AKI by Dr Getachew (1)................ppt

Gtt

1. Acute Kidney Injury
Getachew Wondafrash
(MD , Internist, Nephrologist)
18-3 -14 EC
08/23/24 1

2. •What are the different definitions of AKI
•How we differentiate b/n Prerenal azotemia and ATN
•What are the different cause of AKI in our set up and in other area
• How we differentiate b/n AKI and CKD
•What are the principle of Mx of AKI
•What are the indication of dialysis in AKI
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3. A 64-year-old man presents with symptoms of malaise, shortness of
breath, edema, and no urine output for 24 hours. His past medical
history is not significant, and his only medication is daily aspirin. On
examination his JVP is 4 cm, heart sounds are normal, lungs are clear,
and the abdomen is soft.
A Foley catheter is inserted into his bladder for 200 cc of urine, which is
sent for urinalysis. His urine output still remain slow. Which of the
following is the most appropriate initial diagnostic test?
(A) renal ultrasound
(B) blood cultures
(C) urine cultures
(D) inferior vena cava gram with renal venogram
(E) blood urea nitrogen (BUN)/creatinine ratio
Aspirin, also known as acetylsalicylic acid, is a medication used to
reduce pain, fever, or inflammation. Specific inflammatory conditions
which aspirin is used to treat include Kawasaki disease, pericarditis,
and rheumatic fever
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4. • A 74-year-old woman develops acute sepsis from pneumonia and is
admitted to the intensive care unit because of hypotension.
•She is started on antibiotics, and intravenous normal saline .
•Despite this she remains oliguric. Her urinalysis has muddy brown
granular casts and the urine sodium is 56 mEq/L.
•Which of the following is the most likely cause of her ARF(AKI)
(A) nephrotoxic antibiotics
(B) acute infectious GN
(C) acute tubular necrosis (ATN)
(D) contrast nephropathy
(E) cholesterol emboli
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5. •A 46-year-old woman with nausea and vomiting presents to hospital
because of light- headedness when standing and decreased urine
output.
• She looks unwell; the blood pressure supine is 90/60 mm Hg and
80/60 mm Hg when standing.
•Her abdominal, heart, and lung examinations are normal.
•Which of the following laboratory values suggests prerenal azotemia in
this patient?
(A) markedly elevated urea, unchanged
creatinine
(B) unchanged urea, elevated creatinine
(C) little change in either creatinine or urea for several days after
oliguria develops
(D) urea/creatinine ratio <15
(E) urea/creatinine ratio >20
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6. •A 28-year-old woman with HIV on antiretroviral therapy complains of
abdominal pain in the emergency department. Laboratory data show
a creatinine of 3.2 mg/dL; her baseline creatinine is 1.0 mg/dL.
Urinalysis shows large numbers of white blood cells and red blood
cells without epithelial cells, leukocyte esterase, or nitrites. Which test
is indicated next to identify the cause
A. Acid-fast stain of the urine
B. Anti-GBM (glomerular base membrane) antibodies
C. Renal angiogram
D. Renal ultrasound
E. Urine electrolytes
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7. • Eosinophiluria can be found in which of the following conditions
(causes of AKI)
A -Interstitial nephritis
B- Athroembolic Disease
C- Rhabdomylosis
D-A and B
E -B and C
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8. • It is hospital day 5 for a 65-year-old patient with pre renal
azotemia secondary to dehydration.
•His creatinine was initially 3.6 mg/dL on admission, but it has
improved today to 2.1 mg/dL.
•He complains of mild lower back pain, and you prescribe
IBUBROFEN (NSAID) to be taken intermittently.
• By what mechanism might this drug further impair his renal function?
A. Afferent arteriolar vasodilatation

B. Afferent arteriolar vasoconstriction

C. Efferent arteriolar vasoconstriction
D. Proximal tubular toxicity
E Efferent arteriolar vasodilatation
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9. • Which of the following feature suggestive of CRF (CKD) instead of
ARF (AKI) except
A-Reduced kidney size bilaterally on ultrasonography
B-Symptoms or signs of renal osteodystrophy
C-Finding of broad tubular or waxy casts on urine analysis
D-Prolonged symptoms or signs of uremia for>3 months
E-None
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10. •Which of the following statement is not true
A-Oliguria refers to a 24-h urine output <400 mL
B-Anuria is the complete absence of urine formation (<100 mL)
C-Nonoliguria refers to urine output >400 mL/d in patients with
acute or chronic azotemia
D-Polyuria refers to urine output of>1.5 L/d
E-All are true
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11.  A 68-year-old man with acute renal insufficiency presents with
weakness, paresthesias, and progressively worsening shortness of
breath. He has been experiencing these symptoms for 4 days.
Laboratory findings show a potassium level of 7.2 it is very high; an
electrocardiogram reveals peaked T waves and widening of the
QRS complex. Which of the following is NOT indicated in the initial
treatment of this patient?
A. Intravenous calcium
B. Intravenous glucose and insulin
C. Dialysis
D. Sodium polystyrene sulfonate (Kayexalate, Kionex)
E. Beta blockers
 Sodium polystyrene sulfonate (SPS), sold under the brand names
Kayexalate and Kionex, is a potassium-binding resin that has been in
use in the United States. It is used in treating patients who have
hyper-kalemia, a sometimes life-threatening condition marked by an
excessive level of potassium in the blood.
08/23/24 11

12. Ethiopia: Renal Diseases
•In a study with 136 adults(106 women and 30 men) with
acute intrinsic renal failure 71(52.2%) had septic abortion,
29(21.3 %) had falciparum malaria and 12(8.8%) patients
nephrotoxic agents as causes for the renal failure .Overall
case fatality rate 33.8% with 36.3% for septic abortion 37.9%
for malaria and 16.7% fatality rate for nephrotoxic agents.
(Eth. Med J 1994;32:89-97)
•Among children with ARF in Addis Ababa, post-diarrheal
hemolytic uremic syndrome was a leading cause. Out of 30
patients with ARF 23 were diagnosed to have HUS. Very high
mortality of 46.7% (Eth. Med J 2004;42:17-22)
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13. AKI (definition)
AKI is defined as any of the following:
• Increase in SCr by >0.3 mg/dl within 48 hours; or
•Increase in SCr by >1.5-fold above baseline, which is
known or presumed to have occurred within 7 days; or
•Urine volume <0.5 ml/kg/h for 6 hours.
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14. AKI (RIFLE Criteria)
•Risk
•Injury
•Failure
•Loss
•ESKD
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15. Rifle Criteria
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16. Acute kidney Injury Network (AKIN)Acute kidney Injury Network (AKIN)
Classification/Staging for AKIClassification/Staging for AKI
S Creatinine CriteriaS Creatinine CriteriaUrine output CriteriaUrine output Criteria
Increase in S creatinine > 0.3 mg/dl
OR increase to 1.5 – 2 fold
< 0.5 ml/ kg / hr for > 6 hrs
Increase in S creatinine > 2 – 3 fold< 0.5 ml/ kg / hr for > 12 hrs
Increase in S creatinine > 3 fold
OR ≥ 4 mg/dl with acute ↑ of > 0.5
< 0.3 ml/ kg / hr for > 24 hrs
OR Anuria for > 12 hrs
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17. AKI Staging Criteria
Stage S Creatinine Urine output
1 ≥1.5-1.9 times baseline
OR
0.3 mg/dl increase
<0.5 ml/kg/h for 6-12
hours
2 ≥2.0-2.9 times baseline <0.5 ml/kg/h for ≥12
hrs
3
≥3.0 times baseline
OR
increase in SCr to ≥4.0 mg/dl
OR
RRT
<0.3 ml/kg/h for ≥24
hours
OR
Anuria for ≥12 hours
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18. 08/23/24 18
KDIGO definition /classification of AKI
It is Recommended that acute kidney injury/impairment (AKI)
be defined as any of the following :
• Increase in Scr by >0.3 mg/dl within 48 hours, or
• Increase in Scr by >1.5-fold above baseline which is
known or presumed to have occurred within 7 days or
• Urine volume <0.5 ml/kg/h for 6 hours

19. Acute Kidney Injury: Introduction
 AKI, previously known as acute renal failure
 Is characterized by the sudden impairment of kidney
function resulting in the retention of nitrogenous & other
waste products normally cleared by the kidneys.
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20. Epidemiology - AKI
 AKI complicates 5–7% of acute care hospital admissions
and up to 30% of admissions to the ICU.
 AKI is also a major medical complication in the developing
world, particularly in the setting of diarrheal illnesses &
infections like malaria
 Markedly increase risk of death in hospitalized individuals
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21. Etiology and Pathophysiology - AKI
The causes of AKI have traditionally been divided into three
broad categories:
 Prerenal azotemia
 Intrinsic renal parenchymal disease
 Post renal obstruction
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22. 08/23/24 22

23. Prerenal Azotemia
Prerenal azotemia is the most common form of AKI
It is a rise in serum Cr or BUN due to inadequate renal plasma
flow and intraglomerular hydrostatic pressure
The most common clinical conditions associated with prerenal
azotemia are:
 Hypovolemia,
 Decreased cardiac output, and
 Medications that interfere with renal autoregulatory responses
such as NSAIDs & inhibitors of angiotensin II
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24. Prerenal Azotemia…
 Prolonged periods of prerenal azotemia may lead to ischemic
injury, often termed ATN
 By definition, prerenal azotemia involves no parenchymal
damage to the kidney & is rapidly reversible once
intraglomerular hemodynamics are restored
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25. Disturbances of normal autoregulation of GFR
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Abuelo JG, N Engl J Med 2007;357:797-805

26. Prerenal Azotemia…
Drugs can affect the compensatory changes evoked to
maintain GFR.
 NSAIDs inhibit renal prostaglandin production, limiting renal
afferent vasodilation.
Causing renal afferent vasoconstriction
 ACEI & ARBs limit renal efferent vasoconstriction - by causing
renal efferent arterioles vasodilatation
This effect is particularly pronounced in patients with bilateral
renal artery stenosis
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27. Intrinsic AKI
The most common causes of intrinsic AKI are
Sepsis,
Ischemia, and
Nephrotoxins
Other causes of intrinsic AKI are less common and can involve
damage to
 Glomeruli,
Tubulointerstitium, and
Vessels.
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30. Contrast Agents & AKI
 Iodinated contrast agents are a leading cause of AKI
 The risk of "contrast nephropathy," increases markedly in
the setting of CKD , particularly diabetic nephropathy
 The most common clinical course is rise in Cr within 24–48
hrs , peaking within 3–5 days, & resolving in a week
 Pts with multiple myeloma and renal disease are particularly
susceptible to severe disease
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31. Antibiotics & AKI
Aminoglycosides & Amphotericin B cause tubular necrosis
 Nonoliguric AKI may occur even when plasma levels are in Rxic
range
 AKI typically manifests after 5–7 days of Rx & can present even
after drug discontinuation
 Nephrotoxicity from amphotericin B is dose and duration
dependent
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32. Endogenous Toxins & AKI
 A number of endogenous compounds: Myoglobin, hemoglobin, uric
acid, and myeloma light chains.
Light chain myeloma is a rare type of blood cancer and a subtype of
multiple myeloma. It's characterized by the presence of light chain
immunoglobulins in the blood and urine without a heavy chain
component
 Myoglobin can be released by injured muscle cells in cases
rhabdomyolysis
 Hemoglobin can be released during massive hemolysis
 Rhabdomyolysis may result from traumatic crush injuries, compression
during coma /immobilization, prolonged seizure
 Pathogenic factors for AKI: intrarenal vasoconstriction, direct proximal
tubular toxicity, & mechanical obstruction of distal nephron lumen
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33. Endogenous Toxins & AKI…
 TLS may follow initiation of CXT in pts with high-grade lymphomas
& ALL
•Acute lymphoblastic leukaemia is the most common childhood
cancer.
•It occurs when a bone marrow cell develops errors in its DNA.
•Symptoms may include enlarged lymph nodes, bruising, fever, bone
pain, bleeding from the gums and frequent infections.
• Massive release of UA (often >15 mg/dL) leads to precipitation of
UA in the renal tubules and AKI
•Myeloma light chains can also cause AKI by direct tubular toxicity
and by obstructing intratubular lumen
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34. Post renal Acute Kidney Injury
Obstruction to urinary flow may be caused by functional or
structural derangements anywhere from the renal pelvis to the tip
of the urethra
 For AKI to occur in healthy individuals, obstruction must affect both
kidneys unless only one kidney is functional
Bladder neck obstruction can be due to prostate ds (BPH or prostate
Ca), neurogenic bladder, or Rx with anticholinergics
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35. Post renal Acute Kidney Injury…
Other causes of lower tract obstruction are blood clots, calculi,
and urethral strictures
 Ureteric obstruction can occur from:
 Intraluminal obstruction (calculi, blood clots)
 Infiltration of the ureteric wall (neoplasia), or
 External compression (retroperitoneal fibrosis, neoplasia or
abscess)
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36. 08/23/24 36

37. Diagnostic Evaluation - AKI…
 Clues suggestive of CKD
Radiologic studies: Small, shrunken kidneys with cortical thinning on
U/S, or evidence of renal osteodystrophy
Renal osteodystrophy is
 
a broad term that incorporates all the
biochemical abnormalities and skeletal manifestations in patients
suffering from chronic kidney disease or end-stage renal disease or
Laboratory tests: normocytic anemia or 2
0
hyperparathyroidism with
hyperphosphatemia and hypocalcemia
 No set of tests, however, can rule out AKI superimposed on CKD
since AKI is a frequent complication in patients with CKD
Once the dx of AKI is established, its cause needs to be determined
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38. Renal osteodystrophy
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39. History and Physical Examination - AKI
 Prerenal azotemia should be suspected in the setting of vomiting,
diarrhea, glycosuria causing polyuria, & medications including
diuretics, NSAIDs, ACEIs & ARBs
 Signs of orthostatic hypotension, tachycardia, ↓ ed skin turgor, & dry
mucous membranes are often present in prerenal azotemia
 A Hx of prostatic ds, nephrolithiasis, or pelvic or Para aortic
malignancy would suggest the possibility of postrenal AKI
The jugular venous pressure is usually assessed by observing the right
side of the patient's neck.
The normal mean jugular venous pressure, determined as the vertical
distance above the midpoint of the right atrium, is
 6 to 8 cm H
2
O.
08/23/24 39

40. Urine Findings - AKI
 Complete anuria in early AKI is uncommon except in the
following situations:
 Complete urinary tract obstruction
 Renal artery occlusion
 Overwhelming septic shock or
 Severe ischemia (often with cortical necrosis)
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43. Urine Findings - AKI
 A reduction in UOP (oliguria, defined as <400 ml /24 h)
 Oliguria is associated with worse clinical outcomes
 Red or brown urine may be seen +/- gross hematuria
If the color persists in the supernatant after centrifugation,
then pigment nephropathy from rhabdomyolysis or hemolysis
should be suspected
08/23/24 43

44. Urine Findings - AKI …
 AKI from ischemia or nephrotoxins - mild proteinuria (<1 g/d).
 Greater proteinuria in AKI suggests damage to the glomeruli or
excretion of myeloma light chains/aggressive and poor
prognosis.
 Dipstick positive for hemoglobin but few RBCs in the urine
sediment - rhabdomyolysis or hemolysis.
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45. 08/23/24 45

46. Urine Findings - AKI …
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47. 08/23/24 47

48. 08/23/24 48

49. wbc casts
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50. Uric acid crystals
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Uric acid crystals

51. Blood Laboratory Findings - AKI
 Elevated Serum Cr
 CBC may provide diagnostic clues
 Anemia is common & is usually multifactorial in origin
 Severe anemia in the absence of bleeding may reflect hemolysis, MM,
or thrombotic microangiopathy (e.g., HUS or TTP)
Thrombotic Thrombocytopenia Purpura (TTP) is
 
a rare disorder of
the blood coagulation system 
and is considered a true medical
emergency.
TTP is characterised into acquired (idiopathic) and congenital
(familial) and affects 4-6 people per million, affecting women more
than men with a peak incidence in your forties.
 Peripheral eosinophilia can accompany interstitial nephritis,
atheroembolic disease, and Churg-Strauss vasculitis.
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52. Blood Laboratory Findings – AKI…
 AKI often leads to hyperkalemia, hyperphosphatemia, and
hypocalcemia
 Marked hyperphosphatemia with accompanying
hypocalcemia - Rhabdomyolysis or TLS
 CPK & UA levels are elevated in rhabdomyolysis
TLS shows normal or marginally ↑ed CK and markedly ↑ ed
UA
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53. Blood Laboratory Findings – AKI…
The anion gap may be increased due to retention of anions
such as phosphate, sulfate, and urate
 GN & Vasculitis - depressed complement levels and high
titers of ANAs, ANCAs, & anti GBM antibodies
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54. Radiologic Evaluation AKI
Simple bladder catheterization can R/o urethral obstruction
Imaging of the urinary tract with renal ultrasound or CT
 Findings of obstruction include dilation of the collecting system
and hydroureteronephrosis
 Obstruction can be present without radiologic abnormalities in
the setting of volume depletion, RPF & encasement with tumor
08/23/24 54

55. Radiologic Evaluation AKI…
 Antegrade or retrograde pyelography
 Large kidneys - Diabetic nephropathy, HIVAN, infiltrative diseases,
amyloydosis ,PCKD or occasionally acute interstitial nephritis
HIV-associated nephropathy (HIVAN),
 
the classic kidney disease
associated with HIV infection, was first described in 1984 as a
complication of AIDS, although HIVAN may also occur in patients
with less advanced HIV infection or following acute seroconversion.
 Vascular imaging may be useful if venous or arterial obstruction is
suspected - risks of contrast administration
08/23/24 55

56. Renal Failure Indices
 Can help differentiate prerenal azotemia from intrinsic AKI
 The low tubular flow rate &↑ed recycling of urea seen in prerenal
azotemia may cause a disproportionate ↑ of the BUN compared to Cr
FeNa( The fractional excretion of sodium (FeNa) )is the fraction of the
filtered Na load that is excreted in the urine
 With prerenal azotemia, the FeNa may be below 1%, suggesting avid
tubular sodium reabsorption
08/23/24 56

57. Renal Failure Indices…
 The response of UOP to fluid administration may be both
Dxic & therapeutic in prerenal azotemia
 In ischemic AKI, the FeNa is frequently above 1% because of
tubular injury
 In the pt with good baseline kidney function, urine osmolality
may be above 500 mOsm/kg in prerenal azotemia, consistent
with an elevated vasopressin
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58. 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
castscasts08/23/24 58

59. 08/23/24 59

60. Kidney Biopsy
 If the cause of AKI is not apparent based on the clinical
context, P/E, & laboratory , kidney biopsy should be
considered.
 The procedure is most often used in AKI when prerenal
azotemia, postrenal AKI, and ischemic or nephrotoxic AKI have
been deemed unlikely
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61. Complications AKI
1.Uremia a raised level in the blood of urea and other nitrogenous waste
compounds that are normally eliminated by the kidneys.
Hypervolemia and Hypovolemia
HypoNa
+
, HyperK
+
, HyperPo4
-
& HypoCa
+2
Acidosis
Bleeding
Infections
Cardiac Complic (arrhythmias, pericarditis / pericardial effusion)
Malnutrition
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62. Treatment: Acute Kidney Injury
Varies according to the underlying cause
Optimization of hemodynamics, correction of F & lytes, D/C of
nephrotoxic medications, & dose adjustment of medications are
all critical
The kidney may recover remarkably after even severe, dialysis-
requiring AKI
 However, some pts with AKI do not recover fully and may
remain dialysis dependent.
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63. Rx of Ischemia & Nephrotoxic-Associated AKI
General Issues
1. Optimization of systemic & renal hemodynamics through
volume resuscitation & use of vasopressors
2. Elimination of nephrotoxic agents (ACEIs, ARBs, NSAIDs,
aminoglycosides) if possible
3. Initiation of renal replacement therapy when indicated
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64. Specific Issues
1.Nephrotoxin-specific
Rx: a. Rhabdomyolysis: consider forced alkaline diuresis
b. Tumor lysis syndrome: Allopurinol or rasburicase
•Rasburicase is a medication that helps to clear uric acid from the blood.
•It is a recombinant version of urate oxidase, an enzyme that metabolizes
uric acid to allantoin.
• Urate oxidase is known to be present in many mammals but does not
naturally occur in humans.
2. Volume overload
Rx: a. Salt and water restriction
b. Diuretics
c-Ultrafilitretion
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Rx of Ischemia & Nephrotoxin-Ass AKI …

65. Rx of Specific Issues …
3. Hyponatremia
Rx: Restriction of free H2O intake, minimization of hypotonic IV
solutions including those containing dextrose
4.Hyperkalemia
Rx:
Restriction of dietary K
+
intake
D/C potassium-sparing diuretics, ACEIs, ARBs
Loop diuretics to promote urinary K
+
loss
Insulin & glucose to promote entry of K
+
intracellularly
Calcium gluconate or calcium chloride to stabilize the myocardium
08/23/24 65

66. Rx of Specific Issues …
5. Metabolic acidosis
Rx: Sodium bicarbonate (if pH <7.2 to keep HCo3
-
>15 mmol /L)
Renal replacement therapy
6. Hyperphosphatemia
Rx: Restriction of dietary phosphate intake
Phosphate binding agents (calcium acetate, sevelamer,
Al(OH)3)
08/23/24 66

67. Rx of Specific Issues …
7. Hypocalcemia
RX:
Calcium carbonate or calcium gluconate if symptomatic
8. Nutrition
Rx: Sufficient protein & calorie intake to avoid negative
nitrogen balance
9. Drug dosing
Rx: Careful attention to dosages & frequency drugs,
adjustment for degree of renal failure
08/23/24 67

68. Rx - Prerenal Azotemia
 Replacement fluids targeted to the type of fluid lost
 Severe acute b/d loss should be treated with PRBCs
 Crystalloid &/or colloid should be used for less severe
hemorrhage or plasma loss (in burns & pancreatitis)
 Renal hypoperfusion from poor cardiac output may require use
of inotropic agents, preload- and afterload-reducing agents &
antiarrhythmic drugs
08/23/24 68

69. Rx - Postrenal AKI
The site of obstruction defines the treatment approach

Urethral strictures or functional bladder impairment
Rx: Transurethral or suprapubic bladder catheterization
 Ureteric obstruction
Rx: Percutaneous nephrostomy tube or ureteral stent

Relief of obstruction is usually followed by an appropriate
diuresis for several days
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70. Supportive Measures AKI
Volume Management
Hypervolemia in oliguric or anuric AKI may be life threatening due to
acute pulmonary edema
Fluid & Na should be restricted, and diuretics may be used to increase
the urinary flow rate
… There is no evidence that ↑ing UOP itself improves the natural
history of AKI
 In severe cases of volume overload - furosemide as a bolus (200 mg)
followed by an IV drip (10–40 mg/h), with or w/t a thiazide diuretic
Diuretic therapy should be stopped if there is no response
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71. Dialysis Indications in AKI
 When medical management fails to control volume overload,
hyperkalemia, acidosis
When there are severe complications of uremia (astrexis, pericardial
rub/effusion, encephalopathy, uremic bleeding)
The initiation of dialysis should not await the development of a life-
threatening complication of renal failure
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72. Outcome and Prognosis
 AKI is ass with a significantly ↑ed risk of in-hospital & long-term
mortality, longer length of stay & ↑ed costs
 Prerenal azotemia (with the exception of the cardiorenal and
hepatorenal syndromes) and postrenal azotemia carry a better
prognosis than most cases of intrinsic AKI
 Survivors of an episode of AKI requiring temporary dialysis, are at
extremely high risk for progressive CKD, and up to 10% may develop
ESRD
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73. Thank you
08/23/24 73