1. Dr. Ratan Jha (consultant nephrologist)
Dr. Mohd Viquas Uddin Saim (DNB medicine
resident)
Medwin hospital

2. introduction
 Previously known as acute renal failure
 Sudden impairment of kidney function
 Retention of nitrogenous waste products
 Not a single disease
 Designation for conditions sharing common
diagnostic features
 Increase in blood urea and serum creatinine
 Severity ranges from asymptomatic to fatal

3. Why term AKI preferred over ARF ?
 failure reflects only part of the spectrum of damage to the
kidney
 In most cases damage is modest
 Modest damage is not nearly as omnious as frank kidney
failure
 Frank kidney failure often requires acute dialysis therapies
 term renal is not well understood in the general population
 Hence kidney has replaced renal

4. epidemiology
 5–7% of acute care hospital admissions
 30% of admissions to the intensive care unit
 Major complication of diarrheal illnesses, malaria and
leptospirosis
 markedly increased risk of death in hospitalized
individuals
 mortality rates may exceed 50% in ICU patients

5. Etiology

6. Pre renal azotemia
 "azo," meaning nitrogen, and "-emia“
 most common form of AKI
 rise in SCr or BUN concentration due to inadequate renal
plasma flow and intraglomerular hydrostatic pressure to
support normal glomerular filtration
 may coexist with other forms of intrinsic AKI
 When prolonged may lead to ischemic injury called Acute
tubular necrosis
 prerenal azotemia involves no parenchymal damage to the
kidney
 rapidly reversible once intraglomerular hemodynamics are
restored.

7. Pathophysiology of prerenal AKI

8. Renal autoregulation
 Normal GFR is maintained by the relative resistances of the
afferent and efferent renal arterioles
 Renal blood flow accounts for 20% of cardiac output
 renal vasoconstriction and salt and water reabsorption
occur as a homeostatic response to decreased effective
circulating volume or cardiac output
 to maintain blood pressure and increase intravascular
volume to sustain perfusion to the cerebral and coronary
vessels
 Mediators of this response include angiotensin II,
norepinephrine, and vasopressin

9. Renal autoregulation
 Glomerular filtration can be maintained despite
reduced renal blood flow by angiotensin II–mediated
renal efferent vasoconstriction
 Intrarenal biosynthesis of vasodilator prostaglandins
(prostacyclin, prostaglandin E2 also increase in
response to low renal perfusion pressure
 also accomplished by tubuloglomerular feedback
 decreases in solute delivery to the macula densa
(specialized cells within the proximal tubule) elicit
dilation of the juxtaposed afferent arteriole

10. Failure of autoregulation
 There is a limit to autoregulation
 in healthy adults, renal autoregulation usually fails once
the systolic blood pressure falls below 80 mmHg
 Atherosclerosis, long-standing hypertension, and older age
cause impaired capacity for renal afferent vasodilation
 NSAIDs inhibit renal prostaglandin production, limiting
renal afferent vasodilation
 ACE inhibitors and angiotensin receptor blockers (ARBs)
limit renal efferent vasoconstriction
 NSAID’s and ARBs should not be given together.

11. Intrinsic AKI
 most common causes of intrinsic AKI are sepsis,
ischemia, and nephrotoxins
 In many cases, prerenal azotemia advances to tubular
injury
 classically termed "acute tubular necrosis
 Other causes of intrinsic AKI are less common

12. Intrinsic AKI - Glomerular causes
 Post-infectious
 SLE
 ANCA associated
 Henoch schnolen purpura
 Cryoglobulinaemia
 TTP
 HUS
 Accounts for 5 % of cases

13. Intrinsic AKI - tubular causes (ATN)
 Ischemic (50%)
 kidneys are the site of one of the most hypoxic regions in the
body, the renal medulla
 outer medulla is particularly vulnerable to ischemic damage
 AKI more commonly develops when ischemia occurs in the
context of limited renal reserve or coexisting insults such as
sepsis,
 Toxins (35%)
 kidney has very high susceptibility to nephrotoxins due to
extremely high blood perfusion
 Endogenous nephrotoxins : hemoglobin, myoglobin
 Exogenous nephrotoxins : contrast agents, antibiotics, etc,.

14. Intrinsic AKI – interstitial & vascular
causes
 Acute interstitial nephritis
 Drugs : NSAID’s, allopurinol, methicillin
 Granulomatous : tuberculosis, sarcoidosis
 Infective : legionnaire’s disease, pyelonephritis
 Monosodium urate crystals
 Vascular causes
 Renal artery occlusion
 Renal vein thrombosis
 Cholesterol emboli

15. Post renal AKI
 occurs when the unidirectional flow of urine is acutely
blocked either partially or totally
 leads to increased retrograde hydrostatic pressure and
interference with glomerular filtration
 For AKI to occur in healthy individuals, obstruction must
affect both kidneys unless
 Unilateral obstruction may cause AKI in the setting of
significant underlying CKD
 Bladder neck obstruction is a common cause of postrenal
AKI and can be due to prostate disease ,neurogenic
bladder, or therapy with anticholinergic drugs
 Other causes of lower tract obstruction are blood clots,
calculi, and urethral strictures

16. Post renal AKI- ureteric obstruction
 intraluminal obstruction (e.g., calculi, blood clots,
sloughed renal papillae)
 infiltration of the ureteric wall (e.g., neoplasia)
 external compression (e.g., retroperitoneal fibrosis,
neoplasia, abscess, or inadvertent surgical damage)
 pathophysiology of postrenal AKI involves
hemodynamic alterations triggered by an abrupt
increase in intratubular pressures
 Reduced GFR is due to underperfusion of glomeruli

17. Diagnostic evaluation
 presence of AKI is usually inferred by an elevation in
the SCr concentration
 AKI is currently defined by a rise of at least 0.3 mg/dL
or 50% higher than baseline within a 24–48-hours
period or a reduction in urine output to 0.5 mL/kg per
hour for longer than 6 hours
 The distinction between AKI and chronic kidney
disease is important for proper diagnosis and
treatment

18. Diagnostic evaluation
 Features suggestive of CKD than AKI
 from radiologic studies (e.g., small, shrunken kidneys
with cortical thinning on renal ultrasound, or evidence
of renal osteodystrophy)
 laboratory tests such as normocytic anemia or
secondary hyperparathyroidism with
hyperphosphatemia and hypocalcemia, consistent
with CKD
 distinction is straightforward when a recent baseline
SCr concentration is available

19. Diagnostic evaluation : history &
physical evaluation
 Prerenal azotemia : in the setting of vomiting,
diarrhea, glycosuria causing polyuria, and several
medications including diuretics, NSAIDs, ACE
inhibitors, and ARBs
 Postrenal AKI : history of prostatic disease,
nephrolithiasis, or pelvic or paraaortic malignancy .
Abdominal fullness and suprapubic pain can
accompany massive bladder enlargement
 A careful review of all medications is imperative in the
evaluation of an individual with AKI

20. Diagnostic evaluation : Urine
findings
 Anuria is seen in complete urinary tract obstruction, renal
artery occlusion, overwhelming septic shock, severe
ischemia, or severe proliferative glomerulonephritis or
vasculitis
 oliguria, defined as <400 mL/24 husually denotes more
significant AKI than when urine output is preserved
 Preserved urine output can be seen in longstanding urinary
tract obstruction, tubulointerstitial disease, or
nephrotoxicity from cisplatin or aminoglycosides
 In the absence of preexisting proteinuria from CKD, AKI
from ischemia or nephrotoxins leads to mild proteinuria
(<1 g/d)

22. Diagnostic evaluation : blood lab
findings
 Certain forms of AKI are associated with characteristic
patterns in the rise and fall of SCr
 Prerenal azotemia typically leads to modest rises in
SCr that return to baseline with improvement in
hemodynamic status
 Contrast nephropathy leads to a rise in SCr within 24–
48 hours, peak within 3–5 days, and resolution within
5–7 days
 With aminoglycoside antibiotics and cisplatin ,the rise
in SCr is characteristically delayed for 4–5 days to 2
weeks after initial exposure.

23. Diagnostic evaluation : blood lab
findings
 Severe anemia in the absence of bleeding may reflect
hemolysis, multiple myeloma, or thrombotic
microangiopathy
 Peripheral eosinophilia can accompany interstitial
nephritis, atheroembolic disease, polyarteritis nodosa,
and Churg-Strauss vasculitis
 AKI often leads to hyperkalemia, hyperphosphatemia,
and hypocalcemia
 The anion gap may be increased with any cause of
uremia due to retention of anions such as phosphate,
hippurate, sulfate, and urate

24. Diagnostic evaluation : renal failure
indices

25. Diagnostic evaluation : renal failure
indices
The fractional excretion of sodium (FeNa) is the fraction of the filtered sodium load that
is reabsorbed by the tubules and is a measure of both the kidney's ability to reabsorb
sodium

26. Diagnostic evaluation : novel
biomarkers
 BUN and creatinine are functional biomarkers of
glomerular filtration and not tissue injury biomarkers
 suboptimal for the diagnosis of actual parenchymal
kidney damage
 Kidney injury molecule-1 (KIM-1) : for ischemic /
nephrotoxic ATN
 Neutrophil gelatinase associated lipocalin (NGAL), also
known as lipocalin-2 or siderocalin

27. complications
 Uremia
 Hypervolemia/hypovolemia
 Hyponatremia
 Hyperkalemia
 Acidosis
 Hyperphosphatemia/hypocalcemia
 Bleeding
 Cardiac : arrhythmias, pericarditis, and pericardial
effusion

28. treatment
 General issues
 Optimization of systemic and renal hemodynamics
through volume resuscitation and judicious use of
vasopressors
 Elimination of nephrotoxic agents (e.g., ACE
inhibitors, ARBs, NSAIDs, aminoglycosides)
 Initiation of renal replacement therapy when
indicated

29. Treatment : specific issues
 Nephrotoxin-specific
 a. Rhabdomyolysis: consider forced alkaline diuresis
 b. Tumor lysis syndrome: allopurinol or rasburicase
 Volume overload
 a. Salt and water restriction
 b. Diuretics
 c. Ultrafiltration
 Hyperkalemia
 a. Restriction of dietary potassium intake
 b. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARBs, NSAIDs
 c. Loop diuretics to promote urinary potassium loss
 d. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)
 e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry
of potassium intracellularly
 f. Inhaled beta-agonist therapy to promote entry of potassium intracellularly
 g. Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium

30. Treatment : specific issues
 Metabolic acidosis
 a. Sodium bicarbonate (if pH <7.2 to keep serum
bicarbonate >15 mmol/L)
 b. Administration of other bases e.g., THAM
(tromeThamine injection)
 c. Renal replacement therapy
 Hyperphosphatemia
 a. Restriction of dietary phosphate intake
 b. Phosphate binding agents (calcium acetate, sevelamer
hydrochloride, aluminum hydroxide—taken with meals)
 Hypocalcemia
 a. Calcium carbonate or calcium gluconate if symptomatic

31. Indications of dialysis
 indicated when medical management fails to
control
 volume overload
 hyperkalemia
 Acidosis
 in some toxic ingestions
 severe complications of uremia
 Many nephrologists initiate dialysis for AKI empirically when the
BUN exceeds 100 mg/dL

32. Outcome and prognosis
 associated with a significantly increased risk of in-
hospital and long-term mortality
 Prerenal azotemia and postrenal azotemia carry a
better prognosis than most cases of intrinsic AKI
 kidneys may recover even after severe, dialysis-
requiring AKI
 up to 10% may develop end-stage renal disease
 Postdischarge care under the supervision of a
nephrologist for aggressive secondary prevention of
kidney disease is prudent

33. ----------------------------------------
The end
Thank you 