Risk Of Kidney Stone Formation Research Articles

Obesity, Weight Gain, and the Risk of Kidney Stones

Larger body size may result in increased urinary excretion of calcium, oxalate, and uric acid, thereby increasing the risk for calcium-containing kidney stones. It is unclear if obesity increases the risk of stone formation, and it is not known if weight gain influences risk. To determine if weight, weight gain, body mass index (BMI), and waist circumference are associated with kidney stone formation. A prospective study of 3 large cohorts: the Health Professionals Follow-up Study (N = 45,988 men; age range at baseline, 40-75 years), the Nurses' Health Study I (N = 93,758 older women; age range at baseline, 34-59 years), and the Nurses' Health Study II (N = 101,877 younger women; age range at baseline, 27-44 years). Incidence of symptomatic kidney stones. We documented 4827 incident kidney stones over a combined 46 years of follow-up. After adjusting for age, dietary factors, fluid intake, and thiazide use, the relative risk (RR) for stone formation in men weighing more than 220 lb (100.0 kg) vs men less than 150 lb (68.2 kg) was 1.44 (95% confidence interval [CI], 1.11-1.86; P = .002 for trend). In older and younger women, RRs for these weight categories were 1.89 (95% CI, 1.52-2.36; P<.001 for trend) and 1.92 (95% CI, 1.59-2.31; P<.001 for trend), respectively. The RR in men who gained more than 35 lb (15.9 kg) since age 21 years vs men whose weight did not change was 1.39 (95% CI, 1.14-1.70; P = .001 for trend). Corresponding RRs for the same categories of weight gain since age 18 years in older and younger women were 1.70 (95% CI, 1.40-2.05; P<.001 for trend) and 1.82 (95% CI, 1.50-2.21; P<.001 for trend). Body mass index was associated with the risk of kidney stone formation: the RR for men with a BMI of 30 or greater vs those with a BMI of 21 to 22.9 was 1.33 (95% CI, 1.08-1.63; P<.001 for trend). Corresponding RRs for the same categories of BMI in older and younger women were 1.90 (95% CI, 1.61-2.25; P<.001 for trend) and 2.09 (95% CI, 1.77-2.48; P<.001 for trend). Waist circumference was also positively associated with risk in men (P = .002 for trend) and in older and younger women (P<.001 for trend for both). Obesity and weight gain increase the risk of kidney stone formation. The magnitude of the increased risk may be greater in women than in men.

Dietary Factors and the Risk of Incident Kidney Stones in Men

Diet plays an important role in the pathogenesis of kidney stones. Because the metabolism of many dietary factors, such as calcium, may change with age, the relation between diet and kidney stones may be different in older adults. Uncertainty also remains about the association between many dietary factors, such as vitamin C, magnesium, and animal protein, and the risk of kidney stone formation. To examine the association between dietary factors and the risk of incident, symptomatic kidney stones in men and to determine whether these associations vary with age, a prospective cohort study was conducted of 45,619 men without a history of nephrolithiasis. Self-administered food frequency questionnaires were used to assess diet every 4 yr. A total of 1473 incident symptomatic kidney stones were documented during 477,700 person-years of follow-up. For men aged <60 yr, the multivariate relative risk (RR) for stone formation in the highest quintile of dietary calcium as compared with the lowest quintile was 0.69 (95% confidence interval [CI], 0.56 to 0.87; P = 0.01 for trend). By contrast, there was no association between dietary calcium and stone formation in men aged 60 yr or older. The multivariate RR for men who consumed 1000 mg or greater of vitamin C per day compared with those who consumed less than the recommended dietary allowance of 90 mg/d was 1.41 (95% CI, 1.11 to 1.80; P = 0.01 for trend). Other dietary factors showed the following multivariate RR among men in the highest quintile of intake compared with those in the lowest: magnesium, 0.71 (95% CI, 0.56 to 0.89; P = 0.01 for trend); potassium, 0.54 (95% CI, 0.42 to 0.68; P < 0.001 for trend); and fluid, 0.71 (95% CI, 0.59 to 0.85; P < 0.001 for trend). Animal protein was associated with risk only in men with a body mass index <25 kg/m(2) (RR, 1.38; 95% CI, 1.05 to 1.81; P = 0.03 for trend). Sodium, phosphorus, sucrose, phytate, vitamin B(6), vitamin D, and supplemental calcium were not independently associated with risk. In conclusion, the association between calcium intake and kidney stone formation varies with age. Magnesium intake decreases and total vitamin C intake seems to increase the risk of symptomatic nephrolithiasis. Because age and body size affect the relation between diet and kidney stones, dietary recommendations for stone prevention should be tailored to the individual patient.

Oxidative stress in urogenital tuberculosis patients: a predisposing factor for renal stone formation—amelioration by vitamin E supplementation

Background Previous studies have shown that urogenital tuberculosis (GuTb) patients treated or untreated with regular anti-Tb regimen excrete comparatively high levels of urinary stone forming constituents than normal subjects. Enhanced oxidative stress is also considered as a prime factor that accelerates urolithiasis. The present study was aimed to determine antioxidant status and lipid peroxidation of these individuals in order to assess their risk for kidney stone formation. Methods GuTb patients and age-matched normal subjects were divided into four groups: I: normal subjects ( n=60), II: GuTb patients a day before treatment ( n=72), III: GuTb patients after treatment with isoniazid (300 mg), rifampicin (450 mg) and pyrazinamide (1.5 g) per day for 60 days ( n=42), and IV: GuTb patients supplemented with vitamin E (200 mg/day) along with regular chemotherapy for 60 days ( n=30). Blood was collected and tested for various markers of oxidative stress. Results Increased levels of lipid peroxidation, protein carbonyls (PCO), advanced oxidative protein products (AOPP) and reduced antioxidant defenses by impairment in enzyme activities like superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione and decreased plasma concentrations of non enzymatic antioxidants like vitamins C and E were observed in the treated and untreated GuTb patients. Conclusions These biochemical disparities may lead to membrane disintegrity, which is favorable for retention of mirolithis. Advocation of vitamin E enhanced the antioxidant status of the plasma, thereby preventing membrane injury, consequently reducing the risk of stone formation in urogenital tuberculosis patients, who were treated with their routine anti-tuberculosis drug regimen.

Dogmas and controversies in the handling of nitrogenous wastes: excretion of nitrogenous wastes in human subjects.

Two major nitrogenous waste products, urea and ammonium (NH(4)(+)), are produced in humans when proteins are oxidized, and in this manuscript their excretions are examined from two perspectives. First, the specific physiology of each nitrogenous waste is reviewed and the current dogmas summarized. Second, their excretions are considered in the context of integrative physiology, i.e. the need to ensure that the urine composition is appropriate to minimize the risk of kidney stone formation. After the latter analysis, weak links in our understanding of the overall physiology become apparent and a conundrum is defined. The conundrum for the excretion of urea focuses on the fact that urea is not an effective osmole in the medullary-collecting duct when vasopressin acts. As a result, it appears that urinary urea cannot prevent a large decline in the urine flow rate and thereby minimize the risk of forming kidney stones in electrolyte-poor urine. The conundrum for the excretion of NH(4)(+) is: high rates of NH(4)(+) excretion require a low urine pH, yet a pH approximately 6.0 must be maintained in order to reduce the risk of precipitating uric acid in the urine. Possible ways of resolving these conundrums require novel physiological interpretations.

Dietary factors and the risk of incident kidney stones in younger women: Nurses' Health Study II.

In older women and men, greater intakes of dietary calcium, potassium, and total fluid reduce the risk of kidney stone formation, while supplemental calcium, sodium, animal protein, and sucrose may increase the risk. Recently, phytate has been suggested to play a role in stone formation. To our knowledge, no prospective information on the role of dietary factors and risk of kidney stone formation is available in younger women. We prospectively examined, during an 8-year period, the association between dietary factors and the risk of incident symptomatic kidney stones among 96 245 female participants in the Nurses' Health Study II; the participants were aged 27 to 44 years and had no history of kidney stones. Self-administered food frequency questionnaires were used to assess diet in 1991 and 1995. The main outcome measure was an incident symptomatic kidney stone. Cox proportional hazards regression models were used to adjust simultaneously for various risk factors. We documented 1223 incident symptomatic kidney stones during 685 973 person-years of follow-up. After adjusting for relevant risk factors, a higher dietary calcium intake was associated with a reduced risk of kidney stones (P =.007 for trend). The multivariate relative risk among women in the highest quintile of intake of dietary calcium compared with women in the lowest quintile was 0.73 (95% confidence interval, 0.59-0.90). Supplemental calcium intake was not associated with risk of stone formation. Phytate intake was associated with a reduced risk of stone formation. Compared with women in the lowest quintile of phytate intake, the relative risk for those in the highest quintile was 0.63 (95% confidence interval, 0.51-0.78). Other dietary factors showed the following relative risks (95% confidence intervals) among women in the highest quintile of intake compared with those in the lowest quintile: animal protein, 0.84 (0.68-1.04); fluid, 0.68 (0.56-0.83); and sucrose, 1.31 (1.07-1.60). The intakes of sodium, potassium, and magnesium were not independently associated with risk after adjusting for other dietary factors. A higher intake of dietary calcium decreases the risk of kidney stone formation in younger women, but supplemental calcium is not associated with risk. This study also suggests that some dietary risk factors may differ by age and sex. Finally, dietary phytate may be a new, important, and safe addition to our options for stone prevention.

Mechanisms used to dispose of progressively increasing alkali load in rats.

Our objective was to describe the process of alkali disposal in rats. Balance studies were performed while incremental loads of alkali were given to rats fed a low-alkali diet or their usual alkaline ash diet. Control groups received equimolar NaCl or KCl. Virtually all of the alkali was eliminated within 24 h when the dose exceeded 750 micromol. The most sensitive response to alkali input was a decline in the excretion of NH(4)(+). The next level of response was to increase the excretion of unmeasured anions; this rise was quantitatively the most important process in eliminating alkali. The maximum excretion of citrate was approximately 70% of its filtered load. An even higher alkali load augmented the excretion of 2-oxoglutarate to >400% of its filtered load. Only with the largest alkali load did bicarbonaturia become quantitatively important. We conclude that renal mechanisms eliminate alkali while minimizing bicarbonaturia. This provides a way of limiting changes in urine pH without sacrificing acid-base balance, a process that might lessen the risk of kidney stone formation.

Oxalate content of soybean seeds (Glycine max: Leguminosae), soyfoods, and other edible legumes.

Consumption of soybeans and food products made from them is increasing because of their desirable nutritional value. However, the oxalate content of seeds from 11 cultivars of soybean showed relatively high levels of total oxalate from 0.67 to 3.5 g/100 g of dry weight. Oxalate primarily was found as calcium oxalate crystals. Thirteen tested commercial soyfoods contained between 16 and 638 mg of total oxalate per serving. These values compare to those of three other legume foods, peanut butter, refried beans, and lentils, which contained 197, 193, and 100 mg of total oxalate per serving, respectively. After oxalate has been absorbed from the diet, it cannot be metabolized and is excreted by the kidney into urine, where it binds to calcium forming an insoluble salt that may precipitate to form kidney stones. The amounts of total oxalate in soybean seeds, soy foods, and other common legume foods exceed current recommendations for oxalate consumption by individuals who have a history of calcium oxalate kidney/urinary stones. This study serves as the basis to find soybean cultivars lower in oxalate, which will have lower risk for kidney stone formation after human consumption.

Family History and Risk of Kidney Stones

Kidney stones develop more frequently in individuals with a family history of kidney stones than in those without a family history; however, little information is available regarding whether the increased risk is attributable to genetic factors, environmental exposures, or some combination. In this report, the relation between family history and risk of kidney stone formation was studied in a cohort of 37,999 male participants in the Health Professionals Follow-up Study. Information on family history, kidney stone formation, and other exposures of interest, including dietary intake, was obtained by mailed questionnaires. A family history of kidney stones was much more common in men with a personal history of stones at baseline in 1986 than in those without a history of stones (age-adjusted prevalence odds ratio, 3.16; 95% confidence interval [CI], 2.90 to 3.45). During 8 yr of follow-up, 795 incident cases of stones were documented. After adjusting for a variety of risk factors, the relative risk of incident stone formation in men with a positive family history, compared with those without, was 2.57 (95% CI, 2.19 to 3.02). Family history did not modify the inverse association between dietary calcium intake and the risk of stone formation. These results suggest that a family history of kidney stones substantially increases the risk of stone formation. In addition, these data suggest that dietary calcium restriction may increase the risk of stone formation, even among individuals with a family history of kidney stones.

Intake of vitamins B6 and C and the risk of kidney stones in women.

Urinary oxalate is an important determinant of calcium oxalate kidney stone formation. High doses of vitamin B6 may decrease oxalate production, whereas vitamin C can be metabolized to oxalate. This study was conducted to examine the association between the intakes of vitamins B6 and C and risk of kidney stone formation in women. The relation between the intake of vitamins B6 and C and the risk of symptomatic kidney stones were prospectively studied in a cohort of 85,557 women with no history of kidney stones. Semiquantitative food-frequency questionnaires were used to assess vitamin consumption from both foods and supplements. A total of 1078 incident cases of kidney stones was documented during the 14-yr follow-up period. A high intake of vitamin B6 was inversely associated with risk of stone formation. After adjusting for other dietary factors, the relative risk of incident stone formation for women in the highest category of B6 intake (> or =40 mg/d) compared with the lowest category (<3 mg/d) was 0.66 (95% confidence interval, 0.44 to 0.98). In contrast, vitamin C intake was not associated with risk. The multivariate relative risk for women in the highest category of vitamin C intake (> or =1500 mg/d) compared with the lowest category (<250 mg/d) was 1.06 (95% confidence interval, 0.69 to 1.64). Large doses of vitamin B6 may reduce the risk of kidney stone formation in women. Routine restriction of vitamin C to prevent stone formation appears unwarranted.

Predisposition towards urolithiasis associated with the NQO1 null-allele.

The distribution of two alleles of the NQO1 gene encoding NADP(H):quinone oxidoreductase was studied in 140 urolithiasis patients and 271 control individuals. The minor allele encoding a protein lacking quinone reductase activity was significantly more frequent (q = 0.214) among these patients than in control individuals (P = 0.135) indicating an increased risk for kidney stone formation among heterozygotes (odds ratio 1.83, confidence interval 1.17-2.86) and homozygotes for the null-allele (odds ratio 2.97, confidence interval 0.78-11.33). Since NADP(H):quinone oxidoreductase is thought to participate in activation of vitamin K for protein gamma-carboxylation, decreased activity of the enzyme in heterozygotes or in null-allele homozygotes may disturb the post-translational modification of urinary calcium-binding proteins protective against kidney stone formation. The NQO1 null-allele might therefore be a determinant in enhanced risk of urolithiasis.

Body size and risk of kidney stones.

A variety of factors influence the formation of calcium oxalate kidney stones, including gender, diet, and urinary excretion of calcium, oxalate, and uric acid. Several of these factors may be related to body size. Because men on average have a larger body size and a threefold higher lifetime risk of stone formation than women, body size may be an important risk factor for calcium oxalate stone formation. The association between body size (height, weight, and body mass index) and the risk of kidney stone formation was studied in two large cohorts: the Nurses' Health Study (NHS; n = 89,376 women) and the Health Professionals Follow-up Study (HPFS; n = 51,529 men). Information on body size, kidney stone formation, and other exposures of interest was obtained by mailed questionnaires. A total of 1078 incident cases of kidney stones in NHS during 14 yr of follow-up and a total of 956 cases in HPFS during 8 yr of follow-up were confirmed. In both cohorts, the prevalence of a stone disease history and the incidence of stone disease were directly associated with weight and body mass index. However, the magnitude of the associations was consistently greater among women. Specifically, the age-adjusted prevalence odds ratio for women with body mass index > or = 32 kg/m2 compared with 21 to 22.9 kg/m2 was 1.76 (95% confidence interval, 1.50 to 2.07), but 1.38 (95% confidence interval, 1.16 to 1.65) for the same comparison in men. For incident stone formation, the multivariate relative risks for the similar comparisons were 1.89 (1.51 to 2.36) for women and 1.19 (0.83 to 1.70) in men. Height was inversely associated with the prevalence of stone disease but was not associated with incident stone formation. These results suggest that body size is associated with the risk of stone formation and that the magnitude of risk varies by gender. Additional studies are necessary to determine whether a reduction in body weight decreases the risk of stone formation, particularly in women.

Family history and risk of kidney stones.

Kidney stones develop more frequently in individuals with a family history of kidney stones than in those without a family history; however, little information is available regarding whether the increased risk is attributable to genetic factors, environmental exposures, or some combination. In this report, the relation between family history and risk of kidney stone formation was studied in a cohort of 37,999 male participants in the Health Professionals Follow-up Study. Information on family history, kidney stone formation, and other exposures of interest, including dietary intake, was obtained by mailed questionnaires. A family history of kidney stones was much more common in men with a personal history of stones at baseline in 1986 than in those without a history of stones (age-adjusted prevalence odds ratio, 3.16; 95% confidence interval [CI], 2.90 to 3.45). During 8 yr of follow-up, 795 incident cases of stones were documented. After adjusting for a variety of risk factors, the relative risk of incident stone formation in men with a positive family history, compared with those without, was 2.57 (95% CI, 2.19 to 3.02). Family history did not modify the inverse association between dietary calcium intake and the risk of stone formation. These results suggest that a family history of kidney stones substantially increases the risk of stone formation. In addition, these data suggest that dietary calcium restriction may increase the risk of stone formation, even among individuals with a family history of kidney stones.

Intravenous aminophylline increases the degree of saturation of urine with calcium phosphate and struvite.

This study was designed to assess the effect of i.v. treatment with aminophylline (AMPH) on the risk of calcium phosphate and struvite stone formation. We administered AMPH in doses of 4 mg/kg body weight in 15-min i.v. infusions to 60 infants with clinical symptoms of obstructive bronchitis with dyspnoea. During 3 hours after infusion we observed a significant increase in urine saturation with brushite, octocalcium phosphate and struvite. This rise in urine saturation may increase the risk of kidney stone formation.

Limited Risk of Kidney Stone Formation During Long-Term Calcium Citrate Supplementation in Nonstone Forming Subjects

The physiological and physicochemical effects of long-term calcium citrate supplementation (25mmol, calcium per day) were assessed in 7 normal premenopausal women. Calcium citrate increased urinary calcium from 3.27 ± 0.42mmol, per day (standard deviation) before treatment to 5.16 ± 0.75mmol, per day after 1-month of treatment (p <0.0125). After 3 months of treatment urinary calcium decreased from the 1-month value to 4.54 ± 0.67mmol, per day (p <0.0125) but remained higher than the pretreatment value (p <0.0125). Fractional intestinal calcium absorption and serum 1,25-dihydroxyvitamin D levels decreased marginally at 1 month of calcium citrate therapy, from 0.457 ± 0.092 to 0.374 ± 0.035 (p <0.05) and from 103 ± 7 to 77 ± 14 pmol./l. (p <0.05), respectively. After 3 months of treatment fractional intestinal calcium absorption decreased further to 0.341 ± 0.061 (p <0.0125 compared to pretreatment), whereas serum 1,25-dihydroxyvitamin D remained unchanged at 82 ± 14pmol./l.Calcium citrate treatment decreased urinary phosphorus levels significantly from 18.9 ± 3.3 to 15.0 ± 2.5mmol, per day (p <0.0125) and 14.0 ± 2.5mmol, per day (p <0.05) at 1 and 3 months, respectively. Mean urinary oxalate decreased by 15 to 20% and urinary citrate increased marginally during treatment. Urinary saturation of calcium oxalate and brushite did not change during calcium citrate therapy, except at 1 month when the saturation of calcium oxalate increased marginally. The inhibitory activity of urine against spontaneous nucleation of calcium oxalate and brushite (formation product) did not change during treatment.In conclusion, long-term calcium citrate supplementation in normal subjects does not increase the propensity for crystallization of calcium salts in the urine. This protective effect is probably due to the attenuated increase in urinary calcium excretion (from a decrease in fractional intestinal calcium absorption), a decrease in urinary phosphorus and an increase in urinary citrate.

The Potential Role of Salt Abuse on the Risk for Kidney Stone Formation

The kidney stone-forming risk of a high sodium diet was evaluated by assessing the effect of such a diet on the crystallization of stone-forming salts in urine. Fourteen normal subjects participated in 2 phases of study of 10 days duration each, comprising a low sodium phase (basal metabolic diet containing 50mmol. sodium per day) and a high sodium phase (basal diet plus 250mmol. sodium chloride per day). The high sodium intake significantly increased urinary sodium (34 ± 12 to 267 ± 56mmol, per day), calcium (2.73 ± 1.03 to 3.93 ± 1.51mmol. per day) and pH (5.79 ± 0.44 to 6.15 ± 0.25), and significantly decreased urinary citrate (3.14 ± 1.19 to 2.52 ± 0.83mmol. per day). Arterialized venous blood bicarbonate and total serum carbon dioxide concentrations decreased significantly during the high sodium diet, whereas serum chloride concentration increased. However, no change in arterialized venous pH was detected. Thus, a high sodium intake not only increased calcium excretion, but also increased urinary pH and decreased citrate excretion. The latter effects are probably due to sodium-induced bicarbonaturia and a significant decrease in serum bicarbonate concentration, respectively.Commensurate with these changes, the urinary saturation of calcium phosphate (brushite) and monosodium urate increased, and the inhibitor activity against calcium oxalate crystallization (formation product) decreased. The net effect of a high sodium diet was an increased propensity for the crystallization of calcium salts in urine.

Pathogenesis of nephrolithiasis post-partial ileal bypass surgery: Case-control study

Between 1975 and 1983, 838 patients were randomized into the Program on the Surgical Control of Hyperlipidemias (POSCH) trial: 417 to standard medical care and 421 to partial ileal bypass (PIB) surgery. During the course of the trial, an increased incidence of kidney stone formation was found in the surgery group (4%/year) as compared to the control group (0.4%/year). A matched triplet case-control study was conducted to assess the possible causes for the increased incidence of kidney stones. Three groups were studied: PIB stone-formers (S); PIB non-stone formers (N); and non-PIB, non-stone formers in the control group (C). Initially, 162 patients (54 triplets) were selected. Ten percent of the patients declined to participate which resulted in a sample size of 146 patients. The PIB patients had statistically significant (P less than 0.05) lower levels of serum vitamin D metabolites; lower urine volume, pH, citrate, magnesium, carbon dioxide, and sulfate, and higher urinary oxalate, ammonia and relative supersaturation for calcium oxalate and uric acid than the control patients. Although S and N had similar results, those S with no prior history of stones had a higher calcium oxalate supersaturation than similar N with a negative prior history of stones (P less than 0.025). Based on these results, all PIB patients appear to be at risk for kidney stone formation. The combination of reduced urinary volume and calcium oxalate precipitation inhibitor substance with increased calcium oxalate relative supersaturation produced an increase in nephrolithiasis risk in the PIB groups.

Crystallization activities of polyanionic macro-molecules of human urine may indicate risk of kidney stone formation

Urinary polyanionic macromolecules (UPM) from kidney stone-formers (SF) and normal controls (NC) were investigated for their potential to nucleate and inhibit growth of calcium oxalate crystals. UPM were obtained by precipitation with cetylpyridinium chloride. Solutions of UPM (4-8 mg/ml) from either SF or NC were added to ultrafiltrates (10kDa cutoff) of urine samples which had been adjusted to pH 5.3, 1200 mOsmol/Kg and subsequently frozen (16 hrs) and thawed (37°C) for assessment of crystallization of calcium oxalate. Normal UPM indicated a population density of (3.1 ± 0.1) × 10 5 crystals/ml and a size of 8 ± 1 μ, whereas the SF-UPM indicated a significantly higher population density of (108 ± 47) × 10 5 crystals/ml (p

Calcium oxalate kidney stones in patients on continuous ambulatory peritoneal dialysis

AbstractCalcium oxalate kidney stones in patients on continuous ambulatory peritoneal dialysis. Kidney stones were passed by ten out of 186 patients with endstage renal disease who were treated with continuous ambulatory peritoneal dialysis (CAPD). Stones from seven patients were examined by x-ray diffraction. In five of them the stones were composed of calcium oxalate monohydrate. The urine calcium oxalate activity product was determined in 44 CAPD patients, eight of whom were stone formers, and compared to that of 120 normal volunteers. In CAPD patients, mean urine ionic-calcium concentration was lower than in normal subjects whereas mean urine ionic-oxalate concentration was significantly higher than in normal subjects. In normal urine samples, the calcium oxalate activity product showed a significant correlation with both the urine ionic-calcium and the ionic-oxalate concentrations. In contrast, in CAPD patients the calcium oxalate activity product correlated with the ionic-calcium concentration but not with ionic-oxalate. Although the urine ionic-calcium concentration is lower in CAPD patients than in normal subjects, it is the relative increase in its concentration which appears to be associated with the increased risk of kidney stone formation in these patients. This relative hypercalciuria seems to follow 1,25(OH)2 vitamin D3 administration.Calculs rénaux d'oxalate de calcium chez des malades en dialyse péritonéale continue ambulatoire. Des calculs rénaux ont été éliminés par dix de 186 malades avec une néphropathie terminale traitée par dialyse péritonéale continue ambulatoire (CAPD). Les calculs de sept malades ont été examinés par diffraction aux rayons. Dans cinq d'entre eux, les calculs étaient composés d'oxalate de calcium monohydraté. Le produit d'activité urinaire de l'oxalate de calcium à été déterminé chez 44 malades en CAPD, dont huit étaient lithiasiques, et comparés à celui de 120 volontaires normaux. Chez les malades en CAPD, la concentration urinaire moyenne en ions calcium était plus faible que celle de sujets normaux, alors que la concentration moyenne en ion oxalate était significativement plus élevée que chez les normaux. Dans les échantillons urines normales, le produit d'activité de l'oxalate de calcium indiquait une corrélation significative avec les concentrations urinaires d'ions calcium et d'ions oxalate. A l'opposé, chez les malades en CAPD, le produit d'activité de l'oxalate de calcium était corrélé avec la concentration d'ions calcium mais non d'ions oxalate. Bien que la concentration urinaire d'ions calcium soit plus faible chez les malades en CAPD que chez les sujets contrôles, c'est l'augmentation relative de sa concentration qui semble être associée avec l'augmentation de risques de formation calculeuse chez ces malades. Cette relative hypercalciurie semble suivre l'administration de 1,25(OH)2D vitamine D3.