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Here is a comprehensive overview of Acute Renal Failure (ARF) / Acute Kidney Injury (AKI):
Acute Renal Failure (ARF) / Acute Kidney Injury (AKI)
ARF is the older term; AKI is now the preferred name. It refers to a rapid (hours to days) decline in kidney function, resulting in progressive azotemia and disruption of fluid, electrolyte, and acid-base balance.
Definition
The hallmark of AKI is progressive azotemia - accumulation of nitrogenous waste products (BUN, creatinine). When glomerular filtration abruptly ceases, serum creatinine typically rises by 1-2 mg/dL per day.
Classification (3 Categories)
| Category | Mechanism | Common Causes |
|---|---|---|
| Prerenal | Reduced renal blood flow / perfusion | Heart failure, hepatic failure, dehydration, burns, sepsis, shock |
| Intrinsic (Renal) | Parenchymal damage | ATN, AIN, glomerulonephritis, rhabdomyolysis, contrast nephropathy |
| Postrenal | Obstruction of urine flow | BPH, bilateral ureteric obstruction, bladder outlet obstruction |
Diagnostic Approach
Fig. Evaluation of azotemia - Rosen's Emergency Medicine
Step 1: Rule out prerenal causes (correct volume, improve cardiac output)
Step 2: Rule out postrenal obstruction (ultrasound, bladder scan)
Step 3: If both excluded → intrinsic renal disease → urinalysis + urine electrolytes to distinguish vascular, glomerular, AIN, or ATN
Key Diagnostic Labs
| Parameter | Prerenal | Intrinsic (ATN) | Postrenal |
|---|---|---|---|
| Urine Na | < 20 mEq/L | > 40 mEq/L | Variable |
| FENa | < 1% | > 2% | Variable |
| BUN:Cr ratio | > 20:1 | ~10:1 | Variable |
| Urine specific gravity | High (> 1.020) | Low (~1.010) | Variable |
| Urine casts | Hyaline casts | "Muddy brown" granular casts (ATN) | None |
| Urine output | Oliguria | Oliguric or non-oliguric | Anuria/polyuria |
Clinical Features (Systemic Complications)
- Cardiovascular: Pulmonary edema, hypertension, arrhythmia, pericarditis
- Metabolic: Hyperkalemia, metabolic acidosis, hypocalcemia, hyperphosphatemia, hypermagnesemia
- Neurologic: Asterixis, confusion, seizures, coma
- GI: Nausea/vomiting, GI bleeding (~10% of patients), pancreatitis
- Hematologic: Normocytic anemia, platelet dysfunction/bleeding diathesis
- Infectious: Increased susceptibility - pneumonia, septicemia, UTI
The most rapidly lethal complication of AKI is hyperkalemia.
Most Common Intrinsic Cause: Acute Tubular Necrosis (ATN)
ATN is the most common intrinsic cause. It arises from:
- Ischemia - shock, sepsis, severe prolonged prerenal azotemia
- Nephrotoxins:
- Aminoglycoside antibiotics (gradual onset, typically after 1 week)
- Radiocontrast agents (creatinine rises within 3 days, returns to normal in 10-14 days)
- Myoglobinuria (rhabdomyolysis) - test serum CK, not just urine dipstick
- Hemoglobinuria
Risk factors for contrast nephropathy: Pre-existing renal insufficiency (most important), diabetes, age > 60, volume depletion, multiple myeloma, repeated contrast within 72 hours.
Management Principles
- First priority: Address life-threatening complications - hyperkalemia, pulmonary edema
- Treat the underlying cause (e.g., volume resuscitation for prerenal, relieve obstruction for postrenal)
- Avoid further renal insults - nephrotoxic drugs, contrast, hypotension
- Fluid management - avoid overload; monitor daily weights
- Drug dosing adjustment - many drugs require dose modification in renal failure
Indications for urgent dialysis (mnemonic: AEIOU)
- Acidosis (severe, refractory)
- Electrolyte disturbances (refractory hyperkalemia)
- Intoxication (certain toxins)
- Overload (fluid - pulmonary edema)
- Uremia (symptomatic - pericarditis, encephalopathy, bleeding)
Contrast nephropathy prophylaxis
- IV normal saline: 3 mL/kg over 1 hour before, then 1.5 mL/kg/hr for 4 hours after contrast
- Sodium bicarbonate has no advantage over saline
- N-acetylcysteine is not supported by current evidence
AKI vs CKD Differentiation
| Feature favoring CKD | Notes |
|---|---|
| Small kidneys on imaging | Most reliable |
| Bone changes of 2° hyperparathyroidism | Chronic marker |
Note: Anemia, hypocalcemia, and hyperphosphatemia can develop rapidly in AKI and should not be used alone to confirm CKD.
Sources: Rosen's Emergency Medicine, 9e; Harrison's Principles of Internal Medicine, 22e; Washington Manual of Medical Therapeutics
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