What is the best approach to manage a patient presenting with anuria, considering potential underlying conditions and current medications such as NSAIDs or ACEIs?

Management of Anuria

Immediately discontinue NSAIDs and ACE inhibitors/ARBs in any patient presenting with anuria, as these medications synergistically compromise renal perfusion and can precipitate or worsen acute kidney injury. 1, 2

Immediate Medication Review and Discontinuation

Stop Nephrotoxic Combinations

• Discontinue NSAIDs immediately in patients with anuria, as these drugs inhibit prostaglandin-dependent renal blood flow and glomerular filtration, particularly when the kidney is in a salt-retaining state or has vascular damage. 3
• Stop ACE inhibitors or ARBs immediately if kidney function continues to worsen beyond an initial 30% creatinine rise, or if anuria develops, as continuation removes critical hemodynamic compensation mechanisms. 4, 5
• The combination of NSAIDs with ACE inhibitors/ARBs and diuretics (the "triple whammy") increases acute kidney injury risk with an adjusted rate ratio of 1.64, and this risk is highest in patients over 75 years or those with baseline renal impairment. 2
• Even dual combinations of NSAIDs with either ACE inhibitors (rate ratio 1.60) or diuretics alone (rate ratio 1.64) significantly increase AKI risk, contrary to older studies that relied on hospital coding. 2

Critical Caveat on ACE Inhibitor/ARB Use

• Do not restart ACE inhibitors or ARBs until anuria resolves and renal function stabilizes, especially if minimal change disease or abrupt-onset nephrotic syndrome is suspected, as these drugs can cause additional acute kidney injury in this context. 4, 6
• The FDA label for furosemide explicitly warns that combined use with ACE inhibitors or ARBs may lead to severe hypotension and deterioration in renal function, including renal failure, requiring interruption or dose reduction. 1

Diagnostic Evaluation for Underlying Cause

Rule Out Obstructive and Vascular Causes

• Obtain urgent renal ultrasound to exclude bilateral ureteral obstruction or bladder outlet obstruction, as furosemide can cause acute urinary retention in patients with bladder emptying disorders, prostatic hyperplasia, or urethral narrowing. 1
• Consider renal isotope scanning and arteriography if acute renal artery occlusion is suspected (particularly in patients with pre-existing vascular disease, hypertension, or atrial fibrillation), as revascularization within 2-14 days can restore function even after prolonged anuria. 7
• Anuria from bilateral renal artery occlusion or occlusion of a solitary kidney is unusual but salvageable with surgical revascularization, especially when collateral circulation exists from pre-existing arterial disease. 7

Assess Volume Status and Prerenal Factors

• Evaluate for volume depletion, as excessive diuresis with furosemide may cause dehydration, blood volume reduction, circulatory collapse, and vascular thrombosis, particularly in elderly patients. 1
• The KDIGO guidelines recommend counseling patients to hold ACE inhibitors/ARBs and diuretics when at risk for volume depletion or during "sick days" to prevent hemodynamic AKI. 4

Initial Management Strategy

Fluid Resuscitation (if hypovolemic)

• Administer intravenous isotonic saline if clinical assessment suggests prerenal azotemia from volume depletion, monitoring for fluid overload in anuric patients.
• Reversible elevations of BUN associated with dehydration should be corrected, particularly in patients with renal insufficiency. 1

Diuretic Trial (if euvolemic or hypervolemic)

• Administer high-dose intravenous furosemide (80-200 mg IV bolus) to attempt conversion from anuric to oliguric acute kidney injury, which improves outcomes and simplifies management. 1
• If no response within 1-2 hours, consider a second dose or continuous infusion, but recognize that lack of response indicates severe tubular injury requiring renal replacement therapy.
• The usual initial oral dose of furosemide for edema is 20-80 mg, but doses may be carefully titrated up to 600 mg/day in clinically severe edematous states with careful monitoring. 1

Avoid Further Nephrotoxic Insults

• Do not administer radiocontrast agents without adequate hydration, as furosemide can lead to higher incidence of contrast nephropathy in high-risk patients compared to those receiving only intravenous hydration. 1
• Avoid aminoglycosides, cisplatin, and other nephrotoxic drugs, as furosemide may increase ototoxic and nephrotoxic potential, especially in the presence of impaired renal function. 1

Monitoring and Supportive Care

Laboratory Surveillance

• Check serum electrolytes (particularly potassium), CO2, creatinine, and BUN frequently during initial management and periodically thereafter, as electrolyte depletion may occur during furosemide therapy. 1
• Monitor for signs of fluid or electrolyte imbalance including hyponatremia, hypochloremic alkalosis, hypokalemia, hypomagnesemia, or hypocalcemia. 1
• Serum and urine electrolyte determinations are particularly important when the patient is vomiting profusely or receiving parenteral fluids. 1

Prepare for Renal Replacement Therapy

• Initiate urgent nephrology consultation for consideration of hemodialysis or continuous renal replacement therapy if anuria persists beyond 24 hours despite conservative management.
• Dialysis may be necessary for 30-45 days even after successful revascularization in patients with previously normal kidneys who develop acute renal artery occlusion. 7

Common Pitfalls to Avoid

• Do not assume anuria is always from acute tubular necrosis—always exclude obstruction and vascular causes with imaging, as these are potentially reversible with intervention. 7
• Do not continue NSAIDs "because the patient needs them for pain"—the nephrotoxic risk is particularly high with NSAIDs having half-lives ≥4 hours (adjusted OR 2.6), and alternative analgesics must be used. 8
• Do not restart ACE inhibitors/ARBs prematurely after anuria resolves, as renal function must be stable for at least 5-7 days before cautiously reintroducing these agents at low doses. 6
• Do not overlook medication-induced acute interstitial nephritis as a cause of anuria, particularly with NSAIDs, which can cause this syndrome with or without nephrotic syndrome. 3