiesis is reduced in ARF, but platelet dysfunction is also
observed in the setting of uremia, which may predispose to observed in the setting of uremia, which may predispose to
hemorrhage. In addition, volume overload may lead to hemorrhage. In addition, volume overload may lead to
hemodilution, and red cell survival time may be decreased. hemodilution, and red cell survival time may be decreased.
Complications Complications
Polyuric phase of ATN:Polyuric phase of ATN: This complication can lead This complication can lead
to hypovolemia and create a setting for prerenal to hypovolemia and create a setting for prerenal
azotemia and perpetuation of ATN. azotemia and perpetuation of ATN.
Infections:Infections: Infections is the leading cause of Infections is the leading cause of
morbidity and mortality and can occur in 30-70% morbidity and mortality and can occur in 30-70%
of patients with ARF. Infections are more likely in of patients with ARF. Infections are more likely in
these patients because of an impaired immune these patients because of an impaired immune
system and because of increased use of system and because of increased use of
indwelling catheters and intravenous needles.indwelling catheters and intravenous needles.
Polyuric phase of ATN:Polyuric phase of ATN: This complication can lead This complication can lead
to hypovolemia and create a setting for prerenal to hypovolemia and create a setting for prerenal
azotemia and perpetuation of ATN. azotemia and perpetuation of ATN.
Infections:Infections: Infections is the leading cause of Infections is the leading cause of
morbidity and mortality and can occur in 30-70% morbidity and mortality and can occur in 30-70%
of patients with ARF. Infections are more likely in of patients with ARF. Infections are more likely in
these patients because of an impaired immune these patients because of an impaired immune
system and because of increased use of system and because of increased use of
indwelling catheters and intravenous needles.indwelling catheters and intravenous needles.
PreventionPrevention
Ischemic ATNIschemic ATN:: Be attentive to optimizing Be attentive to optimizing
cardiovascular function as well as maintaining cardiovascular function as well as maintaining
intravascular volume, especially in patients intravascular volume, especially in patients
with preexisting risk factors or those taking with preexisting risk factors or those taking
nephrotoxic medications. Medicines that reduce nephrotoxic medications. Medicines that reduce
systemic resistance (e.g. afterload reducers) systemic resistance (e.g. afterload reducers)
may cause renal vasoconstriction or affect the may cause renal vasoconstriction or affect the
kidney’s autoregulatory response (e.g. ACE kidney’s autoregulatory response (e.g. ACE
inhibitors, cyclooxygenase inhibitors) and also inhibitors, cyclooxygenase inhibitors) and also
should be used with caution.should be used with caution.
Dopamine, mannitol and furosemide, etc have Dopamine, mannitol and furosemide, etc have
been tried within 24 hrs of ischemic insult to been tried within 24 hrs of ischemic insult to
prevent progression to ATN, but have no prevent progression to ATN, but have no
proven benefit.proven benefit.
Ischemic ATNIschemic ATN:: Be attentive to optimizing Be attentive to optimizing
cardiovascular function as well as maintaining cardiovascular function as well as maintaining
intravascular volume, especially in patients intravascular volume, especially in patients
with preexisting risk factors or those taking with preexisting risk factors or those taking
nephrotoxic medications. Medicines that reduce nephrotoxic medications. Medicines that reduce
systemic resistance (e.g. afterload reducers) systemic resistance (e.g. afterload reducers)
may cause renal vasoconstriction or affect the may cause renal vasoconstriction or affect the
kidney’s autoregulatory response (e.g. ACE kidney’s autoregulatory response (e.g. ACE
inhibitors, cyclooxygenase inhibitors) and also inhibitors, cyclooxygenase inhibitors) and also
should be used with caution.should be used with caution.
Dopamine, mannitol and furosemide, etc have Dopamine, mannitol and furosemide, etc have
been tried within 24 hrs of ischemic insult to been tried within 24 hrs of ischemic insult to
prevent progression to ATN, but have no prevent progression to ATN, but have no
proven benefit.proven benefit.
PreventionPrevention
•Nephrotoxic ATNNephrotoxic ATN
AminoglycosidesAminoglycosides: Once daily dosing of : Once daily dosing of
aminoglycosides decreases the aminoglycosides decreases the
incidence of nephrotoxicity. incidence of nephrotoxicity.
Amphotericin BAmphotericin B: Minimize the use of : Minimize the use of
this drug and assure that ECF volume this drug and assure that ECF volume
is adequate. is adequate.
Cyclosporin and tacrolimusCyclosporin and tacrolimus: Regular : Regular
monitoring of blood levels. monitoring of blood levels.
Alkalinization of the urine should be Alkalinization of the urine should be
tried in patients with marked tried in patients with marked
myoglobinuria and hemoglobinuria.myoglobinuria and hemoglobinuria.
•Nephrotoxic ATNNephrotoxic ATN
AminoglycosidesAminoglycosides: Once daily dosing of : Once daily dosing of
aminoglycosides decreases the aminoglycosides decreases the
incidence of nephrotoxicity. incidence of nephrotoxicity.
Amphotericin BAmphotericin B: Minimize the use of : Minimize the use of
this drug and assure that ECF volume this drug and assure that ECF volume
is adequate. is adequate.
Cyclosporin and tacrolimusCyclosporin and tacrolimus: Regular : Regular
monitoring of blood levels. monitoring of blood levels.
Alkalinization of the urine should be Alkalinization of the urine should be
tried in patients with marked tried in patients with marked
myoglobinuria and hemoglobinuria.myoglobinuria and hemoglobinuria.
PreventionPrevention
Radiocontrast dyeRadiocontrast dye: Out of all the agents/modalities : Out of all the agents/modalities
that have been investigated for prevention of CIN, only that have been investigated for prevention of CIN, only
the following have been shown to be of some benefit:the following have been shown to be of some benefit:
11..HydrationHydration with isotonic saline infusion has proven with isotonic saline infusion has proven
benefits in prevention of contrast-induced nephropathy. benefits in prevention of contrast-induced nephropathy.
Typically, half isotonic sodium chloride solution Typically, half isotonic sodium chloride solution
(0.45%) administered at a rate of 50-100 mL/h 12 (0.45%) administered at a rate of 50-100 mL/h 12
hours before and 12 hours after the administration of hours before and 12 hours after the administration of
the dye load is most effective, especially in the setting the dye load is most effective, especially in the setting
of prior renal insufficiency and diabetes mellitus.of prior renal insufficiency and diabetes mellitus.
2. 2. Low osmolal and iso-osmolalLow osmolal and iso-osmolal nonionic contrastnonionic contrast media media
are also associated with lower incidence of CIN. are also associated with lower incidence of CIN.
3. 3. NN-acetylcysteine-acetylcysteine has been used with success in high- has been used with success in high-
risk patients to prevent contrast-induced risk patients to prevent contrast-induced
nephrotoxicity. nephrotoxicity.
4. Using 4. Using lower doses of contrast medialower doses of contrast media, , avoiding volume avoiding volume
depletion and NSAIDsdepletion and NSAIDs,, both of which can cause renal both of which can cause renal
vasoconstriction are some other useful measures. vasoconstriction are some other useful measures.
5. A new modality recently investigated is use of 5. A new modality recently investigated is use of
prophylacticprophylactic hemofiltrationhemofiltration in patients who need in patients who need
contrast and have baseline renal insufficiency.contrast and have baseline renal insufficiency.
Radiocontrast dyeRadiocontrast dye: Out of all the agents/modalities : Out of all the agents/modalities
that have been investigated for prevention of CIN, only that have been investigated for prevention of CIN, only
the following have been shown to be of some benefit:the following have been shown to be of some benefit:
11..HydrationHydration with isotonic saline infusion has proven with isotonic saline infusion has proven
benefits in prevention of contrast-induced nephropathy. benefits in prevention of contrast-induced nephropathy.
Typically, half isotonic sodium chloride solution Typically, half isotonic sodium chloride solution
(0.45%) administered at a rate of 50-100 mL/h 12 (0.45%) administered at a rate of 50-100 mL/h 12
hours before and 12 hours after the administration of hours before and 12 hours after the administration of
the dye load is most effective, especially in the setting the dye load is most effective, especially in the setting
of prior renal insufficiency and diabetes mellitus.of prior renal insufficiency and diabetes mellitus.
2. 2. Low osmolal and iso-osmolalLow osmolal and iso-osmolal nonionic contrastnonionic contrast media media
are also associated with lower incidence of CIN. are also associated with lower incidence of CIN.
3. 3. NN-acetylcysteine-acetylcysteine has been used with success in high- has been used with success in high-
risk patients to prevent contrast-induced risk patients to prevent contrast-induced
nephrotoxicity. nephrotoxicity.
4. Using 4. Using lower doses of contrast medialower doses of contrast media, , avoiding volume avoiding volume
depletion and NSAIDsdepletion and NSAIDs,, both of which can cause renal both of which can cause renal
vasoconstriction are some other useful measures. vasoconstriction are some other useful measures.
5. A new modality recently investigated is use of 5. A new modality recently investigated is use of
prophylacticprophylactic hemofiltrationhemofiltration in patients who need in patients who need
contrast and have baseline renal insufficiency.contrast and have baseline renal insufficiency.
The Prevention of Radiocontrast-Agent–Induced
Nephropathy by Hemofiltration
Giancarlo Marenzi, M.D., et al.
NEJM October 2
nd
, 2003.
114 consecutive patients with chronic renal failure (serum creatinine
concentration, >2 mg/dl, who were undergoing coronary interventions, were
Randomly assigned to either hemofiltration in an intensive care unit (ICU) or
isotonic-saline hydration at a rate of 1 ml per kilogram of body weight per
hour given in a step-down unit. Hemofiltration and saline hydration were
initiated 4 to 8 hours before the coronary intervention and were continued for
18 to 24 hours after the procedure was completed.
Results: Compared with intravenous saline, hemofiltration was associated
with the following significant benefits
1. A lesser likelihood of an increase in the serum creatinine concentration of
greater than 25 percent from baseline values (5 versus 50 percent)
2. A lesser likelihood of requirement for temporary renal replacement
therapy (3 versus 25 percent)
3. A reduction in both in-house mortality (2 versus 14 percent) and one-year
mortality (10 versus 30 percent).
4. Greatest benefit was seen in patients with higher Cr (>4 mg/dl).
Until additional data are available, routine use of hemofiltration for prevention of
CIN is not recommended. However, consideration should be given to the use of
hemofiltration (in combination with other preventive measures) among patients at highest
risk of contrast nephropathy, particularly the diabetic patient with a baseline serum
creatinine concentration of 4 mg/dL or greater.
Nephropathy by Hemofiltration
Giancarlo Marenzi, M.D., et al.
NEJM October 2
nd
, 2003.
114 consecutive patients with chronic renal failure (serum creatinine
concentration, >2 mg/dl, who were undergoing coronary interventions, were
Randomly assigned to either hemofiltration in an intensive care unit (ICU) or
isotonic-saline hydration at a rate of 1 ml per kilogram of body weight per
hour given in a step-down unit. Hemofiltration and saline hydration were
initiated 4 to 8 hours before the coronary intervention and were continued for
18 to 24 hours after the procedure was completed.
Results: Compared with intravenous saline, hemofiltration was associated
with the following significant benefits
1. A lesser likelihood of an increase in the serum creatinine concentration of
greater than 25 percent from baseline values (5 versus 50 percent)
2. A lesser likelihood of requirement for temporary renal replacement
therapy (3 versus 25 percent)
3. A reduction in both in-house mortality (2 versus 14 percent) and one-year
mortality (10 versus 30 percent).
4. Greatest benefit was seen in patients with higher Cr (>4 mg/dl).
Until additional data are available, routine use of hemofiltration for prevention of
CIN is not recommended. However, consideration should be given to the use of
hemofiltration (in combination with other preventive measures) among patients at highest
risk of contrast nephropathy, particularly the diabetic patient with a baseline serum
creatinine concentration of 4 mg/dL or greater.
TreatmentTreatment
General treatmentGeneral treatment
The main goal of treatment is to prevent further injury to The main goal of treatment is to prevent further injury to
the kidney. ECF volume should be assessed promptly, the kidney. ECF volume should be assessed promptly,
either on clinical grounds or by invasive means (Swan-either on clinical grounds or by invasive means (Swan-
Ganz catheter), and repletion of any deficit should be Ganz catheter), and repletion of any deficit should be
initiated promptly. A renal ultrasound should be performed initiated promptly. A renal ultrasound should be performed
to exclude obstruction. to exclude obstruction.
All possible nephrotoxic drugs should be stopped. All possible nephrotoxic drugs should be stopped.
In general, an attempt is made to increase the urine output In general, an attempt is made to increase the urine output
if oliguria is present, by using loop diuretics, although there if oliguria is present, by using loop diuretics, although there
is some controversy about this in the literature. One is some controversy about this in the literature. One
retrospective study showed that diuretics may even retrospective study showed that diuretics may even
increase the risk of death and non-recovery of renal increase the risk of death and non-recovery of renal
function. function. OnlyOnly use diuretics use diuretics ifif ECF volume and cardiac ECF volume and cardiac
function are first carefully assessed and found adequate.function are first carefully assessed and found adequate.
The only true The only true indicationindication for diuretic use is for diuretic use is volume overloadvolume overload. .
Furosemide and bumetanide are the commonly used Furosemide and bumetanide are the commonly used
diuretics. diuretics.
General treatmentGeneral treatment
The main goal of treatment is to prevent further injury to The main goal of treatment is to prevent further injury to
the kidney. ECF volume should be assessed promptly, the kidney. ECF volume should be assessed promptly,
either on clinical grounds or by invasive means (Swan-either on clinical grounds or by invasive means (Swan-
Ganz catheter), and repletion of any deficit should be Ganz catheter), and repletion of any deficit should be
initiated promptly. A renal ultrasound should be performed initiated promptly. A renal ultrasound should be performed
to exclude obstruction. to exclude obstruction.
All possible nephrotoxic drugs should be stopped. All possible nephrotoxic drugs should be stopped.
In general, an attempt is made to increase the urine output In general, an attempt is made to increase the urine output
if oliguria is present, by using loop diuretics, although there if oliguria is present, by using loop diuretics, although there
is some controversy about this in the literature. One is some controversy about this in the literature. One
retrospective study showed that diuretics may even retrospective study showed that diuretics may even
increase the risk of death and non-recovery of renal increase the risk of death and non-recovery of renal
function. function. OnlyOnly use diuretics use diuretics ifif ECF volume and cardiac ECF volume and cardiac
function are first carefully assessed and found adequate.function are first carefully assessed and found adequate.
The only true The only true indicationindication for diuretic use is for diuretic use is volume overloadvolume overload. .
Furosemide and bumetanide are the commonly used Furosemide and bumetanide are the commonly used
diuretics. diuretics.
Treatment Treatment
Aggressively treat any complications that develop. Aggressively treat any complications that develop.
Remember that sepsis is a common cause of death Remember that sepsis is a common cause of death
with severe ARF, so aggressive treatment of with severe ARF, so aggressive treatment of
infections is prudent. However, prophylactic antibiotic infections is prudent. However, prophylactic antibiotic
has not been proven to be of any benefit.has not been proven to be of any benefit.
Also, adjust doses of all medications if the kidney Also, adjust doses of all medications if the kidney
eliminates them.eliminates them.
Various agents have been studied for their possible Various agents have been studied for their possible
role in hastening tubular regeneration and functional role in hastening tubular regeneration and functional
recovery in ATN including growth factors (IGF-I), low recovery in ATN including growth factors (IGF-I), low
dose DA, combination of DA and ANP and anaritide (a dose DA, combination of DA and ANP and anaritide (a
synthetic form of ANP) but have shown no benefit in synthetic form of ANP) but have shown no benefit in
recovery or survival.recovery or survival.
Aggressively treat any complications that develop. Aggressively treat any complications that develop.
Remember that sepsis is a common cause of death Remember that sepsis is a common cause of death
with severe ARF, so aggressive treatment of with severe ARF, so aggressive treatment of
infections is prudent. However, prophylactic antibiotic infections is prudent. However, prophylactic antibiotic
has not been proven to be of any benefit.has not been proven to be of any benefit.
Also, adjust doses of all medications if the kidney Also, adjust doses of all medications if the kidney
eliminates them.eliminates them.
Various agents have been studied for their possible Various agents have been studied for their possible
role in hastening tubular regeneration and functional role in hastening tubular regeneration and functional
recovery in ATN including growth factors (IGF-I), low recovery in ATN including growth factors (IGF-I), low
dose DA, combination of DA and ANP and anaritide (a dose DA, combination of DA and ANP and anaritide (a
synthetic form of ANP) but have shown no benefit in synthetic form of ANP) but have shown no benefit in
recovery or survival.recovery or survival.
Treatment Treatment
Dialysis treatmentDialysis treatment
In general, no clear consensus is established on In general, no clear consensus is established on
when or how often to perform hemodialysis in the when or how often to perform hemodialysis in the
setting of ARF. Some studies have suggested that setting of ARF. Some studies have suggested that
early initiation may be beneficial, but, in one early initiation may be beneficial, but, in one
prospective trial, aggressive dialysis did not improve prospective trial, aggressive dialysis did not improve
recovery or survival rates. However, hemodialysis is recovery or survival rates. However, hemodialysis is
still considered standard therapy in severe ARF. In still considered standard therapy in severe ARF. In
addition, continuous hemodialysis (continuous addition, continuous hemodialysis (continuous
venovenous hemofiltration [CVVHD] and continuous venovenous hemofiltration [CVVHD] and continuous
arteriovenous hemofiltration with dialysis (CAVHD) arteriovenous hemofiltration with dialysis (CAVHD)
and peritoneal dialysis are also available. No and peritoneal dialysis are also available. No
compelling studies suggest that one mode is better compelling studies suggest that one mode is better
than another. In general, patients with multiorgan than another. In general, patients with multiorgan
failure and hemodynamic instability may benefit from failure and hemodynamic instability may benefit from
a continuous mode because it is typically less taxing a continuous mode because it is typically less taxing
on the hemodynamics. on the hemodynamics.
Indications for dialysisIndications for dialysis: Clinical evidence of uremia, : Clinical evidence of uremia,
intractable intravascular volume overload, intractable intravascular volume overload,
hyperkalemia or severe acidosis resistant to hyperkalemia or severe acidosis resistant to
conservative measures.conservative measures.
Dialysis treatmentDialysis treatment
In general, no clear consensus is established on In general, no clear consensus is established on
when or how often to perform hemodialysis in the when or how often to perform hemodialysis in the
setting of ARF. Some studies have suggested that setting of ARF. Some studies have suggested that
early initiation may be beneficial, but, in one early initiation may be beneficial, but, in one
prospective trial, aggressive dialysis did not improve prospective trial, aggressive dialysis did not improve
recovery or survival rates. However, hemodialysis is recovery or survival rates. However, hemodialysis is
still considered standard therapy in severe ARF. In still considered standard therapy in severe ARF. In
addition, continuous hemodialysis (continuous addition, continuous hemodialysis (continuous
venovenous hemofiltration [CVVHD] and continuous venovenous hemofiltration [CVVHD] and continuous
arteriovenous hemofiltration with dialysis (CAVHD) arteriovenous hemofiltration with dialysis (CAVHD)
and peritoneal dialysis are also available. No and peritoneal dialysis are also available. No
compelling studies suggest that one mode is better compelling studies suggest that one mode is better
than another. In general, patients with multiorgan than another. In general, patients with multiorgan
failure and hemodynamic instability may benefit from failure and hemodynamic instability may benefit from
a continuous mode because it is typically less taxing a continuous mode because it is typically less taxing
on the hemodynamics. on the hemodynamics.
Indications for dialysisIndications for dialysis: Clinical evidence of uremia, : Clinical evidence of uremia,
intractable intravascular volume overload, intractable intravascular volume overload,
hyperkalemia or severe acidosis resistant to hyperkalemia or severe acidosis resistant to
conservative measures.conservative measures.
Treatment of ComplicationsTreatment of Complications
Volume overload:Volume overload: Salt and water restriction, diuretics. Salt and water restriction, diuretics.
Dialysis for refractory cases.Dialysis for refractory cases.
Hyperkalemia:Hyperkalemia: Restrict potassium intake, glucose and Restrict potassium intake, glucose and
insulin, sodium bicarbonate, kayexalate, calcium gluconate, insulin, sodium bicarbonate, kayexalate, calcium gluconate,
dialysis.dialysis.
Metabolic acidosis:Metabolic acidosis: Sodium bicarb (only if HCO3 Sodium bicarb (only if HCO3
<15mmol/L or pH<7.2) or dialysis.<15mmol/L or pH<7.2) or dialysis.
Hypocalcemia:Hypocalcemia: Calcium carbonate, calcium gluconate. Calcium carbonate, calcium gluconate.
Infections:Infections: Antibiotics, assess the IV sites. Antibiotics, assess the IV sites.
Hyponatremia:Hyponatremia: Free water restriction. Free water restriction.
Hyperphosphatemia:Hyperphosphatemia: Restrict phosphate intake, phosphate Restrict phosphate intake, phosphate
binding agents.binding agents.
Hypermagnesemia:Hypermagnesemia: Avoid Mg containing antacids. Avoid Mg containing antacids.
Anemia:Anemia: Blood transfusion may be required. Blood transfusion may be required.
Volume overload:Volume overload: Salt and water restriction, diuretics. Salt and water restriction, diuretics.
Dialysis for refractory cases.Dialysis for refractory cases.
Hyperkalemia:Hyperkalemia: Restrict potassium intake, glucose and Restrict potassium intake, glucose and
insulin, sodium bicarbonate, kayexalate, calcium gluconate, insulin, sodium bicarbonate, kayexalate, calcium gluconate,
dialysis.dialysis.
Metabolic acidosis:Metabolic acidosis: Sodium bicarb (only if HCO3 Sodium bicarb (only if HCO3
<15mmol/L or pH<7.2) or dialysis.<15mmol/L or pH<7.2) or dialysis.
Hypocalcemia:Hypocalcemia: Calcium carbonate, calcium gluconate. Calcium carbonate, calcium gluconate.
Infections:Infections: Antibiotics, assess the IV sites. Antibiotics, assess the IV sites.
Hyponatremia:Hyponatremia: Free water restriction. Free water restriction.
Hyperphosphatemia:Hyperphosphatemia: Restrict phosphate intake, phosphate Restrict phosphate intake, phosphate
binding agents.binding agents.
Hypermagnesemia:Hypermagnesemia: Avoid Mg containing antacids. Avoid Mg containing antacids.
Anemia:Anemia: Blood transfusion may be required. Blood transfusion may be required.
NutritionNutrition
Clearly, the maintenance of fluid and electrolyte Clearly, the maintenance of fluid and electrolyte
balance is critical. Aggressive and early balance is critical. Aggressive and early
nutritional support also improves survival rates. nutritional support also improves survival rates.
Adequate caloric intake is essential to avoid Adequate caloric intake is essential to avoid
catabolism and starvation ketoacidosis, while catabolism and starvation ketoacidosis, while
minimizing production of nitrogenous waste. This minimizing production of nitrogenous waste. This
is best achieved by restricting dietary protein to is best achieved by restricting dietary protein to
approximately 0.6g/kg/day of protein of high approximately 0.6g/kg/day of protein of high
biologic value (rich in essential amino acids) and biologic value (rich in essential amino acids) and
provide most calories as carbohydrate provide most calories as carbohydrate
(approximately 100 g/day). (approximately 100 g/day).
Enteral hyperalimentation or parenteral nutrition Enteral hyperalimentation or parenteral nutrition
if recovery prolonged or if patient very catabolic.if recovery prolonged or if patient very catabolic.
Clearly, the maintenance of fluid and electrolyte Clearly, the maintenance of fluid and electrolyte
balance is critical. Aggressive and early balance is critical. Aggressive and early
nutritional support also improves survival rates. nutritional support also improves survival rates.
Adequate caloric intake is essential to avoid Adequate caloric intake is essential to avoid
catabolism and starvation ketoacidosis, while catabolism and starvation ketoacidosis, while
minimizing production of nitrogenous waste. This minimizing production of nitrogenous waste. This
is best achieved by restricting dietary protein to is best achieved by restricting dietary protein to
approximately 0.6g/kg/day of protein of high approximately 0.6g/kg/day of protein of high
biologic value (rich in essential amino acids) and biologic value (rich in essential amino acids) and
provide most calories as carbohydrate provide most calories as carbohydrate
(approximately 100 g/day). (approximately 100 g/day).
Enteral hyperalimentation or parenteral nutrition Enteral hyperalimentation or parenteral nutrition
if recovery prolonged or if patient very catabolic.if recovery prolonged or if patient very catabolic.
Mortality and MorbidityMortality and Morbidity
The The in-hospitalin-hospital survival rate of patients with ATN survival rate of patients with ATN
is about is about 50%50%, with , with 30%30% surviving for surviving for 1 year1 year. .
Factors associated with increased mortalityFactors associated with increased mortality
include:include: poor nutrition status, male sex, the poor nutrition status, male sex, the
presence of oliguria, need for mechanical presence of oliguria, need for mechanical
ventilation, chronic immunosuppression, acute ventilation, chronic immunosuppression, acute
MI, stroke or seizures.MI, stroke or seizures.
The presence of renal failure itself seems to be a The presence of renal failure itself seems to be a
prognostic factor in survival since it weakens prognostic factor in survival since it weakens
immune system and impairs platelet function immune system and impairs platelet function
thus predisposing the patient to sepsis and thus predisposing the patient to sepsis and
bleeding.bleeding.
The The in-hospitalin-hospital survival rate of patients with ATN survival rate of patients with ATN
is about is about 50%50%, with , with 30%30% surviving for surviving for 1 year1 year. .
Factors associated with increased mortalityFactors associated with increased mortality
include:include: poor nutrition status, male sex, the poor nutrition status, male sex, the
presence of oliguria, need for mechanical presence of oliguria, need for mechanical
ventilation, chronic immunosuppression, acute ventilation, chronic immunosuppression, acute
MI, stroke or seizures.MI, stroke or seizures.
The presence of renal failure itself seems to be a The presence of renal failure itself seems to be a
prognostic factor in survival since it weakens prognostic factor in survival since it weakens
immune system and impairs platelet function immune system and impairs platelet function
thus predisposing the patient to sepsis and thus predisposing the patient to sepsis and
bleeding.bleeding.
Mortality and MorbidityMortality and Morbidity
Infections remain the leading cause of death.Infections remain the leading cause of death.
For ARF the mortality rate is For ARF the mortality rate is 20-50%20-50% in patients with in patients with
underlying underlying medical illnessesmedical illnesses, but the mortality rate is as , but the mortality rate is as
high as high as 60-70%60-70% with patients in a with patients in a surgical settingsurgical setting or with or with
severe trauma. severe trauma. If If multiorgan failuremultiorgan failure is present, especially is present, especially
severe hypotension or acute respiratory distress syndrome, severe hypotension or acute respiratory distress syndrome,
the mortality rate ranges from the mortality rate ranges from 50-80%50-80%. .
With dialysis intervention, the frequency of uremia, With dialysis intervention, the frequency of uremia,
hyperkalemia, and volume overload as causes of death hyperkalemia, and volume overload as causes of death
have decreased. have decreased. The most common causes of death now The most common causes of death now
are sepsis, cardiovascular and pulmonary dysfunction, and are sepsis, cardiovascular and pulmonary dysfunction, and
withdrawal of life support. withdrawal of life support.
The type of dialysis membrane utilized during HD may also The type of dialysis membrane utilized during HD may also
affect prognosis.affect prognosis.
Infections remain the leading cause of death.Infections remain the leading cause of death.
For ARF the mortality rate is For ARF the mortality rate is 20-50%20-50% in patients with in patients with
underlying underlying medical illnessesmedical illnesses, but the mortality rate is as , but the mortality rate is as
high as high as 60-70%60-70% with patients in a with patients in a surgical settingsurgical setting or with or with
severe trauma. severe trauma. If If multiorgan failuremultiorgan failure is present, especially is present, especially
severe hypotension or acute respiratory distress syndrome, severe hypotension or acute respiratory distress syndrome,
the mortality rate ranges from the mortality rate ranges from 50-80%50-80%. .
With dialysis intervention, the frequency of uremia, With dialysis intervention, the frequency of uremia,
hyperkalemia, and volume overload as causes of death hyperkalemia, and volume overload as causes of death
have decreased. have decreased. The most common causes of death now The most common causes of death now
are sepsis, cardiovascular and pulmonary dysfunction, and are sepsis, cardiovascular and pulmonary dysfunction, and
withdrawal of life support. withdrawal of life support.
The type of dialysis membrane utilized during HD may also The type of dialysis membrane utilized during HD may also
affect prognosis.affect prognosis.
PrognosisPrognosis
Patients with Patients with oliguric ATNoliguric ATN have a have a worse prognosisworse prognosis
than patients with nonoliguric ATN. This probably than patients with nonoliguric ATN. This probably
is related to more severe necrosis and more is related to more severe necrosis and more
significant disturbances in electrolyte balance.significant disturbances in electrolyte balance.
Rapid increase in serum creatinineRapid increase in serum creatinine (i.e. >3 (i.e. >3
mg/dL) probably also indicates a mg/dL) probably also indicates a poorer poorer
prognosisprognosis. Again, this probably reflects more . Again, this probably reflects more
serious underlying disease.serious underlying disease.
Of the survivors of ATN, approximately Of the survivors of ATN, approximately 50% have 50% have
residual subclinical impairment of renal functionresidual subclinical impairment of renal function, ,
aboutabout 5% 5% continue to undergo a decline in renal continue to undergo a decline in renal
function function following an initialfollowing an initial recovery phase and recovery phase and
about about 5%5% never recover never recover kidney function and kidney function and
require dialysisrequire dialysis..
Patients with Patients with oliguric ATNoliguric ATN have a have a worse prognosisworse prognosis
than patients with nonoliguric ATN. This probably than patients with nonoliguric ATN. This probably
is related to more severe necrosis and more is related to more severe necrosis and more
significant disturbances in electrolyte balance.significant disturbances in electrolyte balance.
Rapid increase in serum creatinineRapid increase in serum creatinine (i.e. >3 (i.e. >3
mg/dL) probably also indicates a mg/dL) probably also indicates a poorer poorer
prognosisprognosis. Again, this probably reflects more . Again, this probably reflects more
serious underlying disease.serious underlying disease.
Of the survivors of ATN, approximately Of the survivors of ATN, approximately 50% have 50% have
residual subclinical impairment of renal functionresidual subclinical impairment of renal function, ,
aboutabout 5% 5% continue to undergo a decline in renal continue to undergo a decline in renal
function function following an initialfollowing an initial recovery phase and recovery phase and
about about 5%5% never recover never recover kidney function and kidney function and
require dialysisrequire dialysis..
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