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PubMedDate not supplied

Association of vitamin D receptor-gene (FokI) polymorphism with calcium oxalate nephrolithiasis.

BACKGROUND AND PURPOSE: Formation of kidney stones is still not understood but is hypothesized to be associated with the vitamin D receptor gene (VDR). In order to assess the eventual role of VDR start-codon FokI polymorphism in stone formation, we evaluated the association between calcium stone disease and this polymorphism in a North Indian population. PATIENTS AND METHODS: A control group comprised of 166 healthy individuals (age range 22-58 years) and a group of 138 patients with calcium oxalate stones (age range 21-72 years) were examined. The polymorphism was detected using polymerase chain reaction-based restriction analysis. An unexcisable length of 265 bp (CC) and two fragments of 169 bp and 96 bp (TT) were obtained by FokI restriction digestion. RESULTS: There was a statistically significant difference between the control and patient groups (X2 test, P<0.001) for the genotype of the VDR FokI start-codon polymorphism. The odds ratio (with 95% CI) for the C allele in those at risk of stone disease was 1.654 (1.041, 2.628). The VDR frequency distribution was also statistically significant (P<0.001) in case of male sex. The frequency distribution for this genetic polymorphism was not statistically different in normocalciuric and hypercalciuric stone patients (P=0.355). CONCLUSION: The VDR FokI polymorphism may be a good candidate for a marker for calcium oxalate-stone disease. These findings may contribute a small piece to the understanding of the pathogenesis of urinary calculi.

Adult↗
PubMed1977

Hyperoxaluria and calcium oxalate nephrolithiasis after jejunoileal bypass.

Patients with ileal disease, ileal resection, and jejunoileal bypass are at increased risk of forming calcium oxalate renal calculi because of enhanced absorption of dietary oxalate. Intraluminal solubility of oxalate is an important determinant for hyperabsorption and may be regulated by intraluminal concentration of calcium and fatty acids. Malabsorbed bile salts and fatty acids may alter intestinal permeability, leading to increased passive diffusion of oxalate. Management includes a diet low in oxalate and fat content, dietary calcium of 750 mg/day, and cholestyramine.

Bile Acids and Salts↗
PubMed1994

Risk factors for low urinary citrate in calcium nephrolithiasis: low vegetable fibre intake and low urine volume to be added to the list.

Risk factors for low urinary citrate excretion were assessed in 34 consecutive male recurrent idiopathic calcium stone formers (RCSF) who collected two 24-h urines while on free-choice diet. Overt hypocitraturia (hypo-cit) was defined as UCit x V < 1.70 mmol/day, and 'low' citraturia (low-cit) as UCit x V between 1.70 and 2.11 mmol/day. Twenty-three RCSF had normocitraturia (normo-cit), six low-cit and five hypo-cit. UCit x V positively correlated with urine volume (VOLUME, r = 0.44, P = 0.009), vegetable fibre intake (fibers, r = 0.46, P = 0.009) and GI-alkali absorption (alkali, r = 0.47, P = 0.006), and volume, fibres and alkali tended to be lower among RCSF with low-/hypo-cit. A 3-day NH4Cl loading test (0.95 mEq/kg BW daily in 3 doses) was performed in RCSF as well as in 14 age-matched healthy male controls (C). On a plot of urine pH versus serum bicarbonate, 10 of 11 RCSF with low-/hypo-cit, but only six of 23 with normo-cit (P = 0.0004) fell off the normal range, indicating incomplete RTA. Two or more risk factors simultaneously occurred in only four of 23 RCSF with normo-cit, but in eight of 11 with low-/hypo-cit (P = 0.002). In conclusion, incomplete RTA is the most prevalent risk factor for low-/hypo-cit in RCSF, and decreases in vegetable fibres and urine volume emerge as two new risk factors for low urinary CIT.

Acidosis, Renal Tubular↗
PubMed1997

Southwestern Internal Medicine Conference: medical management of nephrolithiasis--a new, simplified approach for general practice.

Considerable progress has been made regarding pathophysiology, diagnosis, and medical prevention of recurrent renal stone formation. The medical approach is not applied widely because of the availability of extracorporeal shockwave lithotripsy and the complexity of medical diagnostic and treatment modalities. In this review, a simplified program for the medical management of stones is described. From analysis of stone risk factors in 24-hour urine specimens, uncomplicated calcium stone disease is separated from other stone diseases. The uncomplicated calcium stone disease, comprising the illness in the majority of patients with recurrent renal calculi, is characterized by normocalcemia, normouricemia, calcium stones, and the absence of urinary tract infection, bowel disease, or marked hyperoxaluria. Uncomplicated calcium stone disease is separated into a hypercalciuric group and a normocalciuric group. In the simplified treatment program, the hypercalciuric group would be offered thiazide plus potassium citrate, whereas the normocalciuric group would receive potassium citrate alone.

Benzothiadiazines↗
PubMed1985

Nephrolithiasis and intestinal disease.

Kidney stones in patients with inflammatory bowel disease are usually composed of calcium oxalate. Two factors are important in the increased absorption of dietary oxalate which is responsible for those stones: 1) increased absorption of oxalate in the presence of steatorrhea, and 2) increased permeability of the colon to oxalate. Fortunately, some of the physiologic abnormalities can be corrected. A therapeutic approach is detailed.

Calcium Oxalate↗
PubMed2001

Prevention of nephrolithiasis.

The high incidence of recurrence after an initial stone event underscores the need for an effective medical prophylactic program. Dietary modification and drug therapies have long been advocated to reduce the likelihood of stone recurrence. While the efficacy of a high fluid intake has been validated in a randomized trial, the benefit of other dietary measures is based on modulation of urinary stone risk factors and outcomes derived from observational studies. Several drug therapies have been evaluated in a limited number of prospective, randomized trials and efficacy has been demonstrated for thiazides, allopurinol and alkali citrate in some populations of recurrent stone formers. The role of selective versus nonselective therapy for stone prevention awaits further study.

Allopurinol↗
PubMed2001

Nanobacteria: controversial pathogens in nephrolithiasis and polycystic kidney disease.

Nanobacteria are unconventional agents 100-fold smaller than common bacteria that can replicate apatite-forming units. Nanobacteria are powerful mediators of biogenic apatite nucleation (crystal form of calcium phosphate) and crystal growth under conditions simulating blood and urine. Apatite is found in the central nidus of most kidney stones and in mineral plaques (Randall's plaques) in renal papilla. The direct injection of nanobacteria into rat kidneys resulted in stone formation in the nanobacteria-injected kidney during one month follow-up, but not in the control kidney injected with vehicle. After intravenous administration in rats and rabbits, nanobacteria are rapidly excreted from the blood into the urine, as a major elimination route, and damage renal collecting tubuli. Nanobacteria are cytotoxic to fibroblasts in vitro. Human kidney cyst fluids contain nanobacteria. Nanobacteria thus appear to be potential provocateurs and initiators of kidney stones, tubular damage, and kidney cyst formation. It is hypothesized that nanobacteria are the initial nidi on which kidney stone is built up, at a rate dependent on the supersaturation status of the urine. Those individuals having both nanobacteria and diminished defences against stone formation (i.e. genetic factors, diet and drinking habits) could be at high risk. Kidney cyst formation is hypothesized to involve nanobacteria-induced tubular damage and defective tissue regeneration yielding cyst formation, the extent of which is dependent on genetic vulnerability.

Gram-Negative Bacteria↗