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PubMed1995

Determination of heparan sulphate in kidney tissues of patients with calcium nephrolithiasis.

While the pathogenic mechanisms responsible for calcium nephrolithiasis remain unknown, the influence of heparan sulphate proteoglycan (HSPG) on disease progression of other diseases, such as polycystic kidneys and diabetic glomerulosclerosis, makes it an important candidate for the study of stone formation. Using the indirect immunofluorescence assay and image analysis, we were able to quantify and visualize the loss of HSPG localized in the basement membrane of the glomerulus and the mucosa of ureter or renal pelvis in patients with recurrent calcium nephrolithiasis as compared to normal subjects. However, no significant change in HSPG was observed in the basement membrane of the tubular epithelium. The decreased HSPG in the glomerulus may reflect the potentially disrupted anion/neutral barrier for glomerular filtration, which would encourage the accumulation of stone solutes. The drop in HSPG staining intensity in the basement membrane of the mucosa of ureter/renal pelvis may suggest the tendency of adhesion of crystal to urothelial surfaces. Based on these immunological data, it appears that HSPG plays a modulatory role in the pathogenesis of this disease.

Adult↗

PubMed1991

Effects of the oral administration of glycosaminoglycans on cellular abnormalities associated with idiopathic calcium oxalate nephrolithiasis.

Oral administration of mixture of extractive glycosaminoglycans to a group of renal stone formers led to a significant decrease in oxalate self-exchange and in erythrocytes membrane protein phosphorylation traits that are abnormal in the majority of patients with idiopathic calcium nephrolithiasis. The action of glycosaminoglycans at the cellular level is probably due to their modulating activity on certain membrane protein kinases. The proven effect of the glycosaminoglycans opens a new pharmacological approach to the prevention of recurrent nephrolithiasis.

Administration, Oral↗

PubMed1995

Aetiology of nephrolithiasis in north Indian children.

The aetiology of nephrolithiasis was investigated in 32 north Indian children (25 boys, 7 girls, mean age 7.9 +/- 3.3 years). An underlying disorder was detected in 16 (50%) patients and included idiopathic hypercalciuria (8 patients), hyperoxaluria (3 patients) and renal tubular acidosis, primary hyperparathyroidism and hyperuricosuria (1 patient each). Magnesium ammonium phosphate calculi were found in 2 patients with recurrent urinary tract infections, 1 of whom had a duplex pelvic collecting system. In 16 patients (50%) a cause for renal calculi was not identified. Our findings suggest that an underlying disorder is present in a large proportion of children with nephrolithiasis where appropriate treatment may be beneficial.

Calcium↗

PubMed1995

Nephrocalcinosis and nephrolithiasis due to subcutaneous fat necrosis with hypercalcemia in two full-term asphyxiated neonates: sonographic findings.

Subcutaneous fat necrosis leading to hypercalcemia is rare but well documented in asphyxiated neonates. This paper presents two such neonates in whom sonography revealed the development of nephrocalcinosis and nephrolithiasis. The kidneys had initially been shown to be normal sonographically. In one infant, nephrocalcinosis developed as increasing echogenicity of the medullary pyramids. In the other, increased echogenicity of the renal cortex of uncertain cause developed together with nephrolithiasis. These sonographic appearances have not been described previously in this entity.

Asphyxia Neonatorum↗

PubMed2003

Occupational risk for nephrolithiasis and bladder dysfunction in a chauffeur.

The occupational risks for nephrolithiasis have not been widely studied. The published literature focuses on exposure to heat stress and toxic substances, not on the equally important behavioral risk factor of limited water consumption over many years. Urologic morbidity has been associated with suppressing the need to drink or void under restrictive work environments; however, no such studies link work related behavioral change with the development of kidney stones. This case report is the first to associate a restrictive work environment with limited fluid consumption, resulting in the development of nephrolithiasis.

Automobile Driving↗

PubMed2005

Nephrolithiasis and nephrocalcinosis in rats with small bowel resection.

Intestinal resection (IR) may lead to hyperoxaluria and nephrolithiasis. A rat model of IR was developed, in which kidney stones form. We describe the urine chemistries and histopathologic features. Rats underwent resection of 40-45 cm of distal ileum (n=16) or sham resection (SR) (n=8), and were then fed a 1% Na oxalate, 0.02% Ca diet. After 1 week on the diet, 24 h urine samples were obtained for stone chemistries. At 4-7 months after surgery, kidneys were examined grossly and by light microscopy. The extent and location of crystallization was assessed by polarized light. Histochemistry and infrared spectroscopy were used to determine crystal composition. IR rats had higher urine oxalate excretion (P<0.01) and concentration (P<0.001) than SR rats, and lower urine citrate excretion; only IR rats formed kidney stones (12/15 surviving rats). Tissue calcification was found only in kidneys from IR rats, located in the cortex (83% of kidneys), medulla (73%) and papillary tip (47%). Crystals, composed of CaOx, apatite, and calcium carbonate, filled collecting duct lumens, and were associated with tubular obstruction, and interstitial inflammation. Crystals in the papillary interstitium incited inflammation with tubular destruction and development of progressive papillary erosion. This new rat model of nephrolithiasis and nephrocalcinosis resembles the pattern of urinary abnormalities and tissue calcification that may be seen in humans with small bowel resection. The model allows further studies of the mechanisms of renal crystal formation, and possible therapeutic interventions.

Animals↗

PubMed1998

Quantitative analysis on the localization of chondroitin sulfate proteoglycan in renal tissues of patients with calcium nephrolithiasis.

Previous studies have shown a significant decrease of heparin sulfate proteoglycan (HSPG) in the basement membrane of the glomerulus and the mucosa of the ureter/renal pelvis in patients with calcium nephrolithiasis. In this study, we looked at the localization of another influential proteoglycan, chondroitin sulfate (CSPG), using similar study groups by indirect immunofluorescence staining. Microscopic images were digitized and image analysis was used to quantitate the staining intensity of CSPG present in the basement membrane of the nephron. Our data showed significant loss of CSPG in the Bowman's capsule and the basement membrane of the mucosa of the ureter/renal pelvis using Mann-Whitney U-Wilcoxon Rank Sum W test with P-values of 0.0043 and 0.0041, respectively. However, absence of staining was noted in the basement membrane of the glomerulus and no significant change in the basement membrane of the tubular epithelium was observed. In conclusion, our results showed changes in the localization of CSPG in the basement membrane of the nephron, accompanied with HSPG, which may contribute to the pathological condition of calcium nephrolithiasis.

Adult↗

PubMed2003

Ceftriaxone-associated nephrolithiasis and biliary pseudolithiasis in a child.

Ceftriaxone is a widely used third-generation cephalosporin. It is generally very safe, but complications of biliary pseudolithiasis and, rarely, nephrolithiasis have been reported in children. These complications generally resolve spontaneously with cessation of the ceftriaxone therapy; however, they may symptomatically mimic more serious clinical problems, such as cholecystitis. We report a case of both ceftriaxone-induced biliary pseudolithiasis and nephrolithiasis.

Adolescent↗

PubMed2005

Nephrolithiasis in a worker with cadmium exposure in the past.

OBJECTIVES: A clinical case regarding a cadmium-exposed worker is described. CLINICAL CASE: The subject during the work as welder (male, 42-years-old at the time of the first investigation) developed a Fanconi-like syndrome due to high exposure to cadmium fumes. Ten years after exposure removal, the subject showed clinical and laboratory evidence of nephrolithiasis (calcium phosphate stones). CONCLUSIONS: The clinical case confirms the possibility of nephrolithiasis in cadmium-exposed workers and suggests that susceptible subjects may develop kidney stones after lesion of the tubular cells.

Adult↗

PubMed1999

Ceftriaxone-associated nephrolithiasis and biliary pseudolithiasis.

Biliary pseudolithiasis has been reported in patients who received ceftriaxone therapy. In addition to biliary sludge formation occasional reports of ceftriaxone-induced nephrolithiasis have been published. In general, these adverse effects will develop after seven to ten days of treatment. We report on a seven-year-old boy with ceftriaxone-associated biliary pseudolithiasis and nephrolithiasis four days after initiation of treatment. Patients receiving a high dose of ceftriaxone and developing colicky abdominal pain should be considered for ultrasound and a change in antibiotic therapy if appropriate.

Bile Duct Diseases↗

PubMed2005

Association of vitamin-D and calcitonin receptor gene polymorphism in paediatric nephrolithiasis.

We investigated the role of vitamin-D receptor gene (VDR) and calcitonin receptor (CTR) gene polymorphism in childhood nephrolithiasis in the north Indian population. A control group of 60 healthy paediatric individuals (age range 4-16 years) and 50 paediatric patients (age range 2-14 years) with kidney stones were examined. Polymorphism in both genes (VDR and CTR) was detected by using PCR-based restriction analysis. There was a statistically significant difference between the two groups for the genotypes of the VDR gene Fok-I polymorphism (P =0.007) and the CTR gene (P =0.048) polymorphism. The odds ratio (95% Confidence Interval) for the C allele in those at risk of stone disease was 1.83 (0.82-4.09) in VDR gene polymorphism and 1.99 (0.90-4.39) in the case of CTR gene polymorphism. Our results suggest that the effects of VDR (Fok-I) and CTR gene polymorphism contribute to the understanding of the pathogenesis of urinary calculi. It is also suggestive of a potential candidate gene in the search for genetic causes of paediatric calcium oxalate nephrolithiasis.

Adolescent↗

PubMed1979

Recurrence of nephrolithiasis. A six-year prospective study.

Retrospective studies of nephrolithiasis tend to overestimate the severity of the disease and mistakenly ascribe benefits to treatment regimens. The results of a three-year study of recurrent nephrolithiasis in three patient groups adhering to a calcium-restricted diet who were treated with phosphate therapy, placebo or diet alone are re-examined at the close of an additional three-year follow-up period. Nearly half the subjects in all groups remained free of stone for the six-year period. A reduction in the need for lithotomies occurred in all groups. The absence of renal calcification at entry into the study as well as increasing age were associated with a marked reduction in stone passage. Drug therapy should probably be avoided in older patients as well as in those who are free of renal calcifications.

Adolescent↗

PubMed1980

Recurrence of autonomous hyperparathyroidism in calcium nephrolithiasis.

In a woman with bilateral recurrent calcium nephrolithiasis and hypercalciuria, hypercalcemia developed and she underwent parathyroid surgery, which led to excision of a histologically-confirmed adenoma. The patient became normocalcemic but remained hypercalciuric despite reduction of dietary calcium intake. Several calculi recurred in both kidneys. Four to six years after parathyroidectomy, hypercalcemia recurred and the patient underwent a new surgical exploration; a parathyroid gland with diffuse adenomatous aspects and another gland with pure hyperplasia were excised. Once again, after surgery the patient became normocalcemic but remained hypercalciuric. Evidence for a "renal calcium leak" hypercalciuria was obtained, and thiazide administration led to normalization of urinary calcium excretion. In calcium nephrolithiasis, persistent hypercalciuria may lead to recurrence of autonomous hyperparathyroidism.

Adenoma↗

PubMed1981

Prevention of calcium nephrolithiasis with low-dose thiazide, amiloride and allopurinol.

We report 5 years' experience with low-dose hydrochlorothiazide, 50 mg/day and amiloride, 5 mg/day, in 519 patients with recurrent calcium nephrolithiasis. Additional treatment with allopurinol, 100 mg/day was prescribed for approximately 50 percent of the patients. All patients had active stone formation, having 3,464 stones in 3,126 patient-years (6.67 stones per patient, 1.10 stones per year). Hypercalciuria was present in 65 percent of the patients and hyperuricosuria in 24 percent. The administration of low-dose hydrochlorothiazide was effective in reducing urinary calcium excretion in most patients. It is possible that the hypocalciuric effect of hydrochlorothiazide were enhanced by amiloride, an agent which has been shown to cause hypocalciuria when given alone. Significant side effects requiring discontinuation of the drug were observed in only 5 percent of the patients. During 872.8 patient-years of treatment, only 53 new stones were formed (0.10 stones per patient, 0.06 stones per year) in contrast with the 916 predicted ones. The difference (chi-square) is statistically significant (p less than 0.001). These results show that the administration of low-dose hydrochlorothiazide and amiloride, either alone or in association with allopurinol, is clinically effective in reducing the rate of recurrence of calcium nephrolithiasis.

Adult↗

PubMed1985

Correction of hypocitraturia and prevention of stone formation by combined thiazide and potassium citrate therapy in thiazide-unresponsive hypercalciuric nephrolithiasis.

Thirteen patients with hypercalciuric calcium nephrolithiasis continued to form calcium stones when treated with thiazide (4.69 +/- 6.62 [mean +/- SD] stones per patient-year to 5.12 +/- 10.87 stones per patient-year), despite adequate hypocalciuric response (a reduction in urinary calcium levels from 303 +/- 119 mg per day to 193 +/- 88 mg per day, p less than 0.01). Because they had hypocitraturia (250 +/- 86 mg per day versus 643 +/- 236 mg per day in normal subjects, p less than 0.001), potassium citrate (10 to 20 meq three times per day) was added to the ongoing treatment program. During combined treatment with thiazide and potassium citrate, urinary pH significantly rose, and normal levels of urinary citrate were restored. Ten patients stopped forming new stones and all 13 had reduced stone formation rate. Thus, potassium citrate supplementation should be considered in patients requiring thiazide therapy for the control of hypercalciuric nephrolithiasis, especially if they have concurrent hypocitraturia or if it develops during thiazide therapy.

Adult↗

PubMed1983

Low urinary citrate excretion in nephrolithiasis.

The urinary citrate excretion was examined in patients with nephrolithiasis who were categorized on the basis of different physiologic or metabolic abnormalities. A wide prevalence of low citrate excretion (hypocitraturia) was observed, with over one half of our patients with stones exhibiting it. Hypocitraturia was found in all patient categories except primary hyperparathyroidism and hyperuricosuric calcium oxalate nephrolithiasis. As expected, hypocitraturia was present in renal tubular acidosis and in enteric hyperoxaluria. However, urinary citrate was also low in absorptive and renal hypercalciurias, and in patients in whom an acid-base disturbance was clearly excluded.

Acidosis, Renal Tubular↗

PubMed1991

Correction of erythrocyte abnormalities in idiopathic calcium-oxalate nephrolithiasis and reduction of urinary oxalate by oral glycosaminoglycans.

Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation. There is evidence that glycosaminoglycans (GAGs) have a regulatory effect on both of these processes. This study tested the hypothesis that modifications of erythrocyte oxalate self-exchange induced by oral GAGs are paralleled by similar changes in overall oxalate metabolism. 40 patients with idiopathic calcium-oxalate nephrolithiasis were treated for 15 days with 60 mg/day of a mixture of GAGs. By day 15 of treatment there were significant reductions from baseline in erythrocyte oxalate self-exchange (mean [SD] 1.67 [1.18] vs 2.59 [1.63] x 10(2) per min; p less than 0.005) and erythrocyte membrane protein phosphorylation (55.8 [7.3] vs 72.9 [6.8] x 10(-3) cpm/mg protein; p less than 0.005), but also in urinary oxalate excretion (0.24 [0.09] vs 0.31 [0.15] mmol/24 h; p less than 0.005). This finding suggests similar changes in both erythrocytes and other cells more important in oxalate handling. The changes had reversed by 15 days after withdrawal of treatment. Acute intravenous administration of GAGs (60 mg) induced a fall in carbon-14-labelled oxalate renal clearance (143 [13] vs 169 [28] ml/min; p less than 0.005), which strongly suggests the participation of the kidney. However, reduced oxalate absorption from the intestine, and even decreased synthesis of oxalate, cannot be ruled out.

Administration, Oral↗

PubMed2004

Furosemide nephrolithiasis causing ureteral obstruction and urinoma in a preterm neonate.

Nephrolithiasis and nephrocalcinosis in low-birth-weight, preterm neonates are well-documented complications of furosemide administration. Perinephric urinomas and urinary ascites have been previously reported as complications of obstruction due to posterior urethral valves or ureteropelvic junction obstruction. We present an unusual case of furosemide-induced nephrolithiasis causing ureteral obstruction, urinoma, and acute renal failure in a preterm neonate.

Acute Kidney Injury↗