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PubMed1978

Hyperglycinuria with nephrolithiasis.

The case of a seven and a half-year-old girl with hyperglycinuria, oxalate nephrolithiasis, and a normal plasma amino acid pattern is presented. Hyperglycinuria amounted to 400 mg of glycine in 24 h urine and the stone was composed of calcium oxalate dihydrate. The metabolic relationship between glycine and oxalate is discussed. It is possible that the association of nephrolithiasis and hyperglycinuria was coincidental, although the case of familial hyperglycinuria with nephrolithiasis reported by De Vries and collaborators and our case suggest the possibility of a relationship between the aforesaid compounds in vivo.

Child↗

PubMed2003

Nephrolithiasis in a child with glucose-galactose malabsorption.

Glucose-galactose malabsorption (GGM) is a rare autosomal recessive disorder of intestinal transport of glucose and galactose, leading to watery diarrhea, dehydration, failure to thrive, or early death. We report a female newborn with GGM, whose clinical diagnosis was confirmed by mutational analysis of the SGTL1 gene. Bilateral nephrolithiasis was discovered after an episode of hematuria. Metabolic causes of nephrolithiasis were not found. The most likely explanation for the development of nephrolithiasis is chronic diarrhea leading to dehydration and highly concentrated urine. High fluid intake and rigorous prevention of dehydration is therefore advised for these patients. Furthermore, life-long monitoring of their renal status, including regular ultrasound examinations, is warranted.

Amino Acid Transport Systems, Basic↗

PubMed1998

Clinical features of X-linked nephrolithiasis in childhood.

X-linked recessive nephrolithiasis (XRN) is a rare hereditary form of progressive renal failure characterized by (1) proximal tubular dysfunction and low molecular weight proteinuria; (2) hypercalciuria with nephrocalcinosis and nephrolithiasis. Because the clinical features are non-specific and variable, affected families in different parts of the world were initially thought to have several distinct syndromes. However, positional cloning of the relevant gene (CLCN5) demonstrated that these families have, in common, mutations affecting a chloride channel expressed throughout the renal tubule. To expand the description of early clinical and pathological manifestations of XRN, we describe three patients diagnosed in the 1st decade of life. Renal tubular dysfunction may be evident even in the neonatal period, hypophosphatemic rickets may develop in the first years of life, and nephrocalcinosis (but not nephrolithiasis) with glomerulosclerosis are consistent features in childhood. One of our patients is indistinguishable from the others on clinical grounds, yet no mutations of the coding regions of the CLCN5 gene were found, raising the possibility of genetic heterogeneity in the XRN syndrome.

Adolescent↗

PubMed2004

Impact of CT scan in patients with first episode of suspected nephrolithiasis.

This prospective observational outcome study assessed the impact of helical computed tomography (CT) scan in patients with a first episode of suspected nephrolithiasis. Before CT scanning, Emergency Physicians completed a questionnaire, including diagnostic certainty of nephrolithiasis and anticipated patient disposition. Primary outcome measure was the comparison of physician diagnostic certainty and CT scan results. Secondary outcome measures included alternate diagnoses and changes in patient disposition after CT scan. Four categories grouped the pre-CT diagnostic certainty: 0-49%, 50-74%, 75-90%, and 90-100%. The CT scan found urinary calculi in 28.6%, 45.7%, 74.2%, and 80.5% of patients in each category, respectively. CT scanning revealed alternate diagnoses in 40 cases (33.1%). Of these, 19 (47.5%) included other significant pathology. Before CT scanning, physicians planned to discharge 115 patients and admit six patients. After CT scanning, six of the former group were admitted, and five of the latter group were discharged. Patients presenting with a first episode of clinically suspected nephrolithiasis should undergo CT scanning because it enhances diagnostic certainty by identifying alternate diagnoses not suspected on clinical grounds alone.

Adult↗

PubMed1999

The incidence of nephrolithiasis in patients with spinal neural tube defects.

PURPOSE: Bladder stones are common in patients with spinal neural tube defects but there are little data on the incidence of renal calculi in this population. We examined the incidence, nature and risk factors of nephrolithiasis in our clinic population of patients with neural tube defects. MATERIALS AND METHODS: We retrospectively reviewed the charts and radiological studies of 327 patients followed at our neural tube defects clinic with routine radiological imaging of the urinary tract. Additional confirmatory studies were performed when stones were noted. RESULTS: Renal calculi were identified in 20 patients with neural tube defects (6.1%). The incidence of nephrolithiasis increased with age. Renal stones were noted in 19 patients (10.7%) 12 years old or older. Management of the stones in these patients resulted in overall 53% stone-free and 87% recurrence rates after intervention. Major risk factors for new and/or recurrent renal stone formation were bacteriuria in 95% of the cases, lower urinary tract reconstruction in 80%, pelvicalicectasis in 70%, vesicoureteral reflux in 65%, a thoracic level spinal defect in 60% and renal scarring in 55%. CONCLUSIONS: These data suggest that there is a higher incidence of nephrolithiasis in patients with neural tube defects than in the general population and the risk of stone recurrence is also elevated. Most patients with stones had undergone lower urinary tract reconstruction. Other risk factors were bacteriuria, pelvicalicectasis, vesicoureteral reflux and a thoracic level neural tube defect.

Adolescent↗

PubMed2002

Expression of osteopontin in rat kidneys: induction during ethylene glycol induced calcium oxalate nephrolithiasis.

PURPOSE: Osteopontin is a well-known component of stone matrix and a strong inhibitor of the nucleation, growth and aggregation of calcium oxalate crystals in vitro. To understand its involvement in vivo in calcium oxalate nephrolithiasis we investigated the renal expression and urinary excretion of osteopontin in normal rats, and rats with hyperoxaluria and calcium oxalate crystal deposits in the kidneys. MATERIALS AND METHODS: Calcium oxalate nephrolithiasis was induced by administering ethylene glycol. Immunohistochemistry and in situ hybridization were done to localize osteopontin and osteopontin messenger RNA in the kidneys, while sensitive reverse transcriptase quantitative competitive template polymerase chain reaction was performed to detect and quantify osteopontin messenger RNA expression. Urinary excretion was determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis, and then quantified by densitometry of the Western blots. RESULTS: Osteopontin expression in the kidneys was significantly increased after hyperoxaluria and it increased further after the deposition of calcium oxalate crystals in the kidneys. Urinary excretion of osteopontin increased concomitantly. The results reveal differences in renal responses after exposure to oxalate and calcium oxalate crystals. In normal kidneys osteopontin expression was limited to a small number of cells of the thin limbs of the loop of Henle and papillary surface epithelium. During hyperoxaluria osteopontin expression in the kidneys was increased but still mostly limited to cells of the thin limb and papillary surface epithelium. However, after calcium oxalate crystal deposition osteopontin expression was observed throughout the kidneys, including segments of the proximal tubules. CONCLUSIONS: In response to exposure to oxalate and calcium oxalate crystals renal epithelial cells increase the production of osteopontin, which may have a significant role in calcium oxalate nephrolithiasis.

Animals↗

PubMed1994

Regional variation in nephrolithiasis incidence and prevalence among United States men.

The southeastern region of the United States has long been considered to have higher rates of nephrolithiasis than other regions. Previous reports examined hospital discharge rates for nephrolithiasis rather than stone incidence rates and did not evaluate potential confounding variables. We studied prospectively the regional rates of incident stone formation within the United States in a cohort of 45,289 men 40 to 75 years old in 1986 who had no history of kidney stones. Dietary intake was measured by a semiquantitative food frequency questionnaire. During 6 years of followup 753 incident cases of kidney stones were documented. We also examined regional prevalence among 4,082 men who had a history of nephrolithiasis at the start of the study. There were no significant differences in age-adjusted incidence rates between the Southeast and other regions. Controlling for other risk factors, including age and relevant nutrients, did not alter the results. The prevalence of stone disease was significantly greater in the Southeast. Using the Southeast as the comparison region, a decreased risk of having a history of kidney stones was found, ranging from 13% (95% confidence interval 4 to 21%) lower in the Mid-Atlantic region to 31% (95% confidence interval 21 to 40%) lower in the Northwest. The prevalence in all other regions combined compared to the Southeast was also lower (odds ratio 0.82, 95% confidence interval 0.76 to 0.89). Therefore, individuals in the Southeast appear to have an overall greater risk of kidney stones. However, the magnitude of this effect is modest compared with previous estimates.

Adult↗

PubMed1991

A new model of nephrolithiasis involving tubular dysfunction/injury.

To better understand the pathogenesis of nephrolithiasis, we developed a new animal model that closely mimics human calcium oxalate stone disease. Rats were treated with a regimen that combines moderate hyperoxaluria (produced by 10 days of feeding with 3% ammonium oxalate) with mild proximal tubular injury/dysfunction (produced by 8 daily injections of gentamicin sulfate -40 mg./kg.). This combined treatment caused a marked increase in the incidence of calcium oxalate crystals and stones over that seen in animals treated with oxalate or gentamicin alone. Using a semiquantitative scoring system for estimating the abundance of crystals in coronal sections of kidneys, we found that 63% of animals receiving gentamicin plus oxalate showed "moderate" numbers of crystal, as compared to 8% of animals receiving oxalate alone; and the majority of the crystals occurred in the papilla, a pattern similar to that seen in human stone disease. Untreated rats and rats treated with gentamicin alone did not exhibit calcium oxalate crystals or stones. Despite the abundance of crystals and stones, animals receiving gentamicin plus oxalate retained relatively normal renal function as judged by creatinine clearance. Thus, the model has several advantages over preexisting models of nephrolithiasis. Crystal and stone deposition develop rapidly (within 14 days). The pattern of deposition resembles that seen in human stone disease and renal function remains relatively normal. These findings indicate that this model of nephrolithiasis may prove useful for studies of the pathogenesis of stone disease. Moreover, they suggest that renal tubular injury and/or dysfunction may produce conditions conducive to the formation and growth of calcium oxalate stones.

Animals↗

PubMed1989

The spectrum of metabolic abnormalities in patients with cystine nephrolithiasis.

To elucidate the pathophysiology of mixed stone formation in cystinuria, 27 patients with documented cystine nephrolithiasis underwent an inpatient evaluation under a constant dietary regimen. All patients had homozygous cystinuria, since the daily urinary cystine excretion exceeded 250 mg. per gm. creatinine. Hypercalciuria was noted in 5 patients (18.5 per cent), 4 of whom had fasting hypercalciuria. Hyperuricosuria was found in 6 patients (22.2 per cent) and it was not caused by a consumption of a diet rich in animal proteins, since urinary pH was higher and urinary sulfate lower than in control subjects. Serum uric acid was slightly lower and uric acid clearance was higher in hyperuricosuric patients than in control subjects. Hypocitraturia was found in 12 patients (44.4 per cent) and it was associated with defective renal acidification in 4 of 5 patients in whom it was tested. Thus, hypercalciuria, hyperuricosuria and hypocitraturia frequently accompany cystinuria in patients with cystine nephrolithiasis. These conditions might be renal in origin, rather than a result of dietary or environmental aberrations. They may contribute to the formation of calcium and uric acid stones, which sometimes complicate cystine nephrolithiasis.

Adolescent↗

PubMed1987

Piridoxilate-induced calcium oxalate calculi: a new drug-induced metabolic nephrolithiasis.

During the last 4 years we collected 27 specimens of calcium oxalate nephrolithiasis in patients receiving long-term treatment with piridoxilate, a drug composed of an equimolar combination of glyoxylate and pyridoxine. The mean duration of treatment was 3.6 years (range 4 months to 10 years) and the mean daily dose was 580 mg. piridoxilate, which contained 160 mg. glyoxylate. Calculi often recurred, with an average number of 9.9 per patient, and an open operation, shock wave lithotripsy or percutaneous nephrolithotomy was required in 22 patients (81 per cent). Oxalate excretion was 727 +/- 246 mumol. per day while on the drug and 382 +/- 201 mumol. per day after the drug was withdrawn. Whewellite was the major component of calculi in all cases but the stones exhibited a peculiar morphological arrangement, with multiple small indentations and a fine mamillary structure. Freshly voided urine specimens contained unusual crystals, which on infrared spectroscopy were composed of calcium oxalate trihydrate, a variety of crystal never observed previously in human urine. Piridoxilate-induced calcium oxalate nephrolithiasis is a new variety of metabolic drug-induced nephrolithiasis. Our observations suggest that even large doses of pyridoxine may be unable to prevent the excessive production of oxalate from glyoxylate.

Adult↗

PubMed2000

Metabolic investigation of recurrent nephrolithiasis: compliance with recommendations.

OBJECTIVES: Nephrolithiasis is a recurrent condition with significant associated morbidity and economic impact. Although urologic intervention addresses symptomatic stone episodes, prevention of recurrences with proven medical therapy is indicated. METHODS: This retrospective study examined 97 patients who presented in 1997 and 1998 with recurrent nephrolithiasis in a large tertiary care center for the presence of an appropriate metabolic investigation as recommended by the National Institutes of Health Consensus Conference. Complete data were abstracted from the hospital and private clinic charts. RESULTS: The average patient age was 50.5 years; 61.9% of patients were men. The mean number of stones per patient was 5.6 (range 2 to 62), with stone analysis performed for 78 patients. Fifty-eight stones (74.4%) were calcium oxalate and/or phosphate, 14 (17.9%) urate, 8 (10.3%) struvite, and 3 (3.8%) cystine. Five patients had two stone types on different occasions. Either lithotripsy or a urologic procedure was required for at least one stone presentation in 89 patients (91.8%). An investigation for stone disease was pending in 54 patients (55.7%). A complete evaluation, satisfying the preset criteria, was performed in 34 patients (35.1%). Six patients who did not undergo evaluation were lost to follow-up. Univariate analysis revealed that referral to a nephrologist (P = 0.001), treatment with medications used for stone disease (P = 0.008), and urate stones (P = 0.005) were associated with a complete investigation. Similarly, these were independently associated with a complete evaluation in regression analysis of 77 complete data sets, with odds ratios of 24.4 (nephrology referral), 4.9 (medication use), and 5.6 (urate stones). CONCLUSIONS: The results of this study demonstrate that a significant proportion of patients with recurrent nephrolithiasis do not undergo appropriate metabolic investigations. Efforts should be made to improve the evaluation of these patients.

Female↗

PubMed2001

Dietary supplementation with cranberry concentrate tablets may increase the risk of nephrolithiasis.

OBJECTIVES: Cranberry juice has been recommended for patients with recurrent urinary tract infections. However, cranberry juice has a moderately high concentration of oxalate, a common component of kidney stones, and should be limited in patients with a history of nephrolithiasis. Cranberry concentrate tablets are currently available at nutrition stores and are sold as promoters of urinary tract health. After one of our patients with a distant history of calcium oxalate nephrolithiasis developed recurrent stones following self-administration of cranberry concentrate tablets, we sought to investigate the potential lithogenic properties of cranberry supplements. METHODS: Five healthy volunteers on a normal diet provided 24-hour urine collection for pH, volume, creatinine, oxalate, calcium, phosphate, uric acid, sodium, citrate, magnesium, and potassium. Cranberry tablets were administered to these volunteers at the manufacturer's recommended dosage for 7 days. On the seventh day, a second 24-hour urine collection was obtained. RESULTS: The urinary oxalate levels in the volunteers significantly increased (P = 0.01) by an average of 43.4% while receiving cranberry tablets. The excretion of potential lithogenic ions calcium, phosphate, and sodium also increased. However, inhibitors of stone formation, magnesium and potassium, rose as well. CONCLUSIONS: Cranberry concentrate tablets are marketed for urinary tract ailments. Physicians and manufacturers of cranberry products should make an effort to educate patients at risk for nephrolithiasis against ingestion of these dietary supplements.

Adult↗

PubMed2001

Nephrolithiasis during pregnancy secondary to primary hyperparathyroidism.

Nephrolithiasis secondary to primary hyperparathyroidism infrequently complicates pregnancy. It can cause severe maternal and fetal complications. We present a case of a pregnant woman with nephrolithiasis and primary hyperparathyroidism. We reviewed the management of nephrolithiasis due to primary hyperparathyroidism during pregnancy. We believe that early recognition and timely intervention can significantly reduce the incidence of complications.

Adult↗

PubMed2003

The association of nephrolithiasis with cystic fibrosis.

BACKGROUND: There is a growing body of evidence regarding the association between cystic fibrosis (CF) and nephrolithiasis and the role that Oxalobacter formigenes may have in that association. METHODS: We performed a MEDLINE search of "cystic fibrosis and nephrolithiasis" and "Oxalobacter formigenes." Epidemiological and experimental evidence and possible mechanisms explaining the association were critically reviewed. RESULTS: Of patients with CF, 3.0% to 6.3% are affected with nephrolithiasis, a percentage greater than that of age-matched controls without CF, in whom the rate is 1% to 2%. Studies have suggested possible mechanisms for the association, including hyperuricosuria, hyperoxaluria, primary defects in calcium handling caused by mutation of the CF transmembrane regulator (CFTR), hypocitraturia, and lack of colonization with O formigenes, an enteric oxalate-degrading bacterium. The absence of colonization could be related to frequent courses of antibiotics. CONCLUSION: Although the incidence of stones in patients with CF may be increased compared with controls without CF, many possible mechanisms are implicated. The relative contributions of these mechanisms remain uncertain. Future directions may include specific identification of lithogenic risks and therapy aimed at stone prevention in this population.

Adolescent↗

PubMed1988

The association of nephrolithiasis and autosomal dominant polycystic kidney disease.

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.

Adult↗

PubMed2003

Polymorphisms in the vitamin D receptor gene and the risk of calcium nephrolithiasis in children.

OBJECTIVE: Polymorphism in the Vitamin D Receptor (VDR) gene has recently been reported to be associated with calcium metabolism disorders. This study was conducted to investigate the association of VDR gene polymorphism with the risk of calcium nephrolithiasis. METHODS: We investigated the VDR ApaI, BsmI and TaqI polymorphisms, in relation to serum calcium, phosphate, intact parathyroid hormone and 1.25(OH)(2)D(3) in 64 hypercalciuric stone-forming children and 90 healthy children. DNA was isolated from peripheral blood, and genotyping was performed with PCR-based methods. RESULTS: The frequency of ApaI AA genotype was significantly higher in the children with calcium nephrolithiasis than the controls (chi(2)=9.5; p=0.008). The distribution of BsmI and TaqI genotypes in stone-forming patients was similar to those in the control group. There was a significant association between TaqI TT genotype and the strength of the family history. The patients with TT genotype were observed to have a 8 times more risk than patients with Tt/tt genotype for recurrent stone episodes (OR 8, 95%CI 1.61-39.6). CONCLUSION: VDR genotype determination may provide a tool to identify individuals who are at a risk for calcium nephrolithiasis.

Adolescent↗

PubMed2002

Pathophysiology of uric acid nephrolithiasis.

Humans although a predominantly ureotylic organism, has preserved the ability to excrete nitrogen as uric acid and ammonia. An imbalance between these two secondary modes of nitrogen excretion has resulted in uric acid precipitation in human urine. Uric acid nephrolithiasis can arise from diverse etiologies all with distinct underlying defects converging to one or more of three defects of hyperuricosuria, acidic urine pH, and low urinary volume, originating from secondary, genetic or heretofore undefined (idiopathic) causes. A subset of idiopathic uric acid nephrolithiasis (gouty diathesis) may be the "tip of the icebergp" of a broader systemic illness characterized by insulin resistance. A novel renal manifestation of insulin resistance is a mild defect in ammonium excretion, which is not severe enough to disturb acid-base homeostasis, but is sufficient to set up the chemical milieu for uric acid nephrolithiasis.

Humans↗

PubMed1995

Erythrocyte transmembrane flux and renal clearance of oxalate in idiopathic calcium nephrolithiasis.

An anomaly in erythrocyte oxalate transport has been reported in patients with idiopathic calcium oxalate nephrolithiasis. Even if clinical and experimental evidence suggests a causal role of this cellular anomaly in calcium nephrolithiasis, a definitive answer to this fundamental question is still lacking. We approached this problem by searching for a possible relationship between the erythrocyte oxalate self-exchange anomaly and the renal clearance of this anion in stone formers. In 10 idiopathic calcium-oxalate renal stone formers, and 10 healthy subjects we evaluated the erythrocyte oxalate flux rate, and the renal fractional clearance of oxalate by a recently described enzymathic procedures for plasma oxalate determination. With respect to controls, stone formers had higher oxalate flux rate in erythrocytes, and higher oxalate renal fractional clearance with a significant direct correlation between the two parameters. These data are compatible with a membrane transport abnormality within the kidney of these stone formers, and the existence of a common defect of the oxalate transport shared by both erythrocytes and tubular renal cells. The latter may be crucial in the pathogenesis of calcium oxalate nephrolithiasis, by modifying the renal handling of oxalate.

Adult↗