Acute Kidney Injury.ppt

Notes for all medical student

1. ACUTE RENAL FAILURE
DR.HARO TADELE (MD)

2. ARF… definition
It is as a rapid (within 48 hours) decline in renal
function characterized by progressive azotaemia,
which may or may not be accompanied by oliguria.
Quantitatively, it is a measurable increase in the
serum creatinine (Cr) concentration of 50% or
absolute increase by 0.5-1.0 mg/dL.
Currently, Acute kidney injury (AKI) is a preferred
nomenclature over acute renal failure (ARF).
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3. Definition…
Oliguric ARF –urine volume <400ml/d
Non-oliguric –urine volume >400ml/d
Anuric –UV<100ml/d
Uremia –clinical syndrome resulting from the
adverse effect of renal failure on other organ systems.
Azotemia –refers to retention of nitrogen waste
products due to renal insufficiency.
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4. Epidemiology
ARF is a common problem in the contemporary
practice of hospital-based medicine.
It complicates ~ 5–7% of hospital admissions and up
to 30% of admissions to ICU.
ARF is associated with significant in-hospital
morbidity and mortality.
Mortality from ARF ranges from 30–60%
It depends on the clinical setting and presence or
absence of non-renal organ system failure.
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5. Clinical features
ARF is usually asymptomatic
It is usually diagnosed when biochemical monitoring
of hospitalized patients reveals a new increase in
BUN and serum creatinine concentrations.
Retention of nitrogenous waste products, oliguria,
and electrolyte and acid-baseabnormalities are
frequent clinical features.
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6. Etiology and Pathophysiology
Underlying etiologies of ARF may vary based on the d/t
setups.
In developed countries, postoperative and
ischemic/nephrotoxic causes of ARF are more common.
In countries with less well-developed health care systems,
infective etiologies predominate.
E.g., in Ethiop septic abortion & severe falcipmalaria
For purposes of diagnosis and management, causes of ARF
are generally divided into three major categories:
1.Pre-renal ARF (~55%)
2.Intrinsic renal ARF (~40%)
3.Post-renal ARF (~5%)
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7. Prerenal ARF (Prerenal Azotaemia)
It’s the most common form of ARF
Occurs in the setting of renal hypo-perfusion
It is generally reversiblewhen renal perfusion
pressure is restored.
There should not be renal parenchymal damage.
More severe or prolonged hypo-perfusion may lead
to ischemic injury, often termed acute tubular
necrosis, or ATN.
prerenal ARF and ischemic ATN fall along a
spectrum of manifestations of renal hypoperfusion.
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8. Prerenal ARF… causes
1.
Hypovolemia

Hemorrhage

GI fluid loss (vomiting,
diarrhea)

Renal fluid loss (diuretics,
nephrogenicDI)

Extravascular sequestration
(burns, pancreatitis, severe
hypoalbuminemia)

Decreased intake
(dehydration, altered
mental status)
2.
Altered renal hemodynamics
resulting in hypoperfusion
Low cardiac output state (HF,
pulmonary HTN)
Systemic vasodilation (sepsis,
antihypertensives, anaphylaxis)
Renal vasoconstriction
(catecholamines, amphotericin
B)
Impairment of renal
autoregulatoryresponses
(NSAID, ACEi, ARB)
Hepatorenalsyndrome
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9. Intrinsic ARF (Diseases that directly involve
the renal parenchyma)
Intrinsic causes of ARF can be conceptually divided based on the
predominant compartment of the kidney that is affected:
1.Renovascularobstruction (bilateral, or unilateral in the setting
of one kidney)
2.Diseases of the glomeruli or vasculature (GN or vasculitis,
malignant HTN, collagen vascular diseases, DIC)
3.Acute tubular necrosis (Ischemia, Infection, Toxins)
4.Interstitial nephritis (Allergic, Infection, Infiltration,
Inflammatory)
5.Intratubularobstruction
Ischemia and nephrotoxinsclassically induce acute tubular injury
(ATN).
`
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10. ATN differs from prerenal ARF in that the renal
tubular epithelial cells are injured in the former.
ATN occurs most frequently in patients undergoing
major cardiovascular surgery or suffering severe
trauma, hemorrhage, sepsis, and/or volume depletion.
Patients with other risk factors for ARF (e.g.,
exposure to nephrotoxins or preexisting chronic
kidney disease) are at increased risk for ATN.
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11. The majority of all hospital-acquired ARF is
secondary to ATN.
Renal hypo-perfusion and renal ischemia are the
most common causes of ATN.
Ischemic and nephrotoxic ATN account for >90% of
cases of intrinsic ARF.
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12. Radiocontrast
Aminoglycosides
chemotherapy (e.g.,
cisplatin)
Amphotericin B
Ethylene glycol
Acyclovir
Calcium
Myoglobin
(rhabdomyolysis)
Hemoglobin
(hemolysis)
Urate
Oxalate
Myeloma light chains
Exogenous nephrotoxins Endogenous nephrotoxins
Common toxic agents that may cause toxic ATN are:
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13. PostrenalARF (Diseases associated with urinary tract
obstruction)
To be the cause of azotemia, urinary tract obstruction
must involve the outflow tract of both normal kidneys
unless preexistingrenal dysfunction is present
1.Ureteric (bilateral, or unilateral in the case of one
kidney)
2.Bladder neck: neurogenic bladder, BPH, calculi,
blood clots, cancer
3.Urethra: stricture or congenital valves
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14. Clinical Assessment & diagnosis
An organized approach for the assessment of ARF
include the following:
A thorough history and physical examination to
assess volume status, potential nephrotoxic insults,
and evidence of systemic disease
Urine output
Urinalysis
Serum and urine electrolytes
Radiologic and renal ultrasonography evaluation
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15. Step 1: History and physical examination
Prerenal Renal Postrenal
Volume depletion, CHF,
severe liver disease or other
edematousstate
ATN
AIN
AGN
Ask for exposure
to toxins and
drugs
Palpable bladder or
hydronephrotickidney, enlarged
prostate, abnormal pelvic
examination, large residual
bladder urine volume, history of
renal caliculi.
Step 2: urine sediment
Eosinophils
Suspect acute
interstitial nephritis
(AIN)
RBC casts
GN or
vasculitis
No abnormality
or hyaline casts
Suspect prerenal
azotemia
Renal tubular
Epithelial cells and
“muddy-brown” casts
Suspect ATN
Broad granular casts are characteristic of chronic kidney disease
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16. URINE DIAGNOSTIC INDICES IN DIFFERENTIATION OF
PRERENAL VERSUS INTRINSIC RENAL AZOTEMIA
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Step 3: urine indices

17. Other investigations for evaluation of ARF are:
U/S of the urinary tract -to exclude post renal ARF
Plain film of the abdomen or CT scan -for patients
with suspected nephrolithiasis.
Pyelography in complex cases and for precise
localization of the site of obstruction
Biopsy is reserved for patients in whom prerenal and
post renal ARF have been excluded and the cause of
intrinsic ARF is unclear.
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18. Complications
ARF impairs renal excretion of sodium, potassium, and water and perturbs
divalent cation homeostasis and urinary acidification mechanisms.
As a result, ARF is frequently complicated by:
Intravascular volume overload (pulmonary edema and peripheral edema)
Hyponatremia
Hyperkalemia
Hyperphosphatemia
Hypocalcemia
Hypermagnesemia
Metabolic acidosis
Anemia
Infection is a common and serious complication of ARF
Prolongation of the bleeding time
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19. Treatment
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20. Prevention
Because there are no specific therapies for ischemic or
nephrotoxic ARF, prevention is of paramount importance.
Many cases of ischemic ARF can be avoided by:
Close monitoring of cardiovascular function and
intravascular volume
The incidence of nephrotoxic ARF can be reduced by tailoring
the administration of nephrotoxic drugs to body size and GFR.
Treatment should focus on providing etiology-specific
supportive care.
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21. Specific Therapies
Prerenal ARF is rapidly reversible upon correction of the
primary hemodynamic abnormality, and post renal ARF
resolves upon relief of obstruction.
There are no specific therapies for established AKI.
Management of these disorders should focus on elimination of
the causative hemodynamic abnormality or toxin, avoidance
of additional insults, and prevention and treatment of
complications.
Specific treatment of other causes of intrinsic renal ARF
depends on the underlying pathology.
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22. Pre-Renal ARF
Severe hypovolemia due to hemorrhage should be
corrected with packed red cells.
Isotonic saline is usually appropriate replacement for
mild to moderate hemorrhage or plasma loss (e.g., burns,
pancreatitis).
Hypotonic solutions (e.g., 0.45% saline) are usually
recommended as initial replacement in patients with
prerenal ARF due to increased urinary or GI fluid losses.
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23. Post-renal ARF
The treatment of urinary tract obstruction often
involves consultation with a urologist.
Interventions as simple as Foley catheter placement
or as complicated as multiple ureteral stents and/or
nephrostomy tubes may be required.
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24. Management
Issue
Therapy
Reversal of Renal Insult
Ischemic ATNRestore systemic hemodynamic and renal perfusion
through volume resuscitation and use of
vasopressors
Nephrotoxic ATNEliminate nephrotoxic agents
Consider toxin-specific measures: e.g., forced
alkaline diuresis for rhabdomyolysis,
allopurinol/rasburicasefor tumorlysis syndrome
Management of Ischemic and Nephrotoxic ARF
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Etiology specific supportive care

25. Prevention and Treatment of Complications
Intravascular
volume
overload
Salt and water restriction
Diuretics
Ultrafiltration
HyponatremiaRestriction of enteral free water intake
Avoidance of hypotonic IV solutions, including dextrose-
containing solutions
Hyperkalemia Restriction of dietary K
+
intake
Eliminate K
+
supplements and K
+
-sparing diuretics
Loop diuretics to promote K
+
excretion
Potassium binding ion-exchange resins (e.g., sodium polystyrene
sulfonate or Kayexelate)
Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to
promote intracellular mobilization
Inhaled β-agonist therapy to promote intracellular mobilization
Calcium gluconate or calcium chloride (1 g) to stabilize the
myocardium
Dialysis25

26. Metabolic acidosis NaHCO
3 (should not be given unless serum HCO
3
-
concentration falls below 15 mmol/L or arterial pH falls below
7.2.
Administration of other bases
Dialysis
Hyperphosphatemi
a
Restriction of dietary phosphate intake
Phosphate binding agents (calcium carbonate, calcium acetate,
sevelamerhydrochloride, aluminumhydroxide)
Hypocalcemia Calcium carbonate or gluconate(if symptomatic)
Hypermagnesemia Discontinue Mg
++
containing antacids
Hyperuricemia Treatment usually not necessary if <890 mol/L or <15mg/dL
Allopurinol, forced alkaline diuresis, rasburicase
Nutrition Protein and calorie intake to avoid net negative nitrogen balance
Dialysis To prevent complications of acute renal failure
Choice of agentsAvoid other nephrotoxins: ACE inhibitors/ARBs,
aminoglycosides, NSAIDs, radiocontrastagents
Drug dosing Adjust doses and frequency of administration for degree of renal
impairment
Prevention and Treatment of Complications…
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27. Indications for Dialysis (RRT)
1.Oliguria or anuria not responsive to diuretics
2.Hyperkalemia (especially when coupled with ECG
changes)
3.Severe acidosis
4.Symptomatic uraemia
Encephalopathy
Pericarditis
Neuropathy/myopathy
5.Fluid overload
6.Drug overdose with a dialyzable toxin
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28. Outcome and Long-Term Prognosis
The in-hospital mortality rate among patients with
ARF ranges from 20 to 50% or more, depending on
underlying conditions.
Obstetric patients -15% mortality
Toxin related –30%
Following trauma or major surgery –60%
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29. Prognosis…
Oliguria (<400ml/d) at the time of presentation & a
rise in serum creatinine >3mg/dL are associated with
a poor prognosis.
Mortality is higher in older debilitated patients & in
those with MOF.
Most patients who survive an episode of ARF
recover sufficient renal function to remain dialysis-
independent, although a fraction (roughly 10–20%)
go on to require maintenance dialysis.
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30. Summary
ARF is a sudden decrease in kidney function, resulting in an
inability to maintain acid-base, fluid and electrolyte balance
and to excrete nitrogenous wastes.
Prerenal azotemia, which commonly occurs due to volume
deficit, is most common and readily reversible type of ARF.
Principles of treatment of ARF includes prevention of
occurrenceand progression of the disease, supportive cares,
treatment of underlying diseases, and management of
complications.
Absolute indications for dialysis include symptoms or signs of
the uremic syndrome and management of refractory
hypervolemia, hyperkalemia, or acidosis.
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