What is the best management approach for a patient with a history of Focal Segmental Glomerulosclerosis (FSGS) presenting with bilateral flank pain and anuria for the last 12 hours?

Acute Management of Anuria with Bilateral Flank Pain in FSGS Patient

This patient requires immediate hospitalization for urgent evaluation of obstructive uropathy or acute kidney injury—anuria for 12 hours is a medical emergency that supersedes routine FSGS management and demands immediate imaging (renal ultrasound or CT) to exclude bilateral ureteral obstruction, followed by emergent nephrology consultation.

Immediate Diagnostic Workup

Critical First Steps

• Obtain emergent renal ultrasound to assess for hydronephrosis indicating bilateral ureteral obstruction, which is the most life-threatening reversible cause of anuria with bilateral flank pain 1
• Measure serum creatinine, BUN, potassium, and bicarbonate immediately to assess degree of acute kidney injury and identify life-threatening hyperkalemia 2
• Place Foley catheter to confirm true anuria versus urinary retention and monitor urine output going forward 1
• Check bladder scan if catheterization unsuccessful to exclude lower urinary tract obstruction 1

Secondary Urgent Evaluation

• Measure blood pressure urgently to exclude hypertensive emergency (systolic ≥180 mmHg or diastolic ≥120 mmHg), which can trigger thrombotic microangiopathy in FSGS patients 3
• Obtain serum electrolytes including calcium and magnesium to identify metabolic derangements that may complicate management 4
• Review medication list for nephrotoxic agents, particularly NSAIDs which cause acute kidney injury when combined with underlying kidney disease and increased prostaglandin synthesis 1

Differential Diagnosis for Anuria in FSGS

Obstructive Causes (Most Urgent)

• Bilateral ureteral obstruction from retroperitoneal fibrosis, which can present with bilateral flank pain and anuria despite patent ureters on imaging—ureteral patency does not ensure actual urine flow 1
• Bilateral nephrolithiasis causing complete obstruction, particularly relevant given bilateral flank pain 1

Intrinsic Renal Causes

• Acute tubular necrosis from volume depletion in nephrotic syndrome, especially if patient taking ACE inhibitors/ARBs and diuretics during intercurrent illness 3
• Calcineurin inhibitor toxicity if patient on cyclosporine or tacrolimus for steroid-resistant FSGS 2, 5
• Thrombotic microangiopathy triggered by malignant hypertension in setting of FSGS 3

Prerenal Causes

• Severe volume depletion from aggressive diuresis in nephrotic syndrome 3
• Hypotension from sepsis or other systemic illness 3

Immediate Management Algorithm

If Obstructive Uropathy Confirmed

• Emergent urology consultation for bilateral nephrostomy tube placement or ureteral stent placement 1
• Do not delay intervention—permanent kidney damage occurs rapidly with complete bilateral obstruction 1

If Hypertensive Emergency (BP ≥180/120)

• Initiate IV labetalol or nicardipine in ICU setting, targeting 20-25% reduction in mean arterial pressure within first hour 3
• Avoid rapid BP reduction which can worsen kidney perfusion 3
• Once stabilized, maximize ACE inhibitor or ARB therapy which is mandatory in FSGS with proteinuria 3

If Acute Tubular Necrosis from Volume Depletion

• Hold ACE inhibitors/ARBs and diuretics immediately 3
• Provide cautious IV fluid resuscitation with isotonic saline, monitoring for volume overload given nephrotic syndrome 3
• Monitor potassium closely and treat hyperkalemia aggressively if present 2

If CNI Toxicity Suspected

• Check cyclosporine or tacrolimus trough level immediately 2
• Reduce CNI dose or hold temporarily if supratherapeutic levels or clinical suspicion high 2
• Consider switching to alternative immunosuppression if toxicity confirmed 2

Critical Monitoring During Acute Phase

Hourly to Every 4 Hours

• Urine output monitoring via Foley catheter to assess response to intervention 1
• Blood pressure monitoring targeting systolic <120 mmHg once acute crisis resolved 3

Every 6-12 Hours Initially

• Serum creatinine and potassium to track kidney function recovery and identify dangerous hyperkalemia 2, 3
• Fluid balance assessment to avoid volume overload in anuric patient 3

Daily

• Clinical examination for signs of volume overload (pulmonary edema, peripheral edema) or uremia (altered mental status, pericardial rub) 3

Indications for Emergent Dialysis

Initiate urgent hemodialysis if any of the following develop:

• Hyperkalemia >6.5 mEq/L or any level with ECG changes 2
• Severe metabolic acidosis with pH <7.1 2
• Volume overload with pulmonary edema refractory to diuretics 3
• Uremic symptoms including pericarditis or encephalopathy 2
• Anuria persisting >24 hours despite treatment of reversible causes 1

Common Pitfalls to Avoid

• Do not assume anuria is simply progression of FSGS—this presentation demands evaluation for reversible causes, particularly obstruction 1
• Do not continue nephrotoxic medications including NSAIDs, which are frequently used for pain but cause acute kidney injury in patients with underlying kidney disease 1
• Do not rapidly correct electrolyte abnormalities if severe hyponatremia present from nephrotic syndrome and diuretics—rapid correction causes more harm than the hyponatremia itself 4
• Do not delay imaging—every hour of bilateral obstruction increases risk of irreversible kidney damage 1

Transition to Long-Term FSGS Management

Once acute crisis resolved and urine output restored:

• Reassess FSGS classification (primary versus secondary versus genetic) as this determines whether immunosuppression is appropriate 2
• Maximize RAS blockade with ACE inhibitor or ARB uptitrated to maximum tolerated dose for antiproteinuric effect 3
• Target blood pressure <120 mmHg systolic using standardized office measurement 3
• Restrict dietary sodium to <2.0 g/day which is synergistic with ACE inhibitor/ARB therapy 3
• Consider genetic testing if steroid-resistant FSGS, as 11-24% of adults have disease-causing variants that would not respond to immunosuppression 2