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PubMed1976

Recurrent nephrolithiasis: natural history and effect of phosphate therapy. A double-blind controlled study.

In a double-blind controlled clinical study, 71 patients with recurrent calcium oxalate stones were divided into three treatment groups: those who received potassium acid phosphate, those who received an inert placebo, and those who received a low calcium diet only. Follow-up periods averaged 2.9 years. Although the mean urinary calcium level of the patients who received phosphate was reduced 33 per cent, their renal stone disease did not diminish. Mean urinary phosphorus increased 88 per cent with phosphate treatment but did not correlate with the decrease in urinary calcium, or with treatment success. The data did not suggest that phosphorus and its metabolites retard calcium oxalate crystallization in urine. No evidence appeared for an association of hypercalciuria with severe stone disease, or with a specific clinical or chemical response to phosphate therapy. Patients whose urinary calcium level fell more than 25 percent when dietary calcium was reduced may have excessive gastrointestinal calcium absorption, which appears to be associated with improved chemical response to phosphate therapy.

Adult↗
PubMed1982

Calcium oxalate nephrolithiasis: an easy way to detect an imbalance between promoting and inhibiting factors.

Calcium oxalate stone formation depends on both urine oversaturation with calcium oxalate--which in turn depends mainly on oxalate excretion--and the excretion of inhibitors; the possibility that a ratio of these variables might differentiate stone-formers from stone-free subjects was explored, 24-h urine samples from 20 control subjects and 53 idiopathic calcium oxalate stone-formers receiving a standard diet were studied. A further group of 2-h urine samples (from 7 to 9 a.m.). collected after a overnight fast from 16 non-stone and 24 stone-forming persons on a normal diet, were also examined. The ratio 'oxalate/citrate X acid mucopolysaccharides; (Ox/Cit X AMPs) seems capable of differentiating more than 80% of stone-formers from non-stone-formers using both 24- and 2-h urine collection.

Adult↗
PubMed1993

Can citrate therapy prevent nephrolithiasis?

This prospective study was done to help determine whether or not oral citrate therapy can elevate urinary citrate levels and reduce the incidence of recurrent calcium stones in patients with hypocitraturia (urinary citrate less than 320 mg/24 hr). The treatment group (Group I) consisted of 10 patients treated with oral citrate and hydration. The control group (Group II) was treated with hydration alone. In Group I, the new stone formation rate (stones per patient year) fell from 1.17 +/- 0.26 to 0.45 +/- 0.32 (p = 0.07) and the twenty-four-hour urinary citrate excretion rose from 69 +/- 14 mg to 473 +/- 96 mg (p = 0.002). In Group II, the new stone formation rate fell from 0.9 +/- 0.25 to 0.27 +/- 0.13 (p = 0.03). The twenty-four-hour urinary citrate excretion increased, though not significantly, from 166 +/- 21 mg to 326 +/- 77 mg (p = 0.06). We conclude that oral citrate therapy can significantly increase urinary citrate levels in patients with recurrent stones associated with hypocitraturia but that oral citrate therapy and hydration were no better than hydration alone in reducing the incidence of recurrent stones.

Calcium Oxalate↗
PubMed2004

Nephrolithiasis: why doesn't our "learning" progress?

OBJECTIVE: Stone research is stagnant with minor clinical fall-out. We wonder whether this, in the ESWL era, depends only on ESWL and the consequent change in our clinical management habits, or is rather due to mistakes made by investigators. We feel that indeed we did and do make some: (1) the patients we are investigating may not be appropriate; and (2) we are missing to properly recognise disease heterogeneity. CONCLUSIONS: From the public health side most likely we are not investigating the right patients, and we probably need to address the large part of the problem, i.e. the rarely relapsing stone formers demanding 80% of all urological interventions. Although there is a consensus that urolithiasis is very heterogeneous, this position is presently under reconsideration. It is necessary to investigate the single or "occasional" stone former, and go back to the epidemiology and clinics with multicentre, prospective studies. Being a multifactorial disease, we will need to evaluate as many aspects as possible contemporaneously in the same patient. It is also necessary to "revisit" the disease in an unbiased manner, because its relationship with relevant aspects could be different than previously thought due to our incomplete knowledge of its pathogenesis and pathophysiology.

Biomedical Research↗
PubMed2006

Renal function in patients with nephrolithiasis.

PURPOSE: We describe kidney function, as measured by creatinine clearance in stone formers, and classified by type of stone formed and systemic etiologies of stone formation. MATERIALS AND METHODS: The mean of 3 pretreatment 24-hour creatinine clearance measurements in each of 1,856 stone formers and creatinine clearance in 153 normal individuals were used. Clearance was adjusted for patient sex, age and body weight using general linear modeling. RESULTS: As a group, all stone formers had decreased clearance adjusted for age, sex and body weight compared to that in normal individuals. Although clearance was particularly low in cystine and struvite stone formers, they were below normal in even common CaOx stone formers. CONCLUSIONS: As a rule, patients with kidney stones do not have normal kidney function. In clinical management all efforts must be made to minimize renal injury, balancing the risks of obstruction from stones against those of urological procedures.

Creatinine↗
PubMed2003

Studies of urinary cystine precipitation in vitro: ontogeny of cystine nephrolithiasis and identification of meso-2,3-dimercaptosuccinic acid as a potential therapy for cystinuria.

Children with fully recessive (Type I/I) cystinuria have a high risk of stone formation in the first decade of life. To assess the tendency for cystine to precipitate in individual urine samples, we developed an in vitro assay in which radiolabelled cystine (4mM) was dissolved in urine at 37 degrees C after alkalization to pH 10. Samples were then brought to pH 5, cooled, and centrifuged. The % decrease in supernatant cpm was used as a measure of cystine precipitation (CP). CP varied widely among normal children (74%+/-34) whereas variability of repeated determinations on a single adult individual was modest (64%+/-3.3). The assay was used to compare various potential therapies for cystinuria. Precipitation of exogenous cystine from normal urine was strongly inhibited by addition of D-penicillamine (CP: 8%+/-3) or dimercaptosuccinic acid (DMSA) (CP: 5%+/-1), at urinary concentrations attained by standard oral doses of each drug. Mercaptopropionylglycine (MPG) was moderately effective (CP: 43%+/-9), whereas captopril was a weak inhibitor (CP: 63%+/-12). Precipitation of endogenous cystine (2191 micromol/L) from a cystinuric patient showed that DMSA and D-penicillamine were again highly effective compared to the other agents. In addition DMSA and penicillamine added to the same patient's urine reduced the free cystine by 50% (as measured by automated amino acid analyzer) whereas MPG and captopril had no effect. In conclusion, DMSA is comparable to D-penicillamine as an in vitro inhibitor.

Adolescent↗
PubMed2004

[Nephrolithiasis and primary hyperarathyroidism in pregnancy].

Diagnosis of hyperparathyroidism is unusual during pregnancy. The presence of a renal stone is a very exceptional finding. Hypercalcemia is often revealed by standard blood tests. We present here a clinical case of renal nephretic colic occurring during the third trimester of a fourth pregnancy. Our investigations led to the diagnosis of primary hyperparathyroidism which was successfully treated. Hyperparathyroidism during pregnancy is associated with a high incidence of fetal and maternal complications, essentially neonatal hypocalcemia. In utero death is rare but has been reported. Calcium metabolism during pregnancy is dependent on PTHrp. The surgical option is usually taken during the second trimester but can only be proposed during the third trimester in the event of medically resistant hypercalcemia.

Adult↗
PubMed1993

Nephrolithiasis, hypocitraturia, and a distal renal tubular acidification defect in type 1 glycogen storage disease.

Renal stones containing calcium can occur in patients with type 1 glycogen storage disease. We studied 11 patients with glycogen storage disease. Five patients had renal calculi, nephrocalcinosis, or both, and five had hypercalciuria. Serum levels of calcium, phosphorus, parathyroid hormone, and urate were normal. Serum levels of 1,25-dihydroxyvitamin D were elevated in each patient. None of the patients had a metabolic acidosis, but all nine who were tested had evidence of impaired acid excretion. In response to an acid load, eight of the nine patients had subnormal titratable acid excretion, and nine had subnormal ammonia excretion; six of nine patients were unable to secrete hydrogen ions in response to bicarbonate administration. These data indicate that patients with type 1 glycogen storage disease have an incomplete form of distal renal tubular acidosis. This may be the cause of hypercalciuria and nephrocalcinosis in these patients.

Acidosis, Renal Tubular↗