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Evidence of possible association of nephrolithiasis and nephroptosis.

Two separate populations, one consisting of 100 patients with renal stones and one consisting of 81 patients with nephroptosis were examined to determine whether an association may exist between excessive renal mobility and renal stone formation. The statistical analysis of the data suggests a direct relationship between nephroptosis and the occurrence of renal stones.

Adolescent↗

Hypercalciuric rickets: a rare cause of nephrolithiasis.

An unusual case of rickets associated with hypercalciuria is described. In addition to proteinuria, the patient had phosphaturia, aminoaciduria, renal glucosuria and impaired renal concentration but no renal tubular acidosis. Studies did not support the diagnosis of primary hyperparathyroidism. The findings in the patient were very similar to those in 4 previously reported cases and are suggestive of a new combination of multiple renal tubular defects.

Acidosis, Renal Tubular↗

Low urine citrate excretion as main risk factor for recurrent calcium oxalate nephrolithiasis in males.

To better define the relative role of metabolic factors in the recurrence of stone formation, we studied the 24-hour urinary excretion of calcium (uCa), citrate (uCit), oxalic acid (uOx) and uric acid (uUa) in 73 male patients with primary calcium oxalate urolithiasis. According to the episodes of stone formation per year, we identified 51 recurrent stone formers (RSF) and 22 single stone formers (SSF). 20 normal adult males constituted the control group (C). uCa and uOx were higher in RSF than in C, but quite similar in SSF and RSF. The only difference between RSF and SSF was uCit, significantly lower (2.06 +/- 1.04 mmol/24 h) in RSF than in SSF (3.22 +/- 1.18 mmol/24 h, p less than 0.001) and in C (3.42 +/- 1.33 mmol/24 h, p less than 0.001). Hypocitraturia (uCit less than 1.5 mmol/24 h) was found in 16 of 51 RSF (31.4%) and in 1 of 22 SSF (4.5%). These data confirm that high levels of uCa and uOx represent a risk factor for lithogenesis, but also strongly indicate the low uCit excretion as the most important urinary abnormality accounting for the recurrence of calcium oxalate stones.

Adult↗

Bone mineral density in patients with hypercalciuric nephrolithiasis.

Bone mineral density was studied in 50 adult patients with renal lithiasis and metabolic diagnosis of idiopathic hypercalciuria. Thirty were premenopausal women and 20 were men under 55 years of age, Bone density at the lumbar spine (LSBD) was 0.940 +/- 0.106 g/cm2 in the hypercalciuric patients compared to 1.112 +/- 0.037 g/cm2 in a cohort of age- and sex-matched controls (p < 0.001). LSBD was independent of age and was negatively correlated with the duration of stone disease (r = -0.52, p < 0.001). Thus we conclude that patients with idiopathic hypercalciuria have a decrease in their LSBD that is probably related to a negative calcium balance sustained over time.

Adult↗

A critical evaluation of the urinary inhibiting activity in idiopathic calcium oxalate nephrolithiasis.

In order to obtain new insights into the relevance of inhibitors in whole urine by focusing on their reciprocal interactions, a statistical approach was followed in 35 controls and 27 calcium oxalate (CaOx) recurrent idiopathic stone formers. The inhibiting activity of CaOx crystal growth and the most widely accepted inhibitors (glycosaminoglycans, citrate, magnesium, pyrophosphate), stone constituents (calcium, oxalate, phosphate, urate) and other normal urinary substances were evaluated. It was seen that the inhibitors played a very small role in total inhibiting activity. On the other hand, considering other normal urinary constituents, almost all the inhibiting power of urine on crystal growth could be explained.

Adult↗

Case history of a prune-belly syndrome with extracorporeal shock wave lithotripsy treatment of allograft nephrolithiasis.

This is a case history of a prune-belly syndrome with multiple urologic disorders leading to a renal transplant due to a chronic renal failure at age 8. After four allograft pyelolithotomies he was referred to us with a staghorn stone in the same graft. He was successfully treated with extracorporeal shock wave lithotripsy and a percutaneous nephrostomy and is now stone-free.

Child↗

Influence of nifedipine on stone formation and renal function in cholesterol-induced nephrolithiasis in rats.

Previous investigations showed that nifedipine limited calcium phosphate stone formation induced by a high-cholesterol diet in rats. This study was performed to obtain further insights into the effects of nifedipine on stone prevention, renal function and urine composition. Male Wistar rats were assigned to one of the following groups: (1) cholesterol diet (n = 22), (2) cholesterol diet plus nifedipine (n = 22) and (3) control (n = 6). A high-cholesterol diet was given for 4 weeks, nifedipine was administered by gavage to group 2 for 4 weeks (50 mg/kg/24 h). During weeks 1 and 4, 5 rats of each group were housed in metabolic cages for urine collection. Sodium (Na), calcium (Ca), magnesium (Mg), phosphate (P(i)), citrate and creatinine were determined in the urine. The kidneys of 4 animals of group 1 and 2 were perfused and removed for histology after 1, 2, 3 and 4 weeks, respectively. Clearance studies (inulin, Na, Ca, Mg, P(i)) were performed (n = 6/group) after 4 weeks. The cholesterol diet induced a marked renal stone formation which was significantly limited by nifedipine [calcification index (week 4) 1.75 +/- 0.5 vs. 0.75 +/- 0.5]. The sequential histological examinations showed that concrement formation started intracellularly after only 1 week in group 1, whereas in group 2 the first concretions were observed only after 3 weeks. The cholesterol diet induced an increased excretion of Ca and P(i) citrate and Mg were reduced. The concomitant application of nifedipine resulted in a higher excretion of Ca, Mg and citrate when compared to the cholesterol group. The inulin clearance was decreased in the latter group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗