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PubMed2004

Schedule of taking calcium supplement and the risk of nephrolithiasis.

BACKGROUND: Variation in the timing of calcium supplement may affect gastrointestinal absorption of both calcium and oxalate differently and may associate with variable risk of calcium oxalate nephrolithiasis. There are few human studies addressing specifically the appropriate time for taking calcium supplement. Therefore, this study was performed to compare calcium bioavailability and the risk of calcium oxalate stone formation for calcium supplement taken with meal vs. taken at bedtime. METHODS: Thirty-two healthy male navy privates, 22.7 +/- 1.9 years old (mean +/- SD), who had normal renal function (serum creatinine less than 150 umol/L) and no history of renal stone, participated in the study. The subjects were randomly allocated into two groups of 16 each. Group A took 1 g of calcium carbonate with meal, 3 times/day; and group B took 3 g/day of calcium carbonate at bedtime. After taking the regimens for 1 week, followed by 1 month of washout period, crossover between both groups was done. The diet was controlled throughout the study. Twenty-four-hour urine collections for the determination of urinary constituents were obtained at baseline and after taking both regimens of calcium supplement. Activity product for calcium oxalate was determined to assess the risk of calcium oxalate stone formation. RESULTS: Urinary excretions of calcium were significantly elevated above the baseline values when taking calcium supplement both with meal (3.48 +/- 2.13 mmol/day vs. 5.17 +/- 2.61 mmol/day, P < 0.05) and at bedtime (3.09 +/- 1.70 mmol/day vs. 5.08 +/- 2.34 mmol/day, P < 0.05). There was no difference between the two regimens in the urinary calcium excretions. The urinary oxalate was decreased significantly when the subjects took calcium supplement with meal compared with the corresponding baseline value (0.13 +/- 0.05 vs. 0.17 +/- 0.07 mmol/d, P= 0.01). In contrast, there was no alteration in urinary oxalate when calcium supplement was taken at bedtime compared to the baseline values (0.15 +/- 0.05 mmol/day vs. 0.15 +/- 0.06 mmol/day, P= 0.9). Compared with the corresponding baseline values, there was no significant increase in the activity product for calcium oxalate when taking calcium with meal (0.54 +/- 0.25 vs. 0.57 +/- 0.22, P= 0.54), but it was increased significantly when calcium supplement was taken at bedtime (0.47 +/- 0.21 vs. 0.72 +/- 0.27, P < 0.01). CONCLUSION: Calcium supplement should be taken with meal in order to avoid increasing the risk of calcium oxalate nephrolithiasis.

Adult↗

PubMed2005

A twin study of genetic and dietary influences on nephrolithiasis: a report from the Vietnam Era Twin (VET) Registry.

BACKGROUND: Nephrolithiasis is a complex phenotype that is influenced by both genetic and environmental factors. We conducted a large twin study to examine genetic and nongenetic factors associated with stones. METHODS: The VET Registry includes approximately 7500 male-male twin pairs born between 1939 to 1955 with both twins having served in the military from 1965 to 1975. In 1990, a mail and telephone health survey was sent to 11,959 VET Registry members; 8870 (74.2%) provided responses. The survey included a question asking if the individual had ever been told of having a kidney stone by a physician. Detailed dietary habits were elicited. In a classic twin study analysis, we compared concordance rates in monozygotic (MZ) and dizygotic (DZ) twins. We also conducted a cotwin control study of dietary risk factors in twins discordant for stones. RESULTS: Among dizygotic twins, there were 17 concordant pairs and 162 discordant pairs for kidney stones. Among monozygotic twins, there were 39 concordant pairs and 163 discordant pairs. The proband concordance rate in MZ twins (32.4%) was significantly greater than the rate in DZ twins (17.3%) (chi(2)= 12.8; P < 0.001), consistent with a genetic influence. The heritability of the risk for stones was 56%. In the multivariate analysis of twin pairs discordant for kidney stones, we found a protective dose-response pattern of coffee drinking (P= 0.03); those who drank 5 or more cups of coffee were half as likely to develop kidney stones as those who did not drink coffee (OR = 0.4, 95% CI 0.2, 0.9). Those who drank at least 1 cup of milk per day were half as likely to report kidney stones (OR = 0.5, 95% CI 0.3, 0.8). There were also marginally significant protective effects of increasing numbers of cups of tea per day and frequent consumption of fruits and vegetables. Other factors such as the use of calcium supplements, alcohol drinking, consumption of solid dairy products, and the amount of animal protein consumed were not significantly related to kidney stones in the multivariate model. CONCLUSION: These results confirm that nephrolithiasis is at least in part a heritable disease. Coffee, and perhaps tea, fruits, and vegetables were found to be protective for stone disease. This is the first twin study of kidney stones, and represents a new approach to elucidating the relative roles of genetic and environmental factors associated with stone formation.

Diet↗

PubMed2005

Diabetes mellitus and the risk of nephrolithiasis.

BACKGROUND: Insulin resistance is a central feature of type 2 diabetes mellitus (DM) and may increase the risk of kidney stone formation. Existing cross-sectional data on the association between DM and nephrolithiasis are limited, and no prospective study to date has evaluated the relation between DM and the risk of kidney stones. METHODS: To evaluate the relation between DM and prevalent kidney stones, we conducted a cross-sectional study of 3 large cohorts including over 200,000 participants: the Nurses' Health Study I (older women), the Nurses' Health Study II (younger women), and the Health Professionals Follow-up Study (men). We then prospectively studied the association between DM and incident nephrolithiasis over a combined 44 years of follow-up. Because insulin resistance can precede the diagnosis of DM by decades, we also prospectively examined the relation between kidney stones and the diagnosis of incident DM. Multivariate regression models adjusted for age, body mass index, thiazide diuretic use, fluid intake, and dietary factors. RESULTS: At baseline, the multivariate relative risk of prevalent stone disease in individuals with DM compared to individuals without was 1.38 (95% CI 1.06-1.79) in older women, 1.67 (95% CI 1.28-2.20) in younger women, and 1.31 (95% CI 1.11-1.54) in men. Prospectively, the multivariate relative risk of incident kidney stone formation in participants with DM compared to participants without was 1.29 (95% CI 1.05-1.58) in older women, 1.60 (95% CI 1.16-2.21) in younger women, and 0.81 (95% CI 0.59-1.09) in men. The multivariate relative risk of incident DM in participants with a history of kidney stones compared to participants without was 1.33 (95% CI 1.18-1.50) in older women, 1.48 (95% CI 1.14-1.91) in younger women, and 1.49 (95% CI 1.29-1.72) in men. CONCLUSION: DM is a risk factor for the development of kidney stones. Additional studies are needed to determine if the increased risk of DM in stone formers is due to subclinical insulin resistance.

Adult↗

PubMed1992

Thiazide therapy for ACTH-induced hypercalciuria and nephrolithiasis.

A one-year-old boy presented with hypercalciuria and nephrolithiasis following a course of ACTH therapy for infantile spasms. After a successful cystolithotripsy, therapy with chlorothiazide was followed by regression of the hypercalciuria within 42 months. Neither nephrolithiasis nor nephrocalcinosis recurred. Therapy with thiazides to prevent hypercalciuria caused by ACTH is proposed.

Adrenocorticotropic Hormone↗

PubMed1998

Magnesium hydrogen carbonate natural mineral water enriched with K(+)-citrate and vitamin B6 improves urinary abnormalities in patients with calcium oxalate nephrolithiasis.

The influence of drinking magnesium hydrogen carbonate natural mineral water enriched with potassium citrate on urinary metabolic abnormalities was prospectively studied in 27 patients with recurrent calcium oxalate nephrolithiasis. The mean 24-hour urinary pH shifted from 6.34 to 6.93 (p < 0.01), the mean urinary magnesium/urinary creatinine ratio rose from 0.47 to 0.67 (p < 0.01), the mean urinary citrate/urinary creatinine ratio increased from 0.26 to 0.35 (p NS), and the mean 24-hour urinary calcium decreased from 7.98 to 6.05 mmol (p < 0.05). The effects of magnesium hydrogen carbonate natural mineral water enriched with potassium citrate were found to be favorable on urinary calcium, urinary magnesium/urinary creatinine ratio and urinary pH in patients with calcium oxalate nephrolithiasis.

Adult↗

PubMed1999

Epidemiology of nephrolithiasis.

The main purpose of the study is to acquire useful information on nephrolithiasis in Italy, given the recent increase in its prevalence. The analysis was based on data from sample surveys of the Italian population carried out in 1983 and 1993-1994 as well as on data obtained from medical records of patients treated at the ASTIF in Fiuggi. An increase in the prevalence of the disease from 11.7 to 17.2 out of 1,000 inhabitants has been observed over the last 10 years; most patients are men and elderly, and the highest frequency is in southern and the lowest in northern Italy. The results of the study confirm the hereditary predisposition, since nephrolithiasis is very common among patients' parents (22.5%) and siblings (14.1%). The patients eat more meat than others and are often overweight or obese; the latter represent 18% of these patients and 11% of the general population.

Adult↗

PubMed1999

Idiopathic calcium nephrolithiasis.

Calcium nephrolithiasis (CaNL) accounts for more than 70% of all renal stones, and its prevalence has increased in the last decades. Under this definition are included patients passing stones, composed of calcium oxalates and/or calcium phosphates. Current views of the pathogenesis of CaNL are based on the role of metabolic abnormalities which concur to render urines more conducive to crystallization. Therefore, the diagnostic approach is aimed at detecting these abnormalities, and the medical treatment assumes that a decrease in the risk of lithogenesis will result in remission or improvement of recurrences. The workup of the patients with CaNL begins with the analysis of passed stones and X-ray, sonography or other imaging techniques. Eligible patients, that is, both recurrent active stone formers and single-stone formers with individual risk factors, are considered for a metabolic evaluation, by which a number of blood and urine parameters are measured and others calculated. These include estimates of urine state of saturation with calcium and uric acid salts, net gastrointestinal alkali absorption, renal threshold of phosphate and other renal clearances and net acid and total nitrogen excretions. Basically, this screening is informative on renal function, metabolic abnormalities and their pathophysiology, risk of stone formation and dietary habits. During treatment it gives information about patient compliance and adverse effects of therapy. The cost of a comprehensive screening in Piedmont is 192,000 ITL (100 Euro) and rises to 300,000 ITL (154 Euro) if hormones and hydroxyproline are measured. In individual patients second- and third-level studies are performed, in order to detect systemic diseases which account for about 20% of CaNL in our series. Cost-to-benefit analysis has shown that the medical procedures for CaNL yield considerable saving in terms of difference between expenditure for drugs and testing and reduction of stone events. However, the current workup cannot be considered exhaustive, because misleading events may hamper the relation between laboratory findings and clinical outcome, and factors other than urine composition have appeared on the scenario of nephrolithiasis. These represent our challenge for the third millennium.

Adult↗

PubMed1999

Effects of water hardness on urinary risk factors for kidney stones in patients with idiopathic nephrolithiasis.

Both amount and timing of dietary calcium intake influence the recurrence of renal calcium stones. We have evaluated whether the hardness of extra meal drinking water modifies the risk for calcium stones. The urinary levels of calcium, oxalate and citrate, i.e., the main urinary risk factors for calcium stones, were measured in 18 patients with idiopathic nephrolithiasis, maintained at fixed dietary intake of calcium (800 mg/day), after drinking for 1 week 2 liters per day, between meals, of tap water and at the end of 1 week of the same amount of bottled hard (Ca2+ 255 mg/l) or soft (Ca2+ 22 mg/l, Fiuggi water) water, in a double-blind randomized, crossover fashion. As compared with both tap and soft water, hard water was associated with a significant 50% increase of the urinary calcium concentration in the absence of changes of oxalate excretion; the calcium-citrate index revealed a significant threefold increase during ingestion of hard water as compared with respect to soft water (Fiuggi water), making the latter preferable even when compared with tap water. This study suggests that, in the preventive approach to calcium nephrolithiasis, the extra meal intake of soft water is preferable to hard water, since it is associated with a lower risk for recurrence of calcium stones.

Biomarkers↗

PubMedDate not supplied

Association between vitamin D receptor gene polymorphism and nephrolithiasis.

AIMS: To study the distribution of vitamin D receptor (VDR) gene alleles in hypercalciuric and nonhypercalciuric nephrolithiasis patients, hypothesizing that distinct biochemical parameters would be associated with different VDR genotypes. METHODS: 12 hypercalciuric, 15 normocalciuric nephrolithiasis patients, and 150 healthy subjects were recruited. The individual genetic pattern for VDR was evaluated by DNA extraction followed by polymerase chain reaction amplification of the VDR gene and digestion with the restriction enzyme BsmI. RESULTS: In the hypercalciuric group, Bb patients represented 50% (6/12); bb patients 33% (4/12), and BB cases were 16% (2/12). The VDR frequency distribution was not statistically different in hypercalciuric patients and controls (Bb 72%; bb 16%; BB 12%). In the nonhypercalciuric group, the prevalence of the bb genotype (7/15; 47%) was thrice the percentage of control subjects, while the percentage of BB patients was similar to that of the control group (2/15; 13%). Patients with the bb haplotype exhibited a higher daily urinary calcium excretion. Among hypercalciuric patients, after a calcium-restricted diet, bb patients showed a 39% reduction in daily urinary calcium excretion in comparison with a nonsignificant 13% reduction observed in BB subjects (p = 0.004). CONCLUSIONS: The effects of VDR gene polymorphism on calcium metabolism contribute to the understanding of the pathogenesis of urinary calculi.

Adult↗

PubMed1983

Hypercalcemia and nephrolithiasis provoked by serum phosphorus reduction in a patient with chronic renal failure and sarcoidosis.

A patient with sarcoidosis and chronic renal failure was treated for hyperphosphatemia with aluminum hydroxide. The subsequent fall in serum phosphorus was followed by the development of hypercalcemia and nephrolithiasis. Corticosteroid therapy normalized the serum calcium and halted the progression of the nephrolithiasis, but did not improve renal function. Hyperphosphatemia may have blocked the expression of sarcoid hypercalcemia in the patient. The mechanism is unclear but inhibition of the synthesis or action of 1,25-dihydroxyvitamin D may have been involved. Reduction of serum phosphorus may lead to severe hypercalcemia in some patients with sarcoidosis.

Adult↗

PubMed1996

Localization of tamm-horsfall protein and osteopontin in a rat nephrolithiasis model.

The possibility of more than one urinary protein being simultaneously associated with calcium oxalate (CaOx) crystallization in vivo was investigated by examining the localization of Tamm-Horsfall protein (THP) and osteopontin (Opn) in a rat model of nephrolithiasis. CaOx crystal deposits were induced in male Sprague-Dawley rats by feeding 0.75% ethylene glycol in drinking water. THP and Opn were localized on kidney sections by immunoperoxidase technique, using specific polyclonal antibodies. When only occasional crystal deposits were seen in the kidney, THP showed a similar to normal pattern of distribution, with positive staining in the thick ascending limbs of the loop of Henle. Opn was localized in some nephrons in the thin limb of loop of Henle and on the papillary surface in the calyceal fornix. In contrast, in samples with a significantly increased number of deposits in the kidneys, the staining for both THP and Opn was strikingly enhanced and altered, with positive staining around the crystals as well as abnormal localization in the papilla. Interestingly, the occurrence of Opn was, however, more consistent than that of THP. This is a first study showing that in this nephrolithiasis model, normal localization of THP and Opn is altered and they are closely and concurrently associated with crystal deposits in vivo.

Animals↗

PubMed1985

Urine glycoprotein crystal growth inhibitors. Evidence for a molecular abnormality in calcium oxalate nephrolithiasis.

One reason that some people are prone to calcium oxalate nephrolithiasis is that they produce urine that is subnormal in its ability to inhibit the growth of calcium oxalate crystals. We have identified in human urine a glycoprotein (GCI) that inhibits calcium oxalate crystal growth strongly, and at low concentrations (10(-7) M); in this study, we have isolated GCI molecules from the urine of normal people and patients with calcium oxalate stones. GCI from stone formers is abnormal in three ways: it contains no detectable gamma-carboxyglutamic acid (Gla), whereas normal GCI contains 2-3 residues of Gla per mole; about half of the GCI in urine of patients inhibits crystal growth 4-20 times less than normal GCI as judged by its performance in a kinetic growth assay, in vitro; at the air-water interface, patient GCI has a film collapse pressure approximately half of normal. GCI molecules from the urine of patients with calcium oxalate nephrolithiasis are intrinsically abnormal, and these abnormalities could play a role in the genesis of stones.

1-Carboxyglutamic Acid↗

PubMed2002

Gender- and age-dependent changes in kidney androgen protein mRNA expression in a knockout mouse model for nephrolithiasis.

Kidney androgen-regulated protein (Kap) is the most abundant protein in the mouse kidney, but its function is unknown. We previously observed a significant decrease in Kap mRNA expression in whole kidney tissue from male mice with adenine phosphoribosyltransferase (APRT) deficiency and 2,8-dihydroxyadenine (DHA) nephrolithiasis. The disease phenotype is more severe in male mice and is age-dependent. To identify the cellular basis for differential Kap expression, we used in situ hybridization (ISH) and reverse transcription-polymerase chain reaction ISH (RT-PCR ISH) to identify the cell types expressing this mRNA in paraffin-embedded kidney sections. In 1-month-old wild-type male mice, Kap was detected primarily in S3 proximal tubule segments, but expression was very low in female mice. In 1-month-old APRT-deficient male mice, Kap expression was decreased significantly and was undetectable in female mice. Kap mRNA was not detected in 3- or 6-month-old mice using our standard ISH protocol, but we observed intense cytoplasmic staining in S3 proximal tubules in wild-type male mice of these age groups using an improved RT-PCR ISH procedure. Our studies demonstrate age-, gender-, and APRT genotype-dependent changes in Kap mRNA expression in mouse kidney. Kap expression is under multihormonal control, and hormonal changes in DHA-induced nephrolithiasis may account for the decreased Kap expression in APRT-deficient mice.

Adenine Phosphoribosyltransferase↗

PubMed2005

Fibroblast growth factor 23 is increased in calcium nephrolithiasis with hypophosphatemia and renal phosphate leak.

CONTEXT: Nephrolithiasis affects about 10% of the population in industrialized countries, with calcium salts composing more than 80% of renal stones. A significant percentage of patients with calcium nephrolithiasis and normal parathyroid function show hypophosphatemia and reduced renal phosphate reabsorption (i.e. a renal phosphate leak). OBJECTIVES: The objective of the study was to compare serum levels of fibroblast growth factor 23 (FGF23), a regulator of phosphate homeostasis, in 110 recurrent stone formers with or without renal phosphate leak, six patients affected by X-linked hypophosphatemic rickets, five patients affected by oncogenic osteomalacia, and 60 unrelated healthy controls. DESIGN: This was a prospective interventional study. METHODS: Renal phosphate leak was identified based on the occurrence of idiopathic hypophosphatemia [serum phosphate concentration < 2.50 mg/dl (<0.80 mmol/liter)] and reduced renal threshold phosphate concentration [<2.2 mg/liter (<0.70 mmol/liter)]. RESULTS: In 22 stone formers with renal phosphate leak, serum FGF23 concentration was significantly higher as compared with 88 stone formers without renal phosphate leak and with controls [83.3 (65.6-101.1) vs. 32.1 (26.8-37.4) and 24.5 (19.8-29.1) reference units (RU)/ml, respectively]. Stone formers with renal phosphate leak showed lower FGF23, compared with patients with oncogenic osteomalacia and X-linked hypophosphatemic rickets [572.3 (235.9-908.7) RU/ml]. Among stone formers and controls, serum FGF23 concentration displayed a strong inverse association with serum phosphate (r = -0.784, P = 0.009) and the rate of tubular phosphate reabsorption (r = -0.791, P = 0.008). CONCLUSIONS: In our study population, renal phosphate leak affected 20% of stone formers and was strongly associated with increased serum FGF23 concentration.

Adult↗

PubMed1993

Acetazolamide-induced nephrolithiasis: implications for treatment of neuromuscular disorders.

Carbonic anhydrase inhibitors can cause nephrolithiasis. We studied 20 patients receiving long-term carbonic anhydrase inhibitor treatment for periodic paralysis and myotonia. Three patients on acetazolamide (15%) developed renal calculi. Extracorporeal lithotripsy successfully removed a renal calculus in one patient and surgery removed a staghorn calculus in another, permitting continued treatment. Renal function remained normal in all patients. Nephrolithiasis is a complication of acetazolamide but does not preclude its use.

Acetazolamide↗

PubMed2004

Topiramate increases biochemical risk of nephrolithiasis.

The incidence of renal stone disease in patients receiving topiramate (Topamax) is 2-4 times that expected in the background population. This has been attributed to a weak carbonic anhydrase inhibitor effect, but published data are scant. Following three cases of renal stones in patients receiving topiramate, we evaluated biochemical risk for nephrolithiasis in eight further unselected patients. Most patients demonstrated inadequate urinary acidification and hypocitraturia; in some cases citrate was undetectable. Several patients also had other risk factors for nephrolithiasis, including increased urinary sodium, calcium and oxalate excretion. The biochemical changes induced by topiramate appear highly penetrant. Experience with this drug is relatively short-lived and it is being prescribed for long-term use in (often) relatively young patients. This report highlights the significantly increased metabolic risk of stone formation in patients receiving topiramate.

Adult↗

PubMedDate not supplied

[Quantification of the stone clinic effect in patients with nephrolithiasis].

BACKGROUND: The "stone clinic effect" refers to the effect of encouraging a high intake of fluid and diet counseling in the clinical evolution of kidney stone disease. OBJECTIVE: Our objective was to determine the extent of this variable in patients with nephrolithiasis. METHODS: Twenty-five patients (11 female and 14 male, 47.64+/-10.55 years old) with recurrent nephrolithiasis were prospectively followed for one year, with 3-month interval medical evaluation. Patients were advised to increase the fluid intake, and to limit the intake of salt and protein. No patient was submitted to pharmacological therapy. Two 24-hour urine samples were collected at baseline (S1) and in the end of follow-up (S2) for the measurement of creatinine, calcium, sodium, uric acid, citrate, oxalate and magnesium. Metabolic and radiological activity was also assessed. Urinary calcium oxalate supersaturation (SS) was calculated by Tiselius index. RESULTS: Eleven (44%) patients had hypocitraturia, 9 (36%) hypercalciuria and 5 (20%) hyperuricosuria. Urinary volume increased (1903+/-811 vs. 2381+/-919 ml/day, p<0.05) and SS decreased significantly (1.13+/-0.8 vs. 0.6+/-0.2, p<0.01). During follow-up, the number of stones decreased when compared to baseline (S1 = 2.04+/-1.51 vs. S2 = 0.72+/- 0.23 stones, p<0.001). There was no evidence of new stone formation or growth in 20 of 25 patients (80%). CONCLUSIONS: The "stone clinic effect" significantly decreased urinary SS for calcium oxalate and the formation of new kidney stones in 80% of patients during first year of follow-up.

Adolescent↗

PubMed1995

Characterization of carrier females and affected males with X-linked recessive nephrolithiasis.

X-linked recessive nephrolithiasis (XRN) was described in a large kindred in which nephrolithiasis; proximal tubular dysfunction, proteinuria, nephrocalcinosis, and renal failure occur only in males. Carrier females are asymptomatic, but formal studies of them have not been done. The gene for XRN has been mapped to the pericentromeric region of the X chromosome, close to the loci for several eye disease genes. We studied six affected males, 13 carrier females, and 25 normal members of this family including 7 females whose genetic haplotype predicted them to be carriers. Studies were done in the Clinical Research Unit on a diet containing 400 mg of calcium and 2 g of sodium, and by an additional outpatient urine collection was obtained on a 1-g calcium intake. Hypercalciuria occurred in five of six affected males, 4 of 12 carrier females, and three of seven predicted carriers. Significant proteinuria was present in all affected males and in no other subjects. Low-molecular-weight proteinuria was present in all affected males: the excretion of alpha 1-microglobulin exceeded normal by 3- to 14-fold, of beta 2-microglobulin exceeded normal by 100- to 400-fold, and of retinol-binding protein exceeded normal by 1,000- to 3,000-fold. The excretion of these proteins was less strikingly elevated in carrier females, but the excretion of alpha 1-microglobulin was abnormal in 9 of 15 carriers, beta 2-microglobulin was abnormal in 12 of 15, and retinolbinding protein in was abnormal 12 of 13, and this pattern was similar in predicted carriers. The urinary concentrating ability was abnormal in four affected males with renal insufficiency but normal in all other subjects. Urinary wasting of potassium, phosphorous, and glucose occurred infrequently, and no subject was hypouricemic. Formal ophthalmologic studies were normal in five affected males. Thus, the most consistent urinary abnormalities in XRN are hypercalciuria and low-molecular-weight proteinuria, the latter of which appears to be a marker for the carrier state.

Adolescent↗