Acute KidneyInjury - MiniLecture
IntroductionPreviously known as acute renal failure, is characterized bythe sudden impairment of kidney function resulting...
BackgroundThe incidence of AKI is estimated at 1% of patients that presentto the hospital and 7-50% of patients in the ICU...
AKI can be Prerenal, Intrinsic or Postrenal                                          Acute Kideny Injury       Prerenal   ...
Prerenal AzotemiaPrerenal azotemia is the most common cause of acute kidney injury in theoutpatient setting ◦ Look for pat...
Prerenal azotemiaHistory of poor fluid intake or fluid loss (hemorrhage, diarrhea,vomiting, sequestration into extravascul...
Intrinsic Kidney DiseasesATN - Acute Tubular Necrosis◦ Usually occurs after an ischemic event or exposure to nephrotoxic a...
Intrinsic Kidney DiseasesRecent medication exposure; can have fever, rash arthralgiasskin rash, arthralgias, sinusitis (AG...
Postrenal DiseaseObstruction anywhere in the urinary tract ◦ Bladder outlet obstruction can be seen with bladder scan and ...
Postrenal DiseaseHistory of kidney stones, prostate disease, obstructed bladder catheter,retroperitoneal or pelvic neoplas...
Interpretation of urinary sediment findings in acute kidney injury
ComplicationsUremiaBuildup of nitrogenous waste products, manifested as an elevated BUNconcentration, is a hallmark of AKI...
Management of Ischemia-and Nephrotoxin-Associated Aki1. Optimization of systemic and renal hemodynamics through volumeresu...
Specific Issues1. Nephrotoxin-specifica. Rhabdomyolysis: consider forced alkaline diuresisb. Tumor lysis syndrome: allopur...
Specific Issues4. Hyperkalemiaa. Restriction of dietary potassium intakeb. Discontinuation of potassium-sparing diuretics,...
Dialysis IndicationsDialysis is indicated when medical management fails tocontrol volume overload, hyperkalemia, acidosis,...
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  1. 1. Acute KidneyInjury - MiniLecture
  2. 2. IntroductionPreviously known as acute renal failure, is characterized bythe sudden impairment of kidney function resulting in theretention of nitrogenous and other waste products normallycleared by the kidneys.The term failure reflects only part of the spectrum ofdamage to the kidney that occurs clinically. In most cases ofdamage, the reduction in kidney function is modest.
  3. 3. BackgroundThe incidence of AKI is estimated at 1% of patients that presentto the hospital and 7-50% of patients in the ICU.Part of the initial history should be determining every patientsbaseline Cr.May present as Uremia (malaise, anorexia, nausea, vomiting), butis usually asymptomatic.Acute Kidney Injury Network (AKIN) Criteria Stage Cr Criteria UOP Criteria 1 Cr↑by 1.5-2x baseline or < 0.5 ml/kg/hr for 6hr Cr↑by 0.3 mg/dl 2 Cr↑by 2-3x < 0.5 ml/kg/hr for 12hr 3 Cr↑by more than 3x or Cr↑by < 0.3 ml/kg/hr for 24hr 0.5 if baseline >4mg/dl Or anuria for 12h
  4. 4. AKI can be Prerenal, Intrinsic or Postrenal Acute Kideny Injury Prerenal PostrenalUosm > 5000 mosm/kg Uosm: variableUna < 20meq/L Intrinsic Renal Diseases Una: low early, high lateFEna < 1% FEna: variableMicroscopy - bland Microscopy - bland Acute Interstitial Nephritis Acute Glomerulonephritis Ischemic / Toxic ATN Uosm: variable, ~300 mosm.kg Uosm: variable (>400 in early GN)Uosm ~ 300 mosm/kg Una > 40 meq/L Una: variable (<20meq/l in early GN)Una > 40meq/L FEna > 2% FEna: variable, <1% in early GNFEna > 2% Microscopy – leukocytes, Microscopy – hematuria, proteinuriaMicroscopy – dark pigment cast erythrocyts, leukocyte casts Erythrocyte casts (dysmorphic)
  5. 5. Prerenal AzotemiaPrerenal azotemia is the most common cause of acute kidney injury in theoutpatient setting ◦ Look for patients with decreased PO, diarrhea, vomiting, tachycardia, orthostasis…. ◦ Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics)The kidney functions properly in patients with prerenal azotemia. ◦ True volume depletion can be treated with normal saline. ◦ Decreased effective arterial blood volume can be present in CHF, Cirrhosis or nephrotic syndrome. Treatment should focus on the underlying disease.
  6. 6. Prerenal azotemiaHistory of poor fluid intake or fluid loss (hemorrhage, diarrhea,vomiting, sequestration into extravascular space); NSAID/ACE-I/ARB;heart failure; evidence of volume depletion (tachycardia, absolute orpostural hypotension, low jugular venous pressure, dry mucousmembranes), decreased effective circulatory volume (cirrhosis, heartfailure)BUN/creatinine ratio above 20, FeNa <1%, hyaline casts in urinesediment, urine specific gravity >1.018, urine osmolality >500 mOsm/kg
  7. 7. Intrinsic Kidney DiseasesATN - Acute Tubular Necrosis◦ Usually occurs after an ischemic event or exposure to nephrotoxic agents.◦ Look for muddy brown casts and FeNa>2%AIN - Acute Interstitial Nephritis◦ Classic presentation is fever, rash, eosinophilia and Cr bump 7-10 days after drug exposure.◦ Urine may show leukocytes, leukocyte casts and erythrocytes, cultures will be negative.CIN - Contrast Induced Nephropathy◦ Increased Cr of 0.5mg/dl or 25% 48hrs after contrast administration.◦ Prevent with NS or isotonic fluid+sodium bicarb, hold NSAIDs, metformin and diuretics (in patients without fluid overload).Others – Glomerular Disease, Pigmented Nephropathy,Thrombotic Microangiopathy
  8. 8. Intrinsic Kidney DiseasesRecent medication exposure; can have fever, rash arthralgiasskin rash, arthralgias, sinusitis (AGBM disease), lung hemorrhage(AGBM, ANCA, lupus), recent skin infection or pharyngitis(poststreptococcal)Eosinophilia, sterile pyuria; often nonoliguricANA, ANCA, AGBM antibody, hepatitis serologies, cryoglobulins, bloodculture, decreased complement levels, ASO titer (abnormalities of thesetests depending on etiology)
  9. 9. Postrenal DiseaseObstruction anywhere in the urinary tract ◦ Bladder outlet obstruction can be seen with bladder scan and relieved with catheterization ◦ Ureteral obstruction and hydronephrosis may be seen on ultrasound and noncontrast CT ◦ Order: Order: UA, Uosm, Una, Ucr, BMP, Uurea (if on diuretics)Patients often have a history of pelvic tumors, irradiation, congentialabnormalities, kidney stones, genitourinary, procedures or surgeries, andprostatic enlargement.
  10. 10. Postrenal DiseaseHistory of kidney stones, prostate disease, obstructed bladder catheter,retroperitoneal or pelvic neoplasmpyuria or hematuria
  11. 11. Interpretation of urinary sediment findings in acute kidney injury
  12. 12. ComplicationsUremiaBuildup of nitrogenous waste products, manifested as an elevated BUNconcentration, is a hallmark of AKI. Mental status changes and bleedingcomplications can arise.Hypervolemia and HypovolemiaExpansion of extracellular fluid volume is a major complication ofoliguric and anuric AKI, due to impaired salt and water excretion. Theresult can be weight gain, dependent edema, increased jugular venouspressure, and pulmonary edema.
  13. 13. Management of Ischemia-and Nephrotoxin-Associated Aki1. Optimization of systemic and renal hemodynamics through volumeresuscitation and judicious use of vasopressors2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs,aminoglycosides) if possible3. Initiation of renal replacement therapy when indicated
  14. 14. Specific Issues1. Nephrotoxin-specifica. Rhabdomyolysis: consider forced alkaline diuresisb. Tumor lysis syndrome: allopurinol or rasburicase2. Volume overloada. Salt and water restrictionb. Diureticsc. Ultrafiltration3. HyponatremiaRestriction of enteral free water intake, minimization of hypotonicintravenous solutions including those containing dextrose
  15. 15. Specific Issues4. Hyperkalemiaa. Restriction of dietary potassium intakeb. Discontinuation of potassium-sparing diuretics, ACE inhibitors, ARBs, NSAIDsc. Loop diuretics to promote urinary potassium lossd. Potassium binding ion-exchange resin (sodium polystyrene sulfonate)e. Insulin (10 units regular) and glucose (50 mL of 50% dextrose) to promote entry of potassiumintracellularlyf. Inhaled beta-agonist therapy to promote entry of potassium intracellularlyg. Calcium gluconate or calcium chloride (1 g) to stabilize the myocardium5. Metabolic acidosisa. Sodium bicarbonate (if pH <7.2 to keep serum bicarbonate >15 mmol/L)b. Administration of other bases e.g., THAMc. Renal replacement therapy
  16. 16. Dialysis IndicationsDialysis is indicated when medical management fails tocontrol volume overload, hyperkalemia, acidosis, in sometoxic ingestions, and when there are severe complicationsof uremia (asterixis, pericardial rub or effusion,encephalopathy, uremic bleeding).Late initiation of dialysis carries the risk of avoidablevolume, electrolyte, and metabolic complications of AKI.
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