The document discusses acute kidney injury (AKI), including its definition, classification, causes, diagnostic evaluation and management. AKI can be prerenal, intrinsic renal or postrenal. Prerenal AKI is due to reduced renal blood flow and reversible. Intrinsic renal AKI involves direct kidney damage from factors like ischemia or toxins. Postrenal AKI is due to urinary tract obstruction. Evaluation includes urine and blood tests. Management focuses on treating the underlying cause, maintaining fluid/electrolyte balance and preventing complications through supportive care and possibly dialysis.

1. Dr Abhishek Tamrakar
ACUTE
KIDNEY
INJURY

2. Definition: acute kidney injury is a syndrome
characterized by:
• Sudden decline in GFR (hours to days )
• Retention of nitrogenous wastes
• Disturbance in extracellular fluid volume and
• Disturbance in electrolyte and acid base
homeostasis
Acute Kidney Injury

3. Risk
Injury
Failure
Loss of function
End-Stage Renal disease
Rifle Criteria For AKI

4. Risk
 Increase in Cr of 1.5-2.0 X baseline or
 urine output < 0.5 mL/kg/hr for more than 6 hours.
Injury
Failure
Loss of function
End-Stage Renal disease

5. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for more than 6 hrs
Injury
– increase in Cr 2-3 X baseline (loss of 50% of GFR) or
– urine output < 0.5 mL/kg/hr for more than 12 hours.
Failure
Loss of function
End-Stage Renal disease

6. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure
 increase in Cr rises > 3X baseline Cr (loss of 75% of GFR) or
 an increase in serum creatinine greater than 4 mg/dL, or
 urine output < 0.3 mL/kg/hr for more than 24 hours or
anuria for more than 12 hours.
Loss of function
End-Stage Renal disease

7. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr >
24 hrs or anuria for more than 12 hours
Loss of function
 persistent renal failure (i.e. need for dialysis) for more than 4
weeks.
End-Stage Renal disease

8. Risk: Inc Cr 50-100% or U.O. < 0.5 mL/kg/hr for > 6 hrs
Injury: Inc Cr 100-200% or U.O. < 0.5 mL/kg/hr > 12 hrs
Failure: Inc Cr > 200% or > 4 mg/dL or U.O. < 0.3 mL/kg/hr >
24 hrs or anuria for more than 12 hours
Loss of function: Need for dialysis for more than 4 weeks
End-Stage Renal disease
 persistent renal failure (i.e. need for dialysis) for more than 3
months.

9. RIFLE criteria

10. • Azotemia: an abnormal increase in concentration of
urea and other nitrogenous substances in the blood
plasma
• Uremia: the complex of symptoms due to severe
persisting renal failure that can be relieved by
improving clearance
• Oliguria: UOP <~400 ml/24hrs
• Anuria: UOP < ~200 ml/24hrs

11. Etiologic Classification of AKI
Acute kidney injury
Pre-renal Intrinsic Post-renal
Glomerular Interstitial VascularTubular

13. Pre renal AKI
•Most commonest form of acute renal failure
•Represents a physiologic response to mild to
•moderate renal hypo perfusion.
• Prerenal AKI is rapidly reversible upon restoration of
renal blood flow and glomerular ultrafiltration
pressure.

14. • More severe hypoperfusion may lead to ischemic
injury of renal parenchyma and intrinsic renal AKI.
• Thus, prerenal AKI and intrinsic renal AKI due to
ischemia are part of a spectrum of manifestations of
renal hypoperfusion.

15. Causes

16. Etiology and Pathophysiology
I. Hypovolemia
• Hemorrhage, burns, dehydration
• Gastrointestinal fluid loss: vomiting, surgical
drainage, diarrhea

17. • Renal fluid loss: diuretics, osmotic diuresis (e.g.,
diabetes mellitus), hypoadrenalism
• Sequestration in extravascular space:
pancreatitis, peritonitis, trauma, burns,
• Severe hypoalbuminemia

18. II. Low cardiac output
• Diseases of - myocardium, valves, and
pericardium; arrhythmias; tamponade
• Other: pulmonary hypertension, massive
pulmonary embolus

19. Pathophysiology:
• Hypovolemia leads to glomerular hypoperfusion, but
filtration rate are preserved during mild hypoperfusion
through several compensatory mechanisms.
• During states of more severe hypoperfusion, these
compensatory responses are overwhelmed and GFR
falls, leading to prerenal AKI.

20. IV. NSAIDS- they reduce affarent renal
vasodilation
V. ACEIs and ARBs- limit renal efferent vasoconstriction

21. • Prerenal AKI can complicate any disease that
induces :
 hypovolemia,
low cardiac output,
systemic vasodilatation, or
 selective renal vasoconstriction.

22. B. Intrinsic Renal AKI:

23. - accounts for nearly 40% of
all AKI
I.Renovascular obstruction
bilateral or unilateral in the
setting of one functioning
kidney
II.Disease of glomeruli
orrenal microvasculature
• Acute kidney injury
Intrinsic
Glomerular
Interstitial Tubular
Vascular

25. III. Acute tubular necrosis(ATN)
• Ischemia: as for prerenal AKI (hypovolemia, low
cardiac output, renal vasoconstriction, systemic
vasodilatation)

27. Toxins
• Exogenous: radio contrast, cyclosporine, antibiotics
(e.g. aminoglycosides), chemotherapy (e.g. cisplatin),
organic solvents (e.g. ethylene glycol), acetaminophen,
illegal abortifacients
• Endogenous: Mb, Hb, uric acid, oxalate, plasma cell
dyscrasia (e.g. myeloma)
Postoperative AKI

28. C. Post renal AKI (OBSTRUCTION):

29. accounts for ~5% of AKI.
I. Ureteric: calculi, blood
clot, sloughed papillae,
cancer, external
compression(e.g.retroperiton
eal fibrosis)
II. Bladder neck
• Neurogenic bladder,
prostatic hypertrophy,
calculi, cancer, blood clot
III. Urethra: stricture,
congenital valve, phimosis

30. Pathophysiology of postrenal AKI
• It involves hemodynamic alterations triggered
by an abrupt increase in intratubular
pressures
• An initial period of hyperemia from afferent
arteriolar dilation is followed by intrarenal
vasoconstriction from the generation of
angiotensin II, thromboxane A2, and
vasopressin, and a reduction in NO
production.

31. • Reduced GFR is due to underperfusion of
glomeruli and, possibly, changes in the
glomerular ultrafiltration coefficient

32. Diagnostic work up
1. Urinalysis: Microscopic evaluation of
urinary sediment.
• Presence of few formed elements or hyaline casts is
suggestive of prerenal or postrenal azotemia.
• Many RBCs may suggest calculi , trauma , infection
or tumor
• Eosinophilia : occurs in 95 % of patients with acute
allergic nephritis
• Brownish pigmented cellular casts and many renal
epithelia cells are seen in patients with acute tubular
necrosis (ATN )

33. • Pigmented casts without erythrocytes in the sediment
from urine but with positive dipstick for occult blood
indicates hemoglobinuria or myoglobinuria

34. • Dipstick test: trace or no proteinuria with pre-renal
and post-renal AKI;
• mild to moderate proteinuria with ATN and moderate
to severe proteinuria with glomerular diseases.
• RBCs and RBC casts in glomerular diseases
• Crystals, RBCs and WBCs in post-renal ARF.

35. 2. Urine and blood Chemistry:
• Most of these tests help to differentiate prerenal
azotemia, in which tubular reabsorption function is
preserved from acute tubular necrosis where tubular
reabsorption is severely disturbed.
Osmolality or specific gravity: decreased in ATN and
pos-renal AKI (urine is diluted) , while increased in pre-
renal AKI ( urine is concentrated)

36. • Renal failure index: ratio of urine Na+ to urine to
plasma creatinine ratio
• (UNa/Ucr/Pcr) . Values less than 1 % are consistent
with prerenal AKI,where as a
• Value > 1% indicates ATN

37. • Fractional excretion of Na+: is ratio of urine-to-
plasma Na ratio to urine-to-plasma creatinine
expressed as a percentage [ (UNa/PNa)/(Ucr/Pcr )X
100]. Value below 1% suggest prerenal failure , and
values above 1% suggest ATN
• Serum K+ and other electrolytes

38. 3. Radiography/imaging
• Ultrasonography: helps to see the presence of two
kidneys, for evaluating kidney size and shape, and for
detecting hydronephrosis or hydroureter.
• It also helps to see renal calculi, and renal vein
thrombosis.
• Retrograde pyelography: is done when
obstructive uropathy is suspected

39. Complications of AKI
• Intravascular overload: may be recognized by weight
gain , hypertension ,elevated central venous pressure (
raise JVP) , Pulmonary edema
Electrolyte disturbance
• Hyperkalemia: (serum K+ >5.5 mEq/L): decreased
renal excretion combined with tissue necrosis or
hemolysis.
• Hyponatremia : ( serum Na+ concentration < 135 mEq/L
): excessive water intake in the face of excretory failure

40. • Hyperphosphatemia : ( serum Phosphate
concentration of > 5.5 mg /dl ) failure of excretion
or tissue necrosis
• Hypocalcemia : ( serum Ca++ < 8.5 mg/dl ) results
from decreased Active Vit-D , hyperposhphatemia
, or hypoalbuminemia
• Hypercalcemia: (serum Ca++ > 10.5 mg /dl) may
occur during the recovery phase following
rhabdomyolysis induced acute renal failure.

41. • Metabolic acidosis :( arterial blood PH < 7.35 ) is
associated with sepsis or severe heart failure
• Hyperuricemia: due to decreased uric acid excretion
• Bleeding tendency : may occur due to platelet
dysfunction and coagulopathy associated with sepsis
• Seizure: may occur related to uremia

42. Management of AKI
1. Prevention:
• Because there are no specific therapies for ischemic or
nephrotoxic AKI,
Many cases of ischemic AKI can be avoided by close
attention to cardiovascular function and intravascular
volume in high-risk patients, such as the elderly and
those with preexisting renal insufficiency.

43. • Indeed, aggressive restoration of intravascular volume
has been shown to reduce the incidence of ischemic
AKI dramatically after major surgery or trauma, burns,
or cholera prevention is of paramount importance.

44. • The incidence of nephrotoxic ARF can be reduced by
tailoring the dosage of potential nephrotoxins to body
size and GFR; for example, reducing the dose or
frequency of administration of drugs in patients with
preexisting renal impairment

45. • Preliminary measures
• Exclusion of reversible causes: Obstruction should
be relived , infection should be treated
• Correction of prerenal factors: intravascular volume
and cardiac performance should be optimized

46. • Maintenance of urine output: Loop diuretics may be
usefully to convert the oliguric form of ATN to the
nonoliguric form.
• High doses of loop diuretics such as Furosemide (up
to 200 to 400 mg intravenously) may promote
diuresis in patients who fail to respond to
conventional doses

47. • Specific Therapies:
• To date, there are no specific therapies for established
intrinsic renal ARF due to ischemia or nephrotoxicity.
• 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.RPGN ,Collagen
disease ,vasculitis is treated with steroids and
cyclophosphamide.

48. Prerenal ARF:
• The composition of replacement fluids for treatment of
prerenal ARF due to hypovolemia must be tailored
according to the composition of the lost fluid.
• Severe hypovolemia due to hemorrhage should be
corrected with packed red blood cells, whereas isotonic
saline is usually appropriate replacement for mild to
moderate hemorrhage or plasma loss (e.g., burns,
pancreatitis).

49. • Urinary and gastrointestinal fluids can vary greatly in
composition but are usually hypotonic. Hypotonic
solutions (e.g., 0.45% saline) are usually
recommended as initial replacement in patients with
prerenal ARF due to increased urinary or
gastrointestinal fluid losses, although isotonic saline
may be more appropriate in severe cases

50. • Subsequent therapy should be based on
measurements of the volume and ionic content of
excreted or drained fluids. Serum potassium and acid-
base status should be monitored carefully.

51. Postrenal ARF:
• Management of postrenal ARF requires close
collaboration between nephrologist, urologist, and
radiologist.
• Obstruction of the urethra or bladder neck is usually
managed initially by transurethral or suprapubic
placement of a bladder catheter, which provides
temporary relief while the obstructing lesion, is
identified and treated definitively. Similarly, ureteric
obstruction may be treated initially by percutaneous
catheterization of the dilated renal pelvis or ureter.

52. 4. Supportive Measures: (Conservative therapy )
• Dietary management:
• Generally, sufficient calorie reflects a diet that
provides 40-60 gm of protein and 35-50 kcal/kg lean
body weight.
• In some patients, severe catabolism occurs and
protein supplementation to achieve 1.25 gm of
protein /kg body weight is required to maintain
nitrogen balance.
• Restricting dietary protein to approximately 0.6 g/kg
per day of protein of high biologic value (i.e., rich in
essential amino acids) may be recommended in sever
azotemia.

53. Fluid and electrolyte management :
• Following correction of hypovolemia, total oral and
intravenous fluid administration should be equal to
daily sensible losses (via urine, stool, and NG tune o
surgical drainage ) plus estimated insensible ( i.e. ,
respiratory and derma ) losses which usually equals
400 – 500 ml/day. Strict input output monitoring is
important.

54. • Hypervolemia: can usually be managed by restriction
of salt and water intake and diuretics.
• Metabolic acidosis: is not treated unless serum
bicarbonate concentration falls below 15 mmol/L or
arterial pH falls below 7.2.
• More severe acidosis is corrected by oral or
intravenous sodium bicarbonate.

55. • Initial rates of replacement are guided by estimates of
bicarbonate deficit and adjusted thereafter according
to serum levels.
• Patients are monitored for complications of
bicarbonate administration such as hypervolemia,
metabolic alkalosis, hypocalcemia, and hypokalemia.
• From a practical point of view, most patients
requiring sodium bicarbonate need emergency
dialysis within days.

56. • Hyperkalemia: cardiac and neurologic complications
may occur if serum K+ level is > 6.5 mEq/L
o Restrict dietary K+ intake
o Give calcium gluconate 10 ml of 10% solution over 5
minutes
o Glucose solution 50 ml of 50 % glucose plus Insulin
10 units IV
o Give potassium –binding ion exchange resin
o Dialysis: it medial therapy fails or the patient is very
toxic

57. • Hyperphosphatemia is usually controlled by
restriction of dietary phosphate and by oral aluminum
hydroxide or calcium carbonate, which reduce
gastrointestinal absorption of phosphate.
• Hypocalcemia does not usually require treatment.

58. • Anemia: may necessitate blood transfusion if severe or
if recovery is delayed.
• GI bleeding: Regular doses of antacids appear to
reduce the incidence of gastrointestinal hemorrhage
significantly and may be more effective in this regard
than H2 antagonists, or proton pump inhibitors.
• Meticulous care of intravenous cannulae, bladder
catheters, and other invasive devices is mandatory to
avoid infections

59. Dialysis
• Indications and Modalities of Dialysis: - Dialysis
replaces renal function until regeneration and repair
restore renal function. Hemodialysis and peritoneal
dialysis appear equally effective for management of
ARF. Absolute indications for dialysis include:
• 􀂾 Symptoms or signs of the uremic syndrome
• 􀂾 Refractory hypervolemia
• 􀂾 Sever hyperkalemia
• 􀂾 Metabolic acidosis.