Occult Nephrolithiasis in Prospective Kidney Donors: A Source for Hematuria

In their report, Koushik et al. (1) identified causes for persistent, asymptomatic, microscopic hematuria in a series of 512 prospective kidney donors in Minnesota. Fourteen of these had hematuria, of whom two had a urinary tract infection, one had multiple renal arteries, one a renal cyst, two normal kidney biopsies (one with renal cysts), and eight had biopsies with varied findings. We wish to highlight another important cause for hematuria in this population: occult nephrolithiasis. In all, 192 prospective kidney donors underwent evaluation at our center between February 2002 and May 2005 that included renal imaging. Seventy-six were eventually excluded for medical or surgical reasons. Out of those excluded, eight were found to have one or more kidney stones by ultrasound (two patients) or computed tomography (CT) scan (six patients). No patient gave a previous history of hypertension, nephrolithiasis or visible hematuria. Kidney size was 11±0.7 cm, with average asymmetry 0.3 cm. Stone size varied from 1 to 7 mm in diameter with up to three in one kidney; two patients had bilateral stones. Ureteric stones, bladder stones, or renal cysts were not detected in any patient. Their age was 43±13 years, three were male, four were white, three Asian, and one Native American and BMI was 27.1±3. Their fasting and two-hour post 75 gram glucose load blood sugar levels and hemoglobin were normal, but one patient had hypercholesterolemia. All patients had a normal 24-hour urine protein excretion rate or random urine microalbumin-to-creatinine ratio, as well as a normal 24-hour urine creatinine clearance (120±21 ml/min). Although the average blood pressure was normal (124/70 mm Hg by 24-hour ambulatory BP monitoring), seven were nocturnal nondippers. Four out of these eight patients had persistent microscopic hematuria. Seven patients provided a 24-hour urine collection to evaluate for metabolic abnormalities favorable to stone formation. Three had significant hypercalciuria (9.2–16.3 mmol/d, N 0–7.5), three had hypocitraturia (0.4–1.0 mmol/d, N >1.6), two had hyperuricosuria (5.5–5.9 mmol/ d, N 2–4), and two had hyperoxaluria (508–814 μmol/d, N 190–480). Three patients had more than one metabolic abnormality. Nephrolithiasis can cause microscopic hematuria without other clinical manifestations. In one study (2), 195 of 906 subjects with asymptomatic hematuria were found to have renal calculi by ultrasound. Twenty-four of these subsequently required urological management (2). Hypercalciuria and hyperuricosuria may also cause microscopic hematuria in adults, which can resolve with appropriate therapy such as thiazides and allopurinol (3). In addition, hypercalciuria, hyperuricosuria, and nephrolithiasis are associated with thin basement membrane nephropathy, a glomerular disease (4). Although we typically decline these individuals as kidney donors, we agree with Koushik et al. that clear guidelines for managing young and healthy adults with microscopic hematuria are lacking. In summary, in addition to the list provided by Koushik et al., occult nephrolithiasis should be considered as a cause for microscopic hematuria in the prospective kidney donor population. This will enable appropriate diagnosis, counseling, referral, and management of these individuals independent of the transplantation process. G.V. Ramesh Prasad Philip A. McFarlane Division of Nephrology Department of Medicine University of Toronto Toronto, Ontario, Canada Renal Transplant Program St. Michael’s Hospital Toronto, Ontario, Canada

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