Acute Kidney Injury due to Crescentic Glomerulonephritis in a Patient with Polycystic Kidney Disease
A 43-year-old man presented to the emergency department complaining of lower extremity edema for 2 weeks. The patient denied any pertinent past medical or family medical history; though he took metoprolol and hydrochlorthiazide for about 1 month a year earlier, he was not taking either of these agents at the time of presentation. He denied use of nonsteroidal anti-inflammatory agents and recreational drugs (including cocaine, heroin and phencyclidine). Initial physical examination was significant for elevated blood pressure (151/94 mm Hg) and pitting edema in both lower extremities. Initial laboratory analysis at presentation (table ) revealed renal failure (serum creatinine 2.6 mg/dl) and anemia (hemoglobin 10.8 g/dl, hematocrit 33.4% and mean corpuscular volume 85.4 fl). Urinalysis (random urine; table ) showed proteinuria, small blood and pyuria without bacteria. Proteinuria was confirmed on 24-hour urine collection that demonstrated nephrotic-range protein (25 g/24 h). Kidney ultrasound revealed enlarged kidneys bilaterally with multiple cysts and this was confirmed by computed tomography (CT) scanning (fig. ). A complete serologic evaluation, including hepatitis screen, was performed and was unrevealing (table ).\nInitially, the patient was empirically treated with intravenous steroid pulse (methylprednisolone, 1 g daily for 3 days) and then switched to prednisone orally (1 mg per kilogram daily). A CT-guided kidney biopsy was performed and revealed immune complex glomerulonephritis with features of membranous nephropathy with crescent formation (fig. ). Despite treatment with oral prednisone (1 mg/kg), the patient's renal function declined and he became oliguric. Intermittent hemodialysis was initiated. In addition to oral steroid, treatment with mycophenolate (500 mg twice daily; escalated to 1,500 mg twice daily over 2 weeks) was started. Over a 5-month period, urine output increased in association with improvement in kidney function. Concurrently, serum albumin recovered to normal values and proteinuria decreased from 25 to 3 g daily. Because of persistent nephrotic-range proteinuria, cyclosporine 75 mg twice daily was added to his medication regimen. Over the ensuing 3 months, the patient manifested further improvement in physiologic parameters. Accordingly, prednisone dosage was reduced (10 mg orally per day) and mycophenolate mofetil (MMF) was maintained at 1,500 mg orally twice daily and cyclosporine at 75 mg orally twice daily. Hemodialysis was subsequently discontinued and the patient has been off dialysis with stable chronic kidney disease stage 3 (creatinine clearance 45 ml/min by 24-hour urine studies). He continues to be monitored closely in an outpatient setting for any changes in renal function. Immunosuppressive agents are being tapered.