Urolithiasis after renal transplantation is uncommon. However, little
is known about what factors could influence this low incidence of ston
e formation, despite these patients being potentially exposed to a hig
h prevalence of metabolic abnormalities predisposing calculus formatio
n. In order to assess the prevalence of these metabolic abnormalities,
we surveyed 133 unselected renal transplant patients in a cross-secti
onal study. The following were measured: serum creatinine, calcium, ph
osphorus, uric acid, magnesium bicarbonate, PTH, as well as the 24 h u
rinary excretion of calcium, phosphorus, uric acid, citrate, oxalate a
nd magnesium. Hypercalciuria was observed in 17 patients (13%), hiperu
ricosuria in 8 (6%), hyperoxaluria in 30 (22%), hypocitraturia in 102
(77%) and hypomagnesiuria in 15 (11%). Among patients with normal rena
l function (Cr < 2 mg/dl (N = 105 patients) the prevalence of metaboli
c abnormalities were similar to the whole group. The mean 24 h urinary
output was high (2.239 +/- 684 ml). Patients with hypocitraturia show
ed lower serum bicarbonate concentrations (25.3 +/- 2.1 vs 26.6 +/- 1.
6 mmol/l, p = 0.01). Hyperparathyroidism among patients with normal re
nal function was not associated with a higher prevalence of urinary ex
cretion abnormalities. Only 5 patients (4%) developed urolithiasis aft
er transplantation. In one patient no metabolic abnormalities could be
demonstrated. The rest of these patients showed two or three associat
ed metabolic abnormalities (hypocitraturia, hypomagnesiuria, hyperoxal
uria or hypercalciuria). In conclusion, metabolic abnormalities predis
posing urolithiasis after renal transplantation are highly prevalent.
Hypocitraturia is the most common abnormality and its etiology may be
related to acidosis. High urinary output and the lack of oversaturatio
n in urine may prefect these patients from a higher incidence of calcu
lus formation.