[Renal tubular function in children with hypercalciuria]

Renal stone disease is commonly due to hypercalciuria [1, 2], which may be assessed either from a 24-hour urinary collection or from the fasting first morning urine. Hypercalciuria during childhood has been defined by a 24-hour calcium excretion greater than 3.5 mg/kg per day and/or calcium to creatinine ratio greater than 0.20 [3]. The alteration in the calcium transporting systems plays a pathogenetic role in promoting hypercalciuria [4, 5]. Since calcium reabsorption along the nephron is intimately related to that of other electrolytes and substances, it can be hypothesized that patients with hypercalciuria may have other renal tubular defects. The aim of the study was to investigate proximal tubular function (tubular reabsorption of sodium, potassium, phosphate and glucose) and distal tubular function (urinary concentrating capacity and acidifying capacity) in children with hypercalciuria.

Two groups of children were studied: hypercalciuric group included 23 children with hypercalciuria (10 males, aged 11.9 +/- 4.1 years), of whom 6 with nephrolithiasis, and control group included 42 healthy children (20 males, aged 11.2 +/- 3.8 years). All subjects had normal serum values for calcium, sodium, potassium, phosphate and glucose, as well as normal renal function. The urinary excretion of calcium, sodium, potassium, phosphate, glucose and creatinine was measured in a 24-hour urine specimen by standard laboratory methods. Urine osmolality and urinary specific gravity were measured following 12-hour water-deprivation test. A short ammonium chloride loading test was performed in 3 patients with urinary pH above 5.5. The fractional excretion of sodium, tubular phosphate reabsorption and renal threshold phosphate concentration were calculated according to standard formula. Statistical analysis was performed using the t-test and analysis of variance (ANOVA). Kruskal-Wallis method was used to compare urinary phosphate excretion between two groups.

Table 1 summarizes urinary excretion of electrolytes in children with hypercalciuria compared with healthy controls. We found that urinary sodium excretion was significantly increased in patients with hypercalciuria when compared with controls (p < 0.05). Urinary phosphate excretion was significantly higher in patients with hypercalciuria in comparison to controls, and this was accompanied by a significant lowering of the tubular phosphate reabsorptive threshold (p < 0.05). Urinary potassium excretion tended to be lower, although not significantly, in the hypercalciuric children than in normal subjects. Table 2 shows the mean values +/- standard deviation of urinary specific gravity, urinary osmolality and urinary pH. Urinary specific gravity mean value was significantly lower in patients with hypercalciuria in comparison to controls (p < 0.05). Urinary pH was found below 5.5 in all patients. Glycosuria was detected in 3 patients (13.3%). As shown in Graph. 1, a significant correlation between the urinary excretion of calcium and sodium was demonstrated in both groups of children (r = 0.29; p < 0.01).

The present study shows that children with hypercalciuria have significantly higher urinary sodium and urinary phosphate excretion in comparison to controls, while urinary potassium excretion is normal in both groups of children. According to some recent reports [6-9], these findings may indicated defects of the renal tubular transport of sodium and phosphate which may be interpreted as a cause or a consequence of the alteration of the calcium transporting system. Defects in both proximal and distal renal tubular functions have been demonstrated in patients with nephrolithiasis, particularly those with hypercalciuria. Proximal renal tubular defects include defects in sodium, fluid, phosphate and glucose reabsorption, which were evident also in our patients. (ABSTRACT TRUNCATED)