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PubMed2000

Role of macrophages in nephrolithiasis in rats: an analysis of the renal interstitium.

Interstitial calcium oxalate (CaOx) crystals can be found in primary oxalosis and in secondary hyperoxaluria. In a rat model for nephrolithiasis, we investigated whether such crystals can be removed by the surrounding interstitial cells. CaOx crystals were induced by a crystal-inducing diet based on ethylene glycol (EG) and ammonium chloride (CID). Both lithogenic compounds were added to the drinking water. After 9 days, the animals received normal drinking water for 2 days. Using this CID, only the interstitial crystals are retained. Subsequently, half of the population remained on normal drinking water (normo-oxaluria), whereas the other half received a low dose of EG alone (chronic hyperoxaluria). The rats were killed at regular times thereafter. The results showed that the kidney-associated oxalate significantly declined during normo-oxaluria, but remained high during chronic hyperoxaluria. Interstitial cells positive for the leukocyte common antigen (CD45; which identifies all types of leukocytes), the ED1 antigen (which is specific for monocytes and macrophages), and the major histocompatibility class II antigen (MCHII), respectively, had increased in number, with minor differences between both rat populations. The cells around the interstitial crystals were mostly positive for ED1. Multinucleate giant cells were regularly observed. These cells were positive for CD45 and ED1 and sometimes also for MCHII. The crystals in these cells were moderately positive for acid phosphatase and carbonic anhydrase II. It is concluded that interstitial CaOx crystals can be removed under normo-oxaluric conditions and that, in all likelihood, macrophages and multinucleate giant cells are involved in that process.

Ammonium Chloride↗

PubMed2001

Risk for renal failure in nephrolithiasis.

Evaluation of the risk for developing renal insufficiency is generally not considered during the clinical metabolic workup of the stone-forming patient. This review approaches the problem of the severity of nephrolithiasis by addressing the renal risk. Although renal stones are an infrequent cause of renal failure, some lithiasic forms present a greater risk, such as in hereditary stone diseases (eg, cystinuria, primary hyperoxaluria, Dent's disease), primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury. Recurrent bouts of obstruction and/or crystal-specific biological effects on tubular epithelial cells and interstitial renal cells may activate the fibrogenic cascade responsible for the loss of renal parenchyma. In clinical terms, frequent stone relapses, episodes of urinary tract infection and obstruction, number of urological interventions, and size of the gravel are all significantly associated with the risk for renal failure. Percutaneous and extracorporeal urological methods for the treatment of renal stones may also lead to some chronic deterioration of renal function, particularly in recurrent stone formers treated with multiple therapeutic sessions. Although still speculative, concerns exist about the effect of extracorporeal shock wave lithotripsy on small or pathological kidneys. Without doubt, the medical prevention of stones would be more sensible.

Humans↗

PubMed2004

Recurrent calcium nephrolithiasis associated with primary aldosteronism.

Typical manifestations of hyperaldosteronism include salt retention, hypokalemia, and metabolic alkalosis. However, a consequence infrequently recognized and described is hypocitraturia. In combination with hypercalciuria, aldosterone-induced hypocitraturia can trigger calcium nephrolithiasis. The authors report a case of an individual with primary hyperaldosteronism from an adrenal adenoma that resulted in hypocitraturia. The patient had severe recurrent renal calcium calculi that corrected with adrenalectomy. The clinical physiology of renal calcium and citrate handling in hyperaldosteronism is reviewed.

Adrenal Gland Diseases↗

PubMed2005

Fatty acid intake and incident nephrolithiasis.

BACKGROUND: Elevated levels of arachidonic acid in cell membranes may promote the hypercalciuria and hyperoxaluria that are characteristic of idiopathic calcium nephrolithiasis. The intake of n-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may decrease the arachidonic acid content of cell membranes and reduce urinary excretion of calcium and oxalate. It has been proposed that greater intake of EPA and DHA (through dietary sources or fish oil supplementation) may reduce the risk for kidney stone formation. METHODS: After excluding subjects with a prior history of kidney stones, we prospectively examined the relation between fatty acid intake (including fish oil supplements) and incident symptomatic kidney stones in 3 large cohorts: the Health Professionals Follow-Up Study (N = 46,043), the Nurses' Health Study I (NHS I; N = 92,079), and the Nurses' Health Study II (N = 96,304). Self-administered food-frequency questionnaires were used to assess fatty acid intake every 4 years. Cox proportional hazards regression was used to adjust simultaneously for a variety of risk factors. RESULTS: We documented 3,956 incident kidney stones during a combined 36 years of follow-up. After adjustment for intake of other dietary factors, no association was detected between the intake of arachidonic acid or linoleic acid (a metabolic precursor to arachidonic acid) and the risk for incident kidney stones. Older women (NHS I) in the highest quintile of EPA and DHA intake had a multivariate relative risk of 1.28 (95% confidence interval, 1.04 to 1.56; P for trend = 0.04) of stone formation compared with women in the lowest quintile. However, this relation was not observed in the other 2 cohorts. CONCLUSION: Fatty acid intake is not consistently associated with the development of kidney stones. Greater levels of arachidonic and linoleic acid intake do not increase the risk for developing a kidney stone, and greater intake of n-3 fatty acids does not reduce the risk.

Adult↗

PubMed2005

Nephrolithiasis and increased blood pressure among females with high body mass index.

BACKGROUND: We hypothesized that one reason for the heterogeneity in previously reported links between kidney stones and blood pressure (BP) was the differential effects of nephrolithiasis among subgroups of individuals. In particular, we hypothesized that the association between stone history and BP may vary with respect to sex and body size. METHODS: Data from the Third National Health and Nutrition Examination Survey were used to estimate the association between history of stone disease and odds of prior diagnosis of hypertension and mean difference in systolic BP, diastolic BP, and pulse pressure. Nine hundred nineteen persons with a history of stones and 19,120 persons without stones were available for analysis. RESULTS: In women, it was estimated that stone formers (SFs) experienced a 69% increase in odds of self-reported hypertension (95% confidence interval [CI], 1.33 to 2.17; P < 0.001). No significant difference was found in men. The estimated difference in mean systolic and diastolic BP comparing SFs with non-SFs increased with body mass index in both sexes, but was more pronounced in women. Mean systolic BPs in women SFs in quintiles 4 and 5 of body mass index were 7.62 mm Hg (95% CI, 1.04 to 14.2; P = 0.024) and 4.36 mm Hg (95% CI, 0.30 to 8.42; P = 0.036) greater than those in similar women non-SFs, respectively. CONCLUSION: Our findings not only support the link between kidney stone disease and BP, but also suggest that overweight women SFs may be at significantly increased risk for hypertension.

Adolescent↗

PubMed1980

[Diagnosis of hypercalciuria in calcium nephrolithiasis (author's transl)].

An increased calcium excretion in 24-hour urine was found in 32 of 42 out-patients with recurrent calcium nephrolithiasis (calcium excretion > 300 mg in males, > 250 mg in females). Subsequent hospitalization of the 32 patients revealed the following diagnosis after a calcium tolerance test: absorptive hypercalciuria in 18, renal hypercalciuria in 4, primary hyperparathyroidism in 2 and dietary hypercalciuria in 7. Normocalciuria in 10 out-patients was confirmed in 6; in one instance there was, however, primary hyperparathyroidism, in 3 there was absorptive hypercalciuria. In one patient it was not possible to classify the hypercalciuria. Total as well as nephrogenic cAMP showed wide scatter and was unsuitable, therefore, in differential diagnosis. In 2 of 3 cases of hyperparathyroidism the serum level of parathormone was distinctly elevated.

Calcium↗

PubMed1984

A randomized double-blind study of acetohydroxamic acid in struvite nephrolithiasis.

We studied the effects of the bacterial urease inhibitor acetohydroxamic acid on the growth of struvite stones in the urinary tract. Eighteen patients who received acetohydroxamic acid (15 mg per kilogram of body weight per day, in divided oral doses) for a mean of 15.8 months were compared in a randomized double-blind study with 19 patients who received placebo for a mean of 19.6 months. Seven patients given placebo reached a pre-determined end point: a 100 per cent increase in the two-dimensional surface area of their stones. No patient who received acetohydroxamic acid had a doubling of stone size (P less than 0.01). Nine patients receiving the drug and one patient receiving placebo required a decrease in dosage or cessation of treatment because of adverse effects (P less than 0.01). Episodes of tremulousness (n = 5, P less than 0.05), which reversed with a decrease in drug dose, and phlebothrombosis (n = 3, P not significant) were limited to the group given acetohydroxamic acid. We conclude that acetohydroxamic acid effectively inhibits the growth of struvite stones in the short term in patients infected with urea-splitting bacteria, but the prevalence of adverse reactions appears to be high and the toxicity and effectiveness of long-term therapy for struvite nephrolithiasis remain to be defined.

Adult↗

PubMed1996

Adenine phosphoribosyltransferase-deficient mice develop 2,8-dihydroxyadenine nephrolithiasis.

Adenine phosphoribosyltransferase (APRT) deficiency in humans is an autosomal recessive syndrome characterized by the urinary excretion of adenine and the highly insoluble compound 2,8-dihydroxyadenine (DHA) that can produce kidney stones or renal failure. Targeted homologous recombination in embryonic stem cells was used to produce mice that lack APRT. Mice homozygous for a null Aprt allele excrete adenine and DHA crystals in the urine. Renal histopathology showed extensive tubular dilation, inflammation, necrosis, and fibrosis that varied in severity between different mouse backgrounds. Thus, biochemical and histological changes in these mice mimic the human disease and provide a suitable model of human hereditary nephrolithiasis.

Adenine↗

PubMed1981

Nephrolithiasis: causes, classification, and management.

The specific biochemical cause of calcium stone formation can now be reliably identified in close to 80% of cases. By permitting treatment to be targeted to the underlying condition, this has, in recent years, resulted in a documented reduction in stone recurrence. Less common types of nephrolithiasis--uric acid, cystine, and struvite stone formation--are also discussed and their management outlined.

Adult↗

PubMed2002

Unusual clinical presentation of Klebsiella pneumoniae induced endogenous endophthalmitis and xanthogranulomatous pyelonephritis in a non-nephrolithiasis and non-obstructive urinary tract.

The genitourinary tract is well recognized as a route through which bacteria could gain access to the blood circulation. Under some circumstances, metastatic infections may occur in distant organs, including endogenous endophthalmitis. Xanthogranulomatous pyelonephritis (XGP) is an unusual variant of chronic pyelonephritis. It most often occurs in middle-aged women who frequently have a history of recurrent urinary tract infections combined with obstruction and a kidney of poor function. We reported an unusual case of urinary tract infection in a non-nephrolithiasis and non-obstructive urinary tract complicated by Klebsiella pneumoniae endogenous endophthalmitis and developed XGP in two months.

Aged↗

PubMed2001

Identification of a new candidate locus for uric acid nephrolithiasis.

Renal stone formation is a common multifactorial disorder, of unknown etiology, with an established genetic contribution. Lifetime risk for nephrolithiasis is approximately 10% in Western populations, and uric acid stones account for 5%-10% of all stones, depending on climatic, dietary, and ethnic differences. We studied a small, isolated founder population in Sardinia, characterized by an increased prevalence of uric acid stones, and performed a genomewide search in a deep-rooted pedigree comprising many members who formed uric acid renal stones. The pedigree was created by tracing common ancestors of affected individuals through a genealogical database based on archival records kept by the parish church since 1640. This genealogical information was used as the basis for the study strategy, involving screening for alleles shared among affected individuals, originating from common ancestors, and utilization of large pedigrees to obtain greater power for linkage detection. We performed multistep linkage and allele-sharing analyses. In the initial stage, 382 markers were typed in 14 closely related affected subjects; interesting regions were subsequently investigated in the whole sample. We identified two chromosomal regions that may harbor loci with susceptibility genes for uric acid stones. The strongest evidence was observed on 10q21-q22, where a LOD score of 3.07 was obtained for D10S1652 under an affected-only dominant model, and a LOD score of 3.90 was obtained using a dominant pseudomarker assignment. The localization was supported also by multipoint allele-sharing statistics and by haplotype analysis of familial cases and of unrelated affected subjects collected from the isolate. In the second region on 20q13.1-13.3, multipoint nonparametric scores yielded suggestive evidence in a approximately 20-cM region, and further analysis is needed to confirm and fine-map this putative locus. Replication studies are required to investigate the involvement of these regions in the genetic contribution to uric acid stone formation.

Alleles↗

PubMed2003

Identification of a novel gene and a common variant associated with uric acid nephrolithiasis in a Sardinian genetic isolate.

Uric acid nephrolithiasis (UAN) is a common disease with an established genetic component that presents a complex mode of inheritance. While studying an ancient founder population in Talana, a village in Sardinia, we recently identified a susceptibility locus of approximately 2.5 cM for UAN on 10q21-q22 in a relatively small sample that was carefully selected through genealogical information. To refine the critical region and to identify the susceptibility gene, we extended our analysis to severely affected subjects from the same village. We confirm the involvement of this region in UAN through identical-by-descent sharing and autozygosity mapping, and we refine the critical region to an interval of approximately 67 kb associated with UAN by linkage-disequilibrium mapping. After inspecting the genomic sequences available in public databases, we determined that a novel gene overlaps this interval. This gene is divided into 15 exons, spanning a region of approximately 300 kb and generating at least four different proteins (407, 333, 462, and 216 amino acids). Interestingly, the last isoform was completely included in the 67-kb associated interval. Computer-assisted analysis of this isoform revealed at least one membrane-spanning domain and several N- and O-glycosylation consensus sites at N-termini, suggesting that it could be an integral membrane protein. Mutational analysis shows that a coding nucleotide variant (Ala62Thr), causing a missense in exon 12, is in strong association with UAN (P=.0051). Moreover, Ala62Thr modifies predicted protein secondary structure, suggesting that it may have a role in UAN etiology. The present study underscores the value of our small, genealogically well-characterized, isolated population as a model for the identification of susceptibility genes underlying complex diseases. Indeed, using a relatively small sample of affected and unaffected subjects, we identified a candidate gene for multifactorial UAN.

Amino Acid Sequence↗

PubMed1997

Effectiveness of SWL for lower-pole caliceal nephrolithiasis: evaluation of 452 cases.

The authors report on the treatment of lower-pole caliceal nephrolithiasis with extracorporeal shockwave lithotripsy (SWL) using the Czech-made Medilit M-5 lithotripter. In 310 patients, they have performed 452 treatments and evaluated the results 3 months after the last session using plain radiographs and ultrasound examination. The effectiveness of treatment and the success rate of SWL decreased with increasing size of stones: with stones >20 mm, it declined to 30%. This poor success rate was attributable not only to the size of the concrement, but also to its location in a lower calix, which is unfavorable for the passage of fragments. For big lower-pole caliceal stones (>20 mm in the longest diameter), the authors recommend percutaneous nephrolithotomy as the primary management method, the effectiveness of which does not depend on the size of the stone. The success rate achieved in treating the lower-pole caliceal lithiasis using the Medilit M-5 machine was 61.3%, similar to that achieved with other lithotripters.

Adult↗

PubMed1999

Epidemiologic evidence for the role of oxalate in idiopathic nephrolithiasis.

The importance of dietary and urinary oxalate in the formation of calcium oxalate kidney stones is widely accepted. Although the epidemiologic evidence for the role of oxalate remains largely indirect, recent prospective observations suggest its importance. The inverse association between dietary calcium intake and the risk of stone formation may be attributable to decreased gastrointestinal absorption of dietary oxalate and, thus, lower urinary oxalate concentrations. Further, the decreased risk of stone formation in women who consume large doses of vitamin B6 may be secondary to decreased oxalate production. The increased risk of nephrolithiasis observed with increasing body size may also be secondary to increased endogenous oxalate production. However, the frequency of hyperoxaluria is not substantially different in cases and controls for either sex. Notably, men have both higher stone incidence rates and higher mean urinary oxalate concentrations than women. Additional studies are needed to determine more precisely the role of dietary oxalate. More valid and comprehensive information on the oxalate content of food are desperately needed. Because the data on dietary oxalate are inconclusive, the routine restriction of dietary oxalate needs to be reexamined.

Calcium Oxalate↗

PubMedDate not supplied

Nephrolithiasis: "scope," shock or scalpel?

PURPOSE: To evaluate treatment preferences for complex urinary calculi. MATERIALS AND METHODS: A questionnaire was sent to 174 members of the Minnesota Urological Society. Three case scenarios were presented: a 1.5-cm lower-pole calculus with unfavorable anatomy, a 1.4-cm proximalureteral calculus, and a staghorn calculus. The treatment options offered were extracorporeal shockwave lithotripsy (SWL), ureteral stenting, ureteroscopy (URS), percutaneous nephrolithotomy (PCNL), and open surgery. RESULTS: Our survey response rate was 49%. A PCNL for staghorn calculi was more likely to be offered by urologists in metropolitan (100%; P<0.001) and urban (100%; P=0.003) settings than rural settings (57%). Whereas only 22% of urban and metropolitan urologists would offer anatrophic nephrolithotomy, 43% of rural urologists would include this among their treatment options. A PCNL was more likely to be offered by urologists trained after 1980 (100%) than by urologists trained before 1980 (81%; P=0.004). For a large lower-pole calculus with unfavorable anatomy, urologists with >50% managed-care practices were more likely (91%) than urologists with <50% managed-care practices (65%) to select PCNL for such stones (P=0.034). Whereas 82% of metropolitan urologists would select PCNL, 43% of rural urologists would consider SWL as initial therapy. A URS was more likely to be offered by urologists trained after 1980 (16%) than by urologists trained before 1980 (0; P=0.044). For a large proximal-ureteral calculus, metropolitan urologists were most likely (64%) to use stents initially (urban 28%; P=0.014; rural 14%; P=0.017). Rural urologists were more likely to offer SWL (100%) than were metro urologists (55%; P=0.024). CONCLUSIONS: Initial therapy for nephrolithiasis differs significantly according to geographic location, year of residency completion, and the percentage of managed-care patients in a urologist's practice. Future emphasis should be placed on increasing the availability of endoscopic techniques in rural settings.

Decision Making↗

PubMed2006

Association of urokinase gene 3'-UTR polymorphism with calcium oxalate nephrolithiasis.

PURPOSE: Urokinase might play a role in the formation of kidney stones. The aim of this study was to investigate the role of the urokinase gene in calcium oxalate nephrolithiasis. SUBJECTS AND METHODS: A control group of 150 healthy individuals having no history of stone formation (mean age 40 +/- 11.5 years) and a group of 130 patients (mean age 40.5 +/- 10.5 years) with recurrent calcium oxalate stones were examined. The C/T polymorphism of the urokinase gene was detected using polymerase chain reaction (PCR)-based restriction analysis. RESULTS: A marginally significant difference (P = 0.035) was found in the distribution of the urokinase gene 3' untranslated region (UTR) C/T polymorphism between patients with stones and controls. The odds ratio for the risk of the T allele in stone patients was 1.006 (95% CI 0.63-1.62). CONCLUSION: The T allele of 3' UTR of the urokinase gene may not be associated with a higher risk of stone formation.

Adult↗

PubMed1999

Acute effects of moderate dietary protein restriction in patients with idiopathic hypercalciuria and calcium nephrolithiasis.

BACKGROUND: High dietary protein intake is a potential risk factor for nephrolithiasis because of its capacity to increase urinary calcium and to facilitate lithogenesis through many other mechanisms. OBJECTIVE: Our aim was to verify the effects of moderate protein restriction in hypercalciuric patients. DESIGN: We studied 18 patients (10 men and 8 women aged 45.6+/-12.3 y) with idiopathic hypercalciuria and renal calculi. Before and after 15 d of a diet with 0.8 g protein x kg(-1) x d(-1) and 955 mg Ca, all patients were evaluated for the main serum and urinary measures of calcium metabolism as well as for urinary uric acid, oxalate, citrate, and prostaglandin E2. RESULTS: Urinary excretion of urea fell after the diet (P < 0.001). Urinary calcium (P < 0.001), uric acid (P < 0.005), oxalate (P < 0.01), and hydroxyproline (P < 0.01) decreased after protein restriction, whereas urinary citrate increased (P < 0.025). Blood pH increased after the hypoproteic diet (P < 0.05). 1,25-Dihydroxycholecalciferol (calcitriol) concentration fell significantly (P < 0.025) and parathyroid hormone increased (P < 0.001). Creatinine clearance tended to decrease (106.4+/-4.8 compared with 97.5+/-5.7 mL/min) after the diet. The decrease in urinary uric acid after the diet correlated with calcitriol concentration (r = 0.57, P < 0.05) and the decrease in urinary urea correlated positively with that in hydroxyproline excretion (r = 0.58, P < 0.01). CONCLUSIONS: In hypercalciuric patients, moderate protein restriction decreases calcium excretion, mainly through a reduction in bone resorption and renal calcium loss; both are likely due to a decreased exogenous acid load. Moreover, dietary protein restriction ameliorates the entire lithogenic profile in these patients.

Calcium↗

PubMed1997

Characterisation of renal chloride channel, CLCN5, mutations in hypercalciuric nephrolithiasis (kidney stones) disorders.

Mutations of the renal-specific chloride channel (CLCN5) gene, which is located on chromosome Xp11.22, are associated with hypercalciuric nephrolithiasis (kidney stones) in the Northern European and Japanese populations. CLCN5 encodes a 746 amino acid channel (CLC-5) that has approximately 12 transmembrane domains, and heterologous expression of wild-type CLC-5 in Xenopus oocytes has yielded outwardly rectifying chloride currents that were markedly reduced or abolished by these mutations. In order to assess further the structural and functional relationships of this recently cloned chloride channel, additional CLCN5 mutations have been identified in five unrelated families with this disorder. Three of these mutations were missense (G57V, G512R and E527D), one was a nonsense (R648Stop) and one was an insertion (30:H insertion). In addition, two of the mutations (30:H insertion and E527D) were demonstrated to be de novo, and the G57V and E527D mutations were identified in families of Afro-American and Indian origin, respectively. The G57V and 30:H insertion mutations represent the first CLCN5 mutations to be identified in the N-terminus region, and the R648Stop mutation, which has been observed previously in an unrelated family, suggests that this codon may be particularly prone to mutations. Heterologous expression of the mutations resulted in a marked reduction or abolition of the chloride currents, thereby establishing their functional importance. These results help to elucidate further the structure-function relationships of this renal chloride channel.

Adult↗