A 47-year-old woman was evaluated in the Nephrology Clinic at New England Medical Center for autosomal dominant polycystic kidney disease (ADPKD). She had undergone abdominal and pelvic noncontrast computed tomographic scans for the evaluation of dyspareunia and stress incontinence. These studies revealed markedly enlarged cystic kidneys as well as multiple cysts involving most of the liver parenchyma, particularly the superior right lobe; the liver size was normal. Several hepatic Structures with high attenuation values were consistent with complicated hemorrhagic cysts or solid masses. She had questionable minimal intrahepatic biliary ductal dilation but no pancreatic or splenic cysts. The patient had been unaware of her renal diagnosis prior to these studies and referred herself for further evaluation. In the Nephrology Clinic, she specifically denied any history of hypertension, flank or abdominal pain, urinary tract infection, or hematuria. She was gravida 4, para 2; she had never used oral contraceptives. The serum creatinine was reportedly normal until one year previously, when it was 1.5 mg/dl. She was taking no medications, and a review of systems was negative. Her family history revealed that her mother and one sister had end-stage renal failure due to ADPKD. A brother also had ADPKD with hypertension and well-preserved renal function. Physical examination disclosed a blood pressure of 120/90 mm Hg. Mild arteriolar narrowing was present on funduscopic examination. The chest was clear and cardiac examination was normal. The left kidney was markedly enlarged and slightly tender to palpation. The right kidney was not felt. The liver edge was palpable but nontender. Trace pedal edema was present. Gynecologic examination revealed grade-2 uterovaginal prolapse. The serum creatinine and BUN levels were 1.7 and 28 mg/dl, respectively. Hematocrit was 36%. Liver function tests, including bilirubin, LDI-I, AST, and ALT, were within normal limits. Cholesterol was 159 mg/dl.