What is the management of acute renal insufficiency?

Management of Acute Renal Insufficiency

The management of acute kidney injury (AKI) requires immediate identification and reversal of the underlying cause, withdrawal of nephrotoxic agents, optimization of hemodynamics with fluid resuscitation, and close monitoring for progression to determine need for renal replacement therapy.

Initial Assessment and Risk Factor Removal

Immediately review and discontinue all nephrotoxic medications including NSAIDs, aminoglycosides, ACE inhibitors/ARBs in the acute setting, and any other potentially nephrotoxic drugs 1. This is the single most important modifiable intervention.

Medication Management

• Withdraw diuretics in patients with suspected hypovolemia or prerenal AKI 1
• Adjust dosing of renally-cleared medications to prevent accumulation and toxicity 2
• In hepatic cirrhosis with AKI, furosemide should be discontinued if increasing azotemia and oliguria occur during treatment 3
• Avoid standard opioid dosing in renal failure; morphine, codeine, and tramadol should not be used as first-line agents 4

Fluid Management and Hemodynamic Optimization

Restore intravascular volume with crystalloids or albumin in patients with clinical evidence of hypovolemia 1, 2.

Volume Resuscitation Protocol

• For patients with cirrhosis and AKI stage 1: administer intravenous albumin at 1 g/kg body weight daily for two consecutive days to treat prerenal AKI and allow differential diagnosis 1
• Maintain central venous pressure at 6-8 cm H₂O in trauma-related AKI 5
• In patients without cirrhosis, use crystalloids as first-line volume expansion 2

Important Caveat

Dopamine and diuretics have been proven ineffective in ameliorating the course of acute renal failure and should not be used for this purpose 2. The FDA label for furosemide specifically warns that therapy should be discontinued if increasing azotemia and oliguria occur during treatment of severe progressive renal disease 3.

Categorization by Etiology

Determine if AKI is prerenal (60-70% of cases), intrinsic renal, or postrenal through history, examination, and laboratory evaluation 2.

Laboratory Evaluation

• Urinalysis 2
• Fractional excretion of sodium (FENa) 2
• Blood urea nitrogen to creatinine ratio 2
• Basic metabolic panel 2
• Serial serum creatinine measurements to assess progression 1

Staging and Monitoring

Use the KDIGO/ICA-AKI staging criteria to classify severity and guide management intensity 1.

Stage 1 AKI Management

• Close monitoring of renal function 1
• Remove risk factors as outlined above 1
• Plasma volume expansion if hypovolemia present 1
• Reassess within 48-72 hours for response or progression 1

Progression Criteria

If AKI progresses to higher stages despite initial management, escalate to more intensive monitoring and consider nephrology consultation 1. Patients who do not respond to diuretic withdrawal and volume expansion require treatment as stage 2-3 AKI 1.

Specific Interventions by Cause

Prerenal AKI

• Volume repletion with crystalloids or albumin (albumin preferred in cirrhosis) 1, 2
• Discontinue diuretics and nephrotoxic agents 1
• Correct hypotension with fluids first, then vasopressors if needed 6

Intrinsic Renal AKI

• Identify specific cause: acute tubular necrosis, acute interstitial nephritis, crystal-induced nephropathy, or glomerulonephritis 7
• For crystal-induced AKI (acyclovir, sulfonamides, methotrexate, indinavir): discontinue offending agent, volume repletion, and urinary alkalinization when appropriate 7
• Adjust drug dosing for reduced GFR 2

Postrenal AKI

• Urgent bladder catheterization if urinary retention suspected 8
• Imaging (ultrasound) to identify obstruction 8
• Urologic consultation for relief of obstruction 8

Renal Replacement Therapy

Initiate dialysis for life-threatening complications including severe hyperkalemia, metabolic acidosis, uremic symptoms, or volume overload refractory to medical management 6.

Dialysis Considerations

• Early versus late initiation remains controversial; no consistent benefit to early-start dialysis has been demonstrated 6
• In trauma-related AKI with hemorrhagic risk, use intermittent heparinization (73% of cases) or continuous heparinization (14% of cases) as clinically appropriate 5
• Peritoneal dialysis may not be feasible in abdominal/chest trauma 5

Nutritional Support

• Provide high-caloric diet with 100 mg carbohydrates given 3-4 times daily (parenteral or oral) 5
• Restrict potassium intake to prevent cardiac complications 5
• Maintain adequate caloric intake to minimize protein catabolism 5

Special Populations

Cirrhosis with Ascites

• Initiate therapy in hospital setting 3
• Do not start therapy in hepatic coma or electrolyte depletion until basic condition improved 3
• Strict observation during diuresis to prevent hepatic coma 3
• Supplemental potassium chloride and aldosterone antagonist helpful in preventing complications 3

Trauma Patients

• Prompt haemodialysis combined with medical and surgical treatment reduces mortality 5
• Address underlying injuries (abdominal, extremity, liver, chest, kidney) concurrently 5
• Monitor for hemorrhagic syndrome, crush syndrome, or septic conditions 5

Prevention of Further Injury

Avoid additional nephrotoxic exposures including radiocontrast agents when possible 2, 7. If contrast procedures are necessary, consider prophylaxis with acetylcysteine (relative risk reduction 0.11 for serum creatinine elevation) or sodium bicarbonate pretreatment (relative risk reduction 0.13) 2.

Long-Term Implications

Even a single episode of AKI increases risk of cardiovascular disease, chronic kidney disease, and death 8. Therefore, establish long-term nephrology follow-up for all patients with AKI, regardless of recovery 8.