Acute Renal Failure
Definition:
Acute renal failure (ARF), now more commonly termed acute kidney injury (AKI), is a sudden and potentially reversible decline in renal function, characterized by:
- Retention of nitrogenous waste products (elevated urea, creatinine),
- Disturbance in fluid, electrolyte, and acid-base homeostasis, and
- Often associated with oliguria (<400 mL/day) or even anuria (<100 mL/day).
Classification / Etiology:
Acute kidney injury is classified based on the anatomical origin of the cause:
1. Prerenal AKI (due to decreased renal perfusion):
- Most common cause of AKI.
- Mechanism: Hypoperfusion, (when pr goes below 70/40, gfr stops) → ↓ GFR → activation of RAAS & ADH → sodium and water retention.
- Causes:
- Hypovolemia: hemorrhage, dehydration, burns
- Cardiovascular failure: heart failure, shock (esp. BP < 70/40 mmHg)
- Systemic vasodilation: sepsis, anesthesia
- Renal artery stenosis
2. Intrarenal (Renal) AKI (damage to kidney tissue itself):
- Main causes:
- Acute tubular necrosis (ATN) – ischemia or toxins
- Glomerulonephritis (immune-mediated)
- Vasculitis (polyarteritis nodosa, SLE)
- Interstitial nephritis (e.g., due to drugs like NSAIDs, antibiotics)
3. Postrenal AKI (obstruction of urine outflow):
- Mechanism: Obstruction → ↑ backpressure → ↓ GFR
- Causes:
- Intrinsic: nephrolithiasis, blood clots
- Extrinsic: retroperitoneal mass, prostate hyperplasia, tumors
Pathogenesis:
Although the initial mechanism differs (pre-, intra-, or postrenal), prolonged injury always leads to ischemia of tubular epithelium → acute tubular necrosis (ATN):
- ATN is potentially reversible if treated early.
- Ischemic injury leads to:
- Shedding of tubular cells → obstructing casts
- Impaired reabsorption & secretion
- Tubular backleak of filtrate → ↓ effective GFR
Clinical Features:
Early (mild to moderate AKI):
- Fatigue, malaise, nausea
- Oliguria or anuria
- Edema
Progressed (severe AKI):
- Pulmonary edema (dyspnea, orthopnea)
- Peripheral edema
- Altered mental status (due to uremia)
- Kussmaul breathing (metabolic acidosis)
- Third heart sound (S3) may be heard
- Possible pericardial friction rub (uremic pericarditis)
Diagnosis:
Physical Examination:
- Assess for hypotension, dehydration, or volume overload
- Check for palpable kidneys (suggestive of obstructive uropathy)
- Signs of fluid overload: rales, elevated JVP, edema
Laboratory Investigations:
- Urine analysis:
- Proteinuria, hematuria, leukocyturia
- Brown granular casts (ATN)
- Blood tests:
- ↑ Creatinine gold standard, ↑ Urea (azotemia)
- ↑ Potassium → risk of arrhythmias
- Metabolic acidosis (decompensated)
- Elevated uric acid
Instrumental Tests:
- Abdominal ultrasound: check for obstruction or hydronephrosis
- ECG: monitor for hyperkalemia-induced arrhythmias (peaked T waves, QRS widening)
- Chest X-ray: evaluate for pulmonary edema
- Echocardiography: assess cardiac function if HF suspected
- Additional tests for primary cause as needed