Acute Kidney Injury: Symptoms, Causes & Treatment

Acute kidney injury (AKI), formerly acute renal failure, is a sudden decline in renal function over hours to days, characterized by rising serum creatinine and/or reduced urine output. The KDIGO (Kidney Disease: Improving Global Outcomes) staging criteria define AKI as: rise in serum creatinine ≥0.3 mg/dL within 48 hours, OR ≥1.5× baseline within 7 days, OR urine output <0.5 mL/kg/hour for ≥6 hours. AKI is staged 1–3 by severity.

AKI affects 10–15% of all hospitalized patients and >50% of ICU patients, representing one of the most common and serious medical complications worldwide. Mechanistically, AKI is classified as: (1) Prerenal (55–70%): reduced renal perfusion from hypovolemia (hemorrhage, dehydration), cardiogenic shock, sepsis, hepatorenal syndrome — tubular function is initially intact; (2) Intrinsic renal (25–40%): direct parenchymal injury, most commonly acute tubular necrosis (ATN) from prolonged ischemia or nephrotoxins (aminoglycosides, contrast media, NSAIDs, cisplatin, myoglobin in rhabdomyolysis); glomerulonephritis and interstitial nephritis are less common; (3) Postrenal (<5%): obstruction of urine flow (benign prostatic hyperplasia, bilateral ureteral obstruction, retroperitoneal fibrosis).

Outcomes depend critically on early identification and treatment of the underlying cause. Most prerenal AKI reverses rapidly with fluid resuscitation. Established ATN from prolonged ischemia or nephrotoxins may take 1–3 weeks to recover. AKI in critically ill patients carries high mortality (40–60% in ICU-AKI) and significantly increases the risk of subsequent chronic kidney disease (CKD).

• Oliguria (<400 mL/day) or anuria (<100 mL/day) — though urine output may be normal in non-oliguric AKI
• Fluid retention: peripheral edema, pulmonary edema (dyspnea, orthopnea)
• Nausea, vomiting, anorexia, hiccups from uremia
• Altered mental status and encephalopathy in severe uremia
• Hyperkalemia symptoms: muscle weakness, cardiac arrhythmias (peaked T waves, wide QRS on ECG)
• Uremic frost and fetor (severe advanced AKI)

• Reduced renal perfusion (prerenal): dehydration, hemorrhage, septic shock, cardiogenic shock, hepatorenal syndrome, major surgery
• Nephrotoxins: NSAIDs, aminoglycosides (gentamicin), IV contrast media (contrast nephropathy), cisplatin, vancomycin, ACE inhibitors in bilateral RAS, myoglobin (rhabdomyolysis), hemoglobin (hemolysis)
• Rhabdomyolysis: crush injuries, extreme exertion, statins, cocaine, seizures — myoglobin directly injures tubules
• Obstruction (postrenal): BPH, bilateral ureteral obstruction (stones, malignancy), neurogenic bladder
• Glomerulonephritis, acute interstitial nephritis (drug hypersensitivity, infections), thrombotic microangiopathy (HUS/TTP)

Serum creatinine and urea: rising creatinine is the primary diagnostic marker; KDIGO staging guides severity assessment. Urinalysis with microscopy: muddy-brown granular casts and renal tubular epithelial cells indicate ATN; dysmorphic RBCs indicate glomerulonephritis; WBC casts indicate pyelonephritis or interstitial nephritis. Fractional excretion of sodium (FENa <1% = prerenal; >2% = intrinsic renal). Renal ultrasound: essential to exclude obstruction (hydronephrosis); also assesses kidney size (small = CKD, normal/large = AKI). Electrolytes (K+, bicarbonate), arterial blood gas (metabolic acidosis), CBC, coagulation studies. Kidney biopsy for unexplained intrinsic AKI when diagnosis uncertain.

Treat the underlying cause: IV fluid resuscitation for prerenal AKI (isotonic saline/albumin); discontinue nephrotoxins; relieve obstruction (catheterization for urethral obstruction, ureteral stenting for upper tract); treat sepsis aggressively. Electrolyte management: hyperkalemia (calcium gluconate for cardiac protection, insulin-glucose to shift K+ intracellularly, furosemide if urine output present, kayexalate/patiromer, dialysis for refractory hyperkalaemia). Supportive: fluid balance optimization, nutritional support, avoid nephrotoxic drugs, dose-adjust renally cleared medications. Renal replacement therapy (RRT/dialysis): indicated for refractory hyperkalemia (K+ >6.5 mEq/L), severe metabolic acidosis (pH <7.1), pulmonary edema refractory to diuretics, uremic encephalopathy, or pericarditis.

• Life-threatening hyperkalemia with ventricular arrhythmias and cardiac arrest
• Severe metabolic acidosis impairing cardiac function
• Pulmonary edema from fluid overload
• Uremic encephalopathy, pericarditis, bleeding from platelet dysfunction
• Progression to CKD in 25–30% and end-stage renal disease requiring permanent dialysis in 5%
• High ICU mortality (40–60% in severe AKI with multiorgan failure)

• Pre-hydration before iodinated contrast media in high-risk patients; use iso-osmolar contrast and minimum dose
• Avoid concurrent nephrotoxin combinations (e.g., NSAIDs + ACE inhibitors + diuretics — the triple whammy)
• Aggressive fluid resuscitation in sepsis, trauma, and major surgery
• Regular monitoring of renal function in high-risk groups: diabetics, hypertensives, elderly, CKD patients
• Ensure adequate hydration during febrile illness and diarrheal diseases