We describe a patient with previously diagnosed IgA nephropathy presenting with persistent macrohematuria and iron-deficiency anemia, in whom angiography showed multiple bilateral renal aneurysms.

In January 1993, a 31-year-old woman was hospitalized because of persistent macrohematuria and moderate iron-deficiency anemia. She did well until 1987, when she experienced two episodes of gross hematuria. A percutaneous renal biopsy specimen showed a moderate focal and segmental mesangial proliferation associated with a discrete increase in the mesangial matrix in 75% of the glomeruli. Tubulointerstitial changes were minimal, and there was no evidence of vasculitis. The immunopathologic pattern was characterized by diffuse deposits of IgA in the mesangial areas. Special attention was placed on excluding the many diseases commonly associated with mesangial IgA deposits.

In 1992, the number of recurrent episodes of gross hematuria increased, becoming persistent macroscopic hematuria. Blood pressure and renal function remained normal. At hospital admission, urine was grossly hematuric, but erythrocyte casts could not be detected on microscopic examination. The 24-hour urine protein excretion was 0.5 g, and the creatinine clearance was 102 mL/min per 1.73 m² body surface area. Laboratory findings included microcytic hypochromic anemia. The blood hemoglobin level was 8.4 g/dL. A renal biopsy specimen showed only minimal glomerular changes, and immunofluorescence studies were negative. Cystoscopy indicated that gross hematuria originated from the left ureter, but retrograde ureteropyelography did not detect the cause of bleeding. Abdominal aortography with bilateral selective renal angiography showed multiple intraparenchymal aneurysms in the left and right kidneys. All aneurysms were located in the interlobar arteries or arteries distal to the interlobar arteries. The aneurysms were small and relatively uniform in size, with diameters of 2 to 5 mm.

Renal aneurysms in medium- or small-sized arteries have long been recognized in patients with systemic necrotizing vasculitis of the polyarteritis nodosa group [1, 2]. However, they have recently been seen, although more rarely, in patients with severe arterial hypertension, rheumatoid arthritis, temporal arteritis, and diabetes mellitus [2, 3]. Our patient did not have any evidence of the systemic diseases known to be associated with angiographically established visceral aneurysms [1-3]. This report is the first description of bilateral renal aneurysms in primary glomerulonephritis.