What is the treatment for acute renal failure?

Treatment of Acute Renal Failure

Immediately discontinue all nephrotoxic medications, optimize volume status with aggressive fluid resuscitation if volume depleted, and adjust all remaining medications based on current GFR—these three interventions form the cornerstone of acute renal failure management and directly impact mortality. 1

Immediate Nephrotoxin Management (First Priority)

Stop all potentially nephrotoxic drugs immediately upon recognition of acute renal failure, as drugs account for 20-25% of AKI cases and each nephrotoxin increases AKI odds by 53%. 2, 1

Specific medications to discontinue:

• NSAIDs must be stopped immediately, especially when combined with diuretics and ACE inhibitors/ARBs (the "triple whammy"), as this combination more than doubles AKI risk 2, 1
• Hold ACE inhibitors and ARBs during the acute phase when GFR is unstable or volume status is not optimized 2, 1
• Avoid macrolide-statin combinations (clarithromycin or erythromycin with statins) due to rhabdomyolysis risk from CYP3A4 inhibition 2
• Discontinue any medication with temporal relationship to the acute deterioration 1

Critical caveat: Do not delay essential antibiotics for life-threatening infections—start these immediately as each hour of delay increases mortality, but choose the least nephrotoxic option and adjust doses appropriately. 2, 3

Volume Status Optimization (Second Priority)

Assess hydration status immediately and correct volume depletion with aggressive intravenous fluid resuscitation, as this remains the most efficient and evidence-based intervention for preventing and treating acute renal failure. 2, 1, 4

Volume assessment approach:

• Determine if patient is volume depleted, euvolemic, or overloaded 1
• For volume depletion: aggressive IV fluid resuscitation 1
• For volume overload: loop diuretics if clearly fluid overloaded with long CHF history 2
• Monitor hourly urine output with bladder catheter in severe cases 1

When renal failure is secondary to hypoperfusion, the urinary sodium/potassium ratio is characteristically <1, which helps distinguish this from acute tubular necrosis. 2

Comprehensive Medication Reconciliation (Third Priority)

Perform immediate medication reconciliation at transition of care and adjust all doses based on current GFR using validated eGFR equations. 2, 1

Medication adjustment protocol:

• Review every medication for necessity, nephrotoxic potential, and appropriate dosing 2
• Use creatinine-cystatin C equations or measured GFR for narrow therapeutic window drugs 1
• Recognize that AKI impairs hepatic cytochrome P450 activity, affecting drug metabolism beyond just renal clearance 2, 1
• Assess impact of concurrent illness (sepsis, heart failure) on drug pharmacokinetics 2
• Consider that volume of distribution changes in AKI affect drug levels 2

Specific drug considerations:

• Trimethoprim-sulfamethoxazole: avoid if creatinine clearance <15 ml/min 2, 5
• Diuretics: may need progressive dose increases or addition of different mechanism diuretic (e.g., metolazone) 2
• Monitor therapeutic drug levels for medications with narrow therapeutic windows 1

Intensive Laboratory Monitoring

Establish daily monitoring of eGFR and serum creatinine, with daily to twice-daily electrolyte checks (especially potassium). 1

Monitoring protocol:

• Daily eGFR and serum creatinine 1
• Daily to twice-daily electrolytes, with particular attention to potassium 1
• Therapeutic drug levels for narrow therapeutic window medications 1
• Urinalysis and culture if infection suspected 1

Identify and Treat Underlying Causes

Systematically evaluate for reversible prerenal, intrarenal, and postrenal causes while treating underlying infections promptly. 1

Diagnostic approach:

• Obtain urine studies to differentiate causes (urinary sodium, urine nitrogen concentration, urinary sediment) 2, 1
• Acute tubular necrosis shows increased urinary sodium, reduced urine nitrogen, and typical sediment findings 2
• Obtain urine culture before starting antibiotics if infection suspected 1, 5

Renal Replacement Therapy Considerations

For severe renal dysfunction with refractory fluid retention despite diuretics, continuous veno-venous hemofiltration (CVVH) may become necessary. 2

CVVH combined with positive inotropic agents can increase renal blood flow, improve renal function, restore diuretic efficiency, and has been associated with increased urine output, reduced symptoms and filling pressures, and improved laboratory abnormalities including hyponatremia. 2

Critical Pitfalls to Avoid

• Never combine multiple nephrotoxins—each additional nephrotoxin exponentially increases AKI risk 2, 1
• Never fail to document medication restart plans, particularly for ACE inhibitors/ARBs which should only be restarted after GFR stabilizes and volume status is optimized 2, 1
• Never attempt to restore normal blood pressure values rapidly in hypertensive crisis with AKI—aim for initial 30 mmHg reduction over minutes, then progressive decrease over hours to avoid organ hypoperfusion 2
• Never use low-dose dopamine for renal protection—it has never been proven useful in prospective trials and causes significant side effects 4
• Educate patients to avoid NSAIDs and new medications without consulting their physician during recovery phase 2, 1

Electrolyte and Acid-Base Management

Maintain careful electrolyte balance, particularly potassium, calcium, and phosphorus, and treat metabolic acidosis as needed. 6, 7

The kidneys' role in homeostasis means that kidney failure leads to derangements requiring frequent reassessment and treatment plan adjustments in response to the rapidly changing clinical situation. 6