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Dr. Ratan Jha (consultant nephrologist)
Dr. Mohd Viquas Uddin Saim (DNB medicine
resident)
Medwin hospital
introduction
 Previously known as acute renal failure
 Sudden impairment of kidney function
 Retention of nitrogenous w...
Why term AKI preferred over ARF ?
 failure reflects only part of the spectrum of damage to the
kidney
 In most cases dam...
epidemiology
 5–7% of acute care hospital admissions
 30% of admissions to the intensive care unit
 Major complication ...
Etiology
Pre renal azotemia
 "azo," meaning nitrogen, and "-emia“
 most common form of AKI
 rise in SCr or BUN concentration due...
Pathophysiology of prerenal AKI
Renal autoregulation
 Normal GFR is maintained by the relative resistances of the
afferent and efferent renal arterioles
...
Renal autoregulation
 Glomerular filtration can be maintained despite
reduced renal blood flow by angiotensin II–mediated...
Failure of autoregulation
 There is a limit to autoregulation
 in healthy adults, renal autoregulation usually fails onc...
Intrinsic AKI
 most common causes of intrinsic AKI are sepsis,
ischemia, and nephrotoxins
 In many cases, prerenal azote...
Intrinsic AKI - Glomerular causes
 Post-infectious
 SLE
 ANCA associated
 Henoch schnolen purpura
 Cryoglobulinaemia
...
Intrinsic AKI - tubular causes (ATN)
 Ischemic (50%)
 kidneys are the site of one of the most hypoxic regions in the
bod...
Intrinsic AKI – interstitial & vascular
causes
 Acute interstitial nephritis
 Drugs : NSAID’s, allopurinol, methicillin
...
Post renal AKI
 occurs when the unidirectional flow of urine is acutely
blocked either partially or totally
 leads to in...
Post renal AKI- ureteric obstruction
 intraluminal obstruction (e.g., calculi, blood clots,
sloughed renal papillae)
 in...
Diagnostic evaluation
 presence of AKI is usually inferred by an elevation in
the SCr concentration
 AKI is currently de...
Diagnostic evaluation
 Features suggestive of CKD than AKI
 from radiologic studies (e.g., small, shrunken kidneys
with ...
Diagnostic evaluation : history &
physical evaluation
 Prerenal azotemia : in the setting of vomiting,
diarrhea, glycosur...
Diagnostic evaluation : Urine
findings
 Anuria is seen in complete urinary tract obstruction, renal
artery occlusion, ove...
Diagnostic evaluation : blood lab
findings
 Certain forms of AKI are associated with characteristic
patterns in the rise ...
Diagnostic evaluation : blood lab
findings
 Severe anemia in the absence of bleeding may reflect
hemolysis, multiple myel...
Diagnostic evaluation : renal failure
indices
Diagnostic evaluation : renal failure
indices
The fractional excretion of sodium (FeNa) is the fraction of the filtered so...
Diagnostic evaluation : novel
biomarkers
 BUN and creatinine are functional biomarkers of
glomerular filtration and not t...
complications
 Uremia
 Hypervolemia/hypovolemia
 Hyponatremia
 Hyperkalemia
 Acidosis
 Hyperphosphatemia/hypocalcemi...
treatment
 General issues
 Optimization of systemic and renal hemodynamics
through volume resuscitation and judicious us...
Treatment : specific issues
 Nephrotoxin-specific
 a. Rhabdomyolysis: consider forced alkaline diuresis
 b. Tumor lysis...
Treatment : specific issues
 Metabolic acidosis
 a. Sodium bicarbonate (if pH <7.2 to keep serum
bicarbonate >15 mmol/L)...
Indications of dialysis
 indicated when medical management fails to
control
 volume overload
 hyperkalemia
 Acidosis
...
Outcome and prognosis
 associated with a significantly increased risk of in-
hospital and long-term mortality
 Prerenal ...
----------------------------------------
The end
Thank you 
Acute Kidney Injury
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Acute Kidney Injury

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Acute Kidney Injury

  1. 1. Dr. Ratan Jha (consultant nephrologist) Dr. Mohd Viquas Uddin Saim (DNB medicine resident) Medwin hospital
  2. 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. 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. 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. 5. Etiology
  6. 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. 7. Pathophysiology of prerenal AKI
  8. 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. 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. 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. 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. 12. Intrinsic AKI - Glomerular causes  Post-infectious  SLE  ANCA associated  Henoch schnolen purpura  Cryoglobulinaemia  TTP  HUS  Accounts for 5 % of cases
  13. 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. 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. 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. 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. 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. 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. 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. 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)
  21. 21. 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.
  22. 22. 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
  23. 23. Diagnostic evaluation : renal failure indices
  24. 24. 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
  25. 25. 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
  26. 26. complications  Uremia  Hypervolemia/hypovolemia  Hyponatremia  Hyperkalemia  Acidosis  Hyperphosphatemia/hypocalcemia  Bleeding  Cardiac : arrhythmias, pericarditis, and pericardial effusion
  27. 27. 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
  28. 28. 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
  29. 29. 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
  30. 30. 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
  31. 31. 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
  32. 32. ---------------------------------------- The end Thank you 

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