• Like
Acute Kidney Injury
Upcoming SlideShare
Loading in...5

Thanks for flagging this SlideShare!

Oops! An error has occurred.

Acute Kidney Injury



Published in Health & Medicine
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
    Be the first to like this
No Downloads


Total Views
On SlideShare
From Embeds
Number of Embeds



Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

    No notes for slide


  • 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)
  • 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. 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. Diagnostic evaluation : renal failure indices
  • 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. 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. complications  Uremia  Hypervolemia/hypovolemia  Hyponatremia  Hyperkalemia  Acidosis  Hyperphosphatemia/hypocalcemia  Bleeding  Cardiac : arrhythmias, pericarditis, and pericardial effusion
  • 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. 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. 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. 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. 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. ---------------------------------------- The end Thank you 