The causes of nephrolithisis are multifactorial and have not yet been enough investigated [1].
Hypercalciuria is the most common cause of metabolic
nephrolithiasis [2-4]. Close relationship between urinary
calcium and urinary
sodium has been a subject of reported observations in the past, showing that high urinary
sodium is associated with high urinary
calcium [5-7].
Hyperoxaluria, hyperuricosuria and
cystinuria are also metabolic disorders that can lead to
nephrolithiasis. Recent studies have indicated that urinary elimination of
cystine is influenced by urinary
sodium excretion. Based on these observations it has been hypothesised that patients with high urinary
sodium excretion are at high risk of
urinary stone disease. The purpose of the study was to investigate
sodium excretion in a 24-hour urine and first morning urine collected from children with lithogenic metabolic abnormalities (
hypercalciuria,
hyperoxaluria, hyperuricosuria,
cystinuria), both with
nephrolithiasis and without it, in order to determine its significance in
urinary calculi formation.
PATIENTS AND METHODS: Urinary
sodium excretion was investigated in 2 groups of children: patients with lithogenic metabolic abnormalities, but without
urinary stone disease (L group) and patients with
nephrolithiasis (C group). Both groups were divided into 2 subgroups: patients with
hypercalciuria and without it. There were 22 patients in group L (mean age 11.97 +/- 4.13 years), of whom 17 formed a hypercalciuric subgroup and 5 formed a non-hypercalciuric subgroup (3 patients with hyperuricosuria and 2 patients with
hyperoxaluria). Group C consisted of 21 patients with
nephrolithiasis (mean age 12.67 +/- 3.44 years), of whom 6 formed a hypercalciuric subgroup and 15 formed a non-hypercalciuric group (2 patients with
cystinuria and 13 patients without lithogenic metabolic abnormalities). Control group consisted of 42 healthy age-matched children. All subjects had a normal renal function. A detailed history and clinical examination were done, and ultrasonography was performed in all patients. A 24-hour urine, first morning urine and serum specimen were analysed for
sodium,
potassium,
calcium,
uric acid,
urea and
creatinine. Fractional excretion of
sodium, as well as urinary
sodium to creatinin ratio and urinary
sodium to
potassium ratio, were calculated from the findings.
Sodium and
potassium levels were determined by flame photometry,
calcium was measured by atomic absorption technique (Beckman Atomic Spectrophotometer, Synchron CX-5 model, USA),
uric acid by
carbonate method and
creatinine by Jaffe technique.
Cystine and
dibasic amino acids were quantified by ion chromatography. Urinary
oxalate excretion was determined by
enzyme spectrophotometry.
Hypercalciuria was defined by 24-hour
calcium excretion greater than 3.5 mg/kg per day and/or
calcium to
creatinine ratio greater than 0.20 [8].
Uric acid excretion was expressed as
uric acid excretion factored for glomerular filtration, according to Stapleton's and Nash's formula [9]. Normal values were lower than 0.57 mg/dl of glomerular filtration rate in 24-hour samples. Mean values were statistically analyzed by Pearson's linear correlation and analysis of variance (ANOVA).
RESULTS: Urinary
sodium concentration values including urinary
sodium to
potassium ratios, are shown in Table 1. We found that urinary
sodium excretion was significantly increased in patients of both L and C groups when compared with controls (p < 0.05). Further analysis of the subgroups showed that urinary
sodium excretion was significantly higher only in patients with
hypercalciuria of both L and C groups in comparison to controls (p < 0.05) (Table 2). A significant positive correlation was found between 24-hour urinary
sodium to
creatinine ratio and urinary
calcium to
creatinine ratio (r = 0.31; p < 0.001) (Graph 1), as well as between urinary
sodium to
potassium ratio in 24-hour and first morning urine (r = 0.69; p < 0.001) (Graph 2). (A