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Emergency And Acute Medicine – Renal Failure (Acute Kidney Injury)
Acute kidney injury (AKI) is the preferred term for what was previously called acute renal failure. It represents a spectrum of acute changes in glomerular filtration rate and urine output, resulting in accumulation of nitrogenous waste products. Severity is defined by the RIFLE criteria: Risk (creatinine increase ×1.5 or GFR decrease >25%, urine output <0.5 ml />g/h for >6 hours), Injury (creatinine ×2 or GFR decrease >50%, urine output <0.5 ml />g/h for >12 hours), and Failure (creatinine ×3 or GFR decrease >75% or creatinine ≥4 mg/dL with acute rise ≥0.5 mg/dL, urine output <0.3 ml />g/h for 24 hours or anuria for 12 hours). Outcome stages include Loss (>4 weeks of renal dysfunction) and ESRD (>3 months). Higher RIFLE stages correlate with increased short- and intermediate-term mortality.
AKI is categorized as prerenal, intrinsic (intrarenal), or postrenal. Prerenal AKI results from renal hypoperfusion without intrinsic parenchymal damage unless prolonged. Causes include hypovolemia, heart failure, systemic vasodilation from sepsis or anaphylaxis, and low cardiac output states. Intrinsic AKI results from parenchymal disease such as acute tubular necrosis (ATN), glomerulonephritis, vasculitis, allergic interstitial nephritis, hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), rhabdomyolysis, nephrotoxins, or renal vascular thrombosis. Iatrogenic causes include aminoglycosides, radiocontrast, NSAIDs, ACE inhibitors, and angiotensin receptor blockers. Postrenal AKI is due to urinary tract obstruction, commonly from prostatic hypertrophy, prostatitis, stones, or malignancy.
AKI is often asymptomatic and detected incidentally on laboratory testing. Oliguria (<400 ml />ay) may be present. Fluid overload may cause dyspnea, hypertension, jugular venous distention, pulmonary edema, peripheral edema, ascites, pleural effusions, or pericardial effusion. Uremic symptoms include nausea, vomiting, pruritus, confusion, asterixis, seizures, and pericarditis. Fever and rash suggest allergic interstitial nephritis. Flank pain may indicate renal vein thrombosis. Postrenal obstruction may present with abdominal pain, distended bladder, oliguria, or anuria. Hyperkalemia and metabolic acidosis are potentially life-threatening complications.
History should include prior kidney disease, recent illness, medication exposure (especially nephrotoxins), fluid losses, and weight changes. Physical examination evaluates mental status, volume status, cardiac findings (S3, jugular venous distention), pulmonary crackles, abdominal or flank tenderness, edema, and skin changes. Elderly patients are particularly vulnerable to prerenal causes and medication toxicity, and baseline creatinine may underestimate renal impairment due to reduced muscle mass.
Essential evaluation includes serum electrolytes (including calcium, magnesium, and phosphate), BUN, creatinine, CBC, urinalysis with microscopy, and ECG. Fractional excretion of sodium (FENa) or urea may help differentiate prerenal from intrinsic causes. Postvoid residual measurement or renal ultrasound is necessary to exclude obstruction, particularly in older men.
In prerenal AKI, urinalysis typically shows high specific gravity (>1.018), urine osmolality >500 mmol/kg, low urine sodium (<10 mmol />), hyaline casts, BUN/creatinine ratio >20, and FENa <1%, with improvement after restoration of perfusion. intrinsic aki often shows bun />reatinine ratio <10-15 and fena>2%. ATN is associated with brown granular casts, urine sodium >20 mmol/L, and urine osmolality <350 mmol />g. Glomerulonephritis presents with red cell casts and proteinuria. Allergic interstitial nephritis shows white blood cells and WBC casts with possible eosinophilia. Postrenal AKI often has relatively normal urinalysis and is confirmed by imaging showing obstruction. Ultrasound is highly sensitive for detecting obstruction.
Initial management focuses on airway, breathing, and circulation, oxygen for hypoxia, and intravenous normal saline for volume depletion. Nephrotoxic medications should be discontinued. Monitor urine output closely. Indications for emergent dialysis include intractable hypertension, refractory volume overload, uremic encephalopathy, uremic bleeding or pericarditis, BUN >100 mg/dL, severe metabolic acidosis (pH <7.2), and refractory hyperkalemia.< />pan>
Hyperkalemia requires prompt treatment. For potassium >6.5 mEq/L or ECG changes, administer calcium (calcium gluconate in awake patients, calcium chloride in pulseless patients) to stabilize myocardium, followed by insulin with dextrose, nebulized albuterol, and loop diuretics if not anuric. Dialysis is required for refractory cases. Sodium polystyrene sulfonate or calcium polystyrene sulfonate may be used in less urgent cases. Sodium bicarbonate may be considered for severe metabolic acidosis but should be used cautiously due to sodium load, especially in oliguric or anuric patients.
Prerenal AKI is treated with volume resuscitation and correction of underlying hypoperfusion. Intrinsic causes require targeted therapy such as glucocorticoids or plasma exchange for glomerulonephritis, supportive care for ATN, aggressive fluids for rhabdomyolysis, and management of electrolyte disturbances. Postrenal AKI requires relief of obstruction.
Admission is required for new-onset AKI, significant electrolyte abnormalities, hyperkalemia, volume overload with hypoxia, uremia, or altered mental status. Stable patients with mild laboratory abnormalities may be managed with close follow-up. Key pitfalls include inappropriate use of nephrotoxic medications, failure to recognize hyperkalemia, and underdosing insulin in renal or liver disease leading to hypoglycemia. Contrast exposure should be avoided whenever possible in patients with AKI.
Acute kidney injury (AKI) is the preferred term for what was previously called acute renal failure. It represents a spectrum of acute changes in glomerular filtration rate and urine output, resulting in accumulation of nitrogenous waste products. Severity is defined by the RIFLE criteria: Risk (creatinine increase ×1.5 or GFR decrease >25%, urine output <0.5 ml />g/h for >6 hours), Injury (creatinine ×2 or GFR decrease >50%, urine output <0.5 ml />g/h for >12 hours), and Failure (creatinine ×3 or GFR decrease >75% or creatinine ≥4 mg/dL with acute rise ≥0.5 mg/dL, urine output <0.3 ml />g/h for 24 hours or anuria for 12 hours). Outcome stages include Loss (>4 weeks of renal dysfunction) and ESRD (>3 months). Higher RIFLE stages correlate with increased short- and intermediate-term mortality.
AKI is categorized as prerenal, intrinsic (intrarenal), or postrenal. Prerenal AKI results from renal hypoperfusion without intrinsic parenchymal damage unless prolonged. Causes include hypovolemia, heart failure, systemic vasodilation from sepsis or anaphylaxis, and low cardiac output states. Intrinsic AKI results from parenchymal disease such as acute tubular necrosis (ATN), glomerulonephritis, vasculitis, allergic interstitial nephritis, hemolytic uremic syndrome (HUS), thrombotic thrombocytopenic purpura (TTP), rhabdomyolysis, nephrotoxins, or renal vascular thrombosis. Iatrogenic causes include aminoglycosides, radiocontrast, NSAIDs, ACE inhibitors, and angiotensin receptor blockers. Postrenal AKI is due to urinary tract obstruction, commonly from prostatic hypertrophy, prostatitis, stones, or malignancy.
AKI is often asymptomatic and detected incidentally on laboratory testing. Oliguria (<400 ml />ay) may be present. Fluid overload may cause dyspnea, hypertension, jugular venous distention, pulmonary edema, peripheral edema, ascites, pleural effusions, or pericardial effusion. Uremic symptoms include nausea, vomiting, pruritus, confusion, asterixis, seizures, and pericarditis. Fever and rash suggest allergic interstitial nephritis. Flank pain may indicate renal vein thrombosis. Postrenal obstruction may present with abdominal pain, distended bladder, oliguria, or anuria. Hyperkalemia and metabolic acidosis are potentially life-threatening complications.
History should include prior kidney disease, recent illness, medication exposure (especially nephrotoxins), fluid losses, and weight changes. Physical examination evaluates mental status, volume status, cardiac findings (S3, jugular venous distention), pulmonary crackles, abdominal or flank tenderness, edema, and skin changes. Elderly patients are particularly vulnerable to prerenal causes and medication toxicity, and baseline creatinine may underestimate renal impairment due to reduced muscle mass.
Essential evaluation includes serum electrolytes (including calcium, magnesium, and phosphate), BUN, creatinine, CBC, urinalysis with microscopy, and ECG. Fractional excretion of sodium (FENa) or urea may help differentiate prerenal from intrinsic causes. Postvoid residual measurement or renal ultrasound is necessary to exclude obstruction, particularly in older men.
In prerenal AKI, urinalysis typically shows high specific gravity (>1.018), urine osmolality >500 mmol/kg, low urine sodium (<10 mmol />), hyaline casts, BUN/creatinine ratio >20, and FENa <1%, with improvement after restoration of perfusion. intrinsic aki often shows bun />reatinine ratio <10-15 and fena>2%. ATN is associated with brown granular casts, urine sodium >20 mmol/L, and urine osmolality <350 mmol />g. Glomerulonephritis presents with red cell casts and proteinuria. Allergic interstitial nephritis shows white blood cells and WBC casts with possible eosinophilia. Postrenal AKI often has relatively normal urinalysis and is confirmed by imaging showing obstruction. Ultrasound is highly sensitive for detecting obstruction.
Initial management focuses on airway, breathing, and circulation, oxygen for hypoxia, and intravenous normal saline for volume depletion. Nephrotoxic medications should be discontinued. Monitor urine output closely. Indications for emergent dialysis include intractable hypertension, refractory volume overload, uremic encephalopathy, uremic bleeding or pericarditis, BUN >100 mg/dL, severe metabolic acidosis (pH <7.2), and refractory hyperkalemia.< />pan>
Hyperkalemia requires prompt treatment. For potassium >6.5 mEq/L or ECG changes, administer calcium (calcium gluconate in awake patients, calcium chloride in pulseless patients) to stabilize myocardium, followed by insulin with dextrose, nebulized albuterol, and loop diuretics if not anuric. Dialysis is required for refractory cases. Sodium polystyrene sulfonate or calcium polystyrene sulfonate may be used in less urgent cases. Sodium bicarbonate may be considered for severe metabolic acidosis but should be used cautiously due to sodium load, especially in oliguric or anuric patients.
Prerenal AKI is treated with volume resuscitation and correction of underlying hypoperfusion. Intrinsic causes require targeted therapy such as glucocorticoids or plasma exchange for glomerulonephritis, supportive care for ATN, aggressive fluids for rhabdomyolysis, and management of electrolyte disturbances. Postrenal AKI requires relief of obstruction.
Admission is required for new-onset AKI, significant electrolyte abnormalities, hyperkalemia, volume overload with hypoxia, uremia, or altered mental status. Stable patients with mild laboratory abnormalities may be managed with close follow-up. Key pitfalls include inappropriate use of nephrotoxic medications, failure to recognize hyperkalemia, and underdosing insulin in renal or liver disease leading to hypoglycemia. Contrast exposure should be avoided whenever possible in patients with AKI.
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