Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “nephrolithiasis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1992

Transmembrane oxalate exchange: its relationship to idiopathic calcium oxalate nephrolithiasis.

Red blood cell oxalate flux rates were measured in various populations of stone patients and controls. Idiopathic and normocalciuric stone patients and post-prostatectomy patients exhibited rates significantly greater than the nonstone controls. The fact that this abnormality was not limited to patients with calcium oxalate nephrolithiasis suggests that this cellular defect is not universal nor an important etiological factor for calcium oxalate nephrolithiasis.

Adult↗
PubMed1988

Plasma osteocalcin levels in stone disease. A potential aid in the differential diagnosis of calcium nephrolithiasis.

Plasma osteocalcin levels were measured by radioimmunoassay in 70 consecutive patients with recurrent calcium (sterile) nephrolithiasis during diagnostic evaluation for the cause of the disease. Nephrogenous cyclic adenosine 3,5'-monophosphate levels also were measured in most of the subjects. Included in the sampling, as determined by standard diagnostic criteria, were 12 patients with absorptive hypercalciuria type I, 15 with absorptive hypercalciuria type II, 22 with renal leak hypercalciuria, 11 with normocalciuria, 6 with primary hyperparathyroidism, 3 with renal tubular acidosis and 1 with Paget's disease, as well as 12 control subjects. The observed plasma osteocalcin levels (ng. per ml. mean +/- standard error) were absorptive hypercalciuria I 2.6 +/- 0.20, absorptive hypercalciuria II 3.1 +/- 0.21, renal hypercalciuria 8.7 +/- 0.45, normocalciuric nephrolithiasis 3.3 +/- 0.25, primary hyperparathyroidism 13.2 +/- 0.91, renal tubular acidosis (range) 5.2 to 10.6, Paget's disease 18.0 and control 3.1 +/- 0.20. There were significant differences between the plasma osteocalcin levels of renal hypercalciuria versus primary hyperparathyroidism and renal hypercalciuria/primary hyperparathyroidism versus any other group. There was good correlation between plasma osteocalcin and cyclic adenosine 3,5'-monophosphate data (correlation coefficient 0.72, p less than 0.005). Plasma osteocalcin levels are a potential differential diagnostic tool for patients with stone disease. The diagnostic value compares favorably with that of cyclic adenosine 3,5'-monophosphate, with the advantage that the determination of plasma osteocalcin requires only a single test.

Adult↗
PubMed1985

The current role of medical treatment of nephrolithiasis: the impact of improved techniques of stone removal.

To document more clearly the effect of selective medical treatment on the course of nephrolithiasis, we surveyed 103 consecutive patients being followed in our stone clinic. Of the patients who initially had existing stones within the kidneys 69 per cent experienced no symptoms while undergoing medical therapy, compared to 96 per cent of those who had no existing stones. In all subjects studied new stone formation was reduced in more than 95 per cent and no new stones were formed in more than 75 per cent. An operation for newly formed calculi was necessary in only 2 per cent of the patients on medical therapy, whereas 58 to 69 per cent of the patients required an operation for new stones before beginning medical treatment. We believe that selective medical treatment has an important role in the over-all management of nephrolithiasis. Appropriate medical therapy may decrease significantly the number of new stones formed and may obviate the need for a repeat stone operation. Therefore, medical treatment should be an important adjunct to percutaneous nephrostolithotomy and extracorporeal shock wave lithotripsy.

Adult↗
PubMed1981

Triamterene nephrolithiasis complicating dyazide therapy.

A case of triamterene nephrolithiasis is reported in a man after 4 years of hydrochlorothiazide-triamterene therapy for hypertension. The stone passed spontaneously and was found to contain a triamterene metabolite admixed with uric acid salts. Factors affecting triamterene nephrolithiasis are discussed and 2 previously reported cases are reviewed.

Drug Combinations↗
PubMed2002

Bone alterations in patients with idiopathic hypercalciuria and calcium nephrolithiasis.

OBJECTIVES: To verify whether alterations in bone density and turnover in patients with calcium nephrolithiasis and hypercalciuria are observable in various subgroups of patients divided according to the pathogenesis of the hypercalciuria. METHODS: Seventy patients with calcium nephrolithiasis and idiopathic hypercalciuria, 19 to 64 years old, were assessed for spine and femur mineral metabolism and bone density using a Dexa evaluation system. After a low calcium diet, the subjects were classified into two groups: fasting hypercalciuria (FH, 39 patients) and absorptive hypercalciuria (AH, 31 patients). RESULTS: Only in the patients with FH was the lumbar spine bone density lower than in the controls (P <0.001). Also, only the patients with FH had higher bone alkaline phosphatase and urinary hydroxyproline levels than the control group (P <0.005 and <0.015, respectively). The blood pH levels were lower, even though within the normal range, in the hypercalciuric patients than in the controls (P <0.01). There was a negative correlation between the urinary hydroxyproline level and lumbar spine and femoral neck density in patients with FH (P <0.001 and <0.005, respectively), and the blood pH correlated positively with the lumbar spine bone density. CONCLUSIONS: Altered bone metabolism and overall bone loss were found only in the patients with FH. Overloading of acid valences, perhaps of dietary origin, could be the pathogenic factor responsible.

Adult↗
PubMed1984

Raised transmembrane oxalate flux in red blood cells in idiopathic calcium oxalate nephrolithiasis.

Red-blood-cell transmembrane oxalate flux was measured in a group of patients with idiopathic calcium oxalate nephrolithiasis and in normal controls. The mean transmembrane oxalate flux rate was significantly higher in stone-forming patients than in controls (0.93 +/- SD 0.31/min vs 0.29 +/- 0.11/min). 80% of stone-forming patients showed raised (greater than 2SD above the mean in controls) transmembrane oxalate flux. Anomalous cellular oxalate transport may be an important pathogenetic factor in calcium oxalate nephrolithiasis.

Adult↗
PubMed1997

Chronic renal failure and its management and nephrolithiasis.

Chronic renal failure (CRF) is the most common form of renal disease in dogs and cats. Although CRF occurs in dogs and cats of all ages, it is commonly considered a disease of older animals, and the incidence increases with age. This article presents guide-lines for the diagnosis and conservative management of chronic renal failure in dogs and cats. Nephrolithiasis is uncommon in dogs and cats, accounting for less than 3% of all urinary calculi. The mineral composition of the renolith is important in formulation of therapeutic and preventive management strategies. This article briefly reviews the epidemiology, diagnosis, and management of nephrolithiasis in the dog and cat.

Aging↗
PubMed1984

Anorexia nervosa and nephrolithiasis.

A patient with primary anorexia nervosa developed acute abdominal pain and hematuria. Cytoscopy and retrograde pyelography confirmed nephrolithiasis. A calcium oxalate stone was passed. The association between anorexia nervosa and nephrolithiasis has not been previously reported. Dietary factors and chronic dehydration are known to contribute to the development of renal stones; therefore, the association may not be coincidental.

Adolescent↗
PubMed1999

Calcium oxalate nephrolithiasis: effect of renal crystal deposition on the cellular composition of the renal interstitium.

Urinary calcium oxalate (CaOx) crystals and crystal agglomerates are normally harmlessly excreted, but in nephrolithiasis they are retained by tubular epithelial cells and shifted into the renal interstitium. This crystalline material induces an inflammatory response consisting of an increase in the number of interstitial cells and an expansion of the extracellular matrix. The newly arrived cells either derive from the blood or the connective tissue or they are formed by local proliferation. Identification of the cells that surround the interstitial crystals is a first step in investigating the question of whether the interstitial cells could remove the crystalline material. Therefore, we performed an immunohistochemical study on the kidneys of rats made hyperoxaluric by ethylene glycol (EG) and ammonium chloride (AC). Attention was paid to expression of the leukocyte common antigen (LCA), which identifies all types of leukocytes, the ED1 antigen, which is specific for monocytes and macrophages, and the major histocompatibility class II antigen (MHC II), which is present on dendritic cells, B lymphocytes, and activated macrophages. The results obtained were compared with those seen in two human kidney specimens with acute and chronic oxalosis. In both rat and humans, macrophages and multinucleated giant cells are the major cells that encapsulate the interstitial crystals. This similarity in response underlines the relevance of the rat nephrolithiasis model. The rat experiments showed, furthermore, that the number of interstitial crystals and the amount of biochemically measured kidney-associated oxalate both decrease with time, if the nephrolithiatic agents EG and AC are omitted from the drinking water. Further studies must clarify whether macrophages and multinucleated giant cells are able to remove the interstitial crystals and how these cells are recruited at the inflammatory site.

Adult↗
PubMed1979

Histomorphometric analysis of bone changes in surgically proven primary hyperparathyroidism and nephrolithiasis--the importance of bone biopsy in diagnosis.

The morphologic changes in trabecular bone were studied in 60 patients with surgically proven hyperparathyroidism and in 69 patients with nephrolithiasis. The hyperparathyroid bone lesions showed substantial variation in their extent. Four, typical stages were defined. The structure of trabecular bone remained intact in most cases. Bone turnover is significantly higher in the patients with primary hyperparathyroidism. Fifty percent of all patients with nephrolithiasis had bone changes similar to those found in the surgically proven hyperparathyroidism group. In 50% of so-called asymptomatic cases of hyperparathyroidism, the iliac crest biopsy is a useful supplement to clinical and hormonal data in deciding whether to operate on the parathyroid glands. In about 45% of cases, however, no definite diagnoses is possible. The determination of serum parathyroid hormone in primary hyperparathyroidism has a greater importance for diagnostic purposes than morphologic investigation of the bone biopsy.

Adolescent↗
PubMed2002

Medical treatment of nephrolithiasis.

The medical treatment of nephrolithiasis is aimed in particular at the prevention of relapses, even though in some cases, such as cystine or uric acid lithiasis, the calculi also can be dissolved on site. When the diagnosis and metabolic profile have been performed correctly, medical treatment is effective in a large number of patients. The greatest difficulty is the patient's compliance with the most suitable prevention measures and the frequency of follow-up controls. This compliance can be influenced significantly by the amount of time that the doctor spends to explain the origin of the disease. This article reviews the main methods available for the medical treatment of various nephrolithiasis types, namely water intake, diet, and drugs, supplying the relevant information about the mechanism of action, metabolic consequences, indications, evidence provided from studies, dosage, efficacy, and side-effects. Finally, brief simplified guidelines are given for the medical treatment of stone disease caused by calcium oxalate or calcium phosphate, uric acid, cystine, and struvite.

Benzothiadiazines↗
PubMed2002

Urinary analysis of nephrolithiasis markers.

Renal stone disease is an ancient and common affliction, common in industrialised nations. The causes and incidence of nephrolithiasis are presented. Afterwards, the promoters and inhibitors of renal stone formation analysis in urine are described including enzymatic methods, chromatography, capillary electrophoresis and other techniques. Aspects such as sample collection and storage are also included. The review article includes referenced tables that provide summaries of methodology for the analysis of nephrolithiasis related compounds.

Biomarkers↗
PubMed2001

Inhibition of oxalate nephrolithiasis with Ammi visnaga (AI-Khillah).

We investigated the effect of Ammi visnaga seeds on experimentally - induced kidney stones - in male Wistar albino rats. Oxalate nephrolithiasis was experimentally induced by 3% glycolic acid (added in their diet) given for the period of four weeks. A highly significant amount of deposits were found in the kidneys, which were analyzed quantitatively. These deposits were mainly of calcium oxalate in composition. Daily oral (gavage) treatment with Ammi visnaga (500 mg/kg) highly reduced the incidence of nephrolithiasis (calcium oxalate deposition in the kidneys). Ammi visnaga seeds extract showed highly potent diuretic activity. The reduction in body weight, increase in kidneys weight, increase in water intake, decrease in urine output found in glycolic acid control group were prevented to various extent on Ammi visnaga treatment; and the values became to insignificant difference with control group. The changes in weights of liver, heart and lungs of the three groups were insignificant. Uraemia and hyperbilirubinaemia observed in glycolic acid control group were found to be ameliorated by Ammi visnaga seed extract treatment.

Ammi↗
PubMed2003

Hospitalized nephrolithiasis after renal transplantation in the United States.

The national incidence of and risk factors for hospitalized nephrolithiasis (NEP) in renal transplant (RT) recipients has not been reported. We conducted a historical cohort study of 42 096 RT recipients in the United States Renal Data System between 1 July 1994 and 30 June 1998. The 1-year incidence of NEP (ICD-9 codes 592.x) after RT in 1997 was compared to the rate of NEP in the general population using the National Hospital Discharge Survey. Associations with time to hospitalizations for a primary diagnosis of nephrolithiasis were assessed by Cox Regression. NEP was uncommon after RT (104 cases per 100 000 person years in 1997). However, females, but not males, had a statistically significant increased risk of NEP compared to the general population (rate ratio for females, 2.84, 95% confidence interval, 2.35-3.58). Kidney stones were more common than ureteral stones, and percutaneous procedures were more common than ureteroscopy or extracorporeal shock wave lithotripsy (ESWL). The only risk factor identified for NEP was renal failure due to stone disease (only one case). NEP was uncommon after RT, but was still more common than in the general population. We identified differences in the presentation and management of NEP after RT in comparison to the general population.

Female↗
PubMed1980

Uric acid saturation in calcium nephrolithiasis.

Hyperuricosuria appears to cause calcium oxalate nephrolithiasis by promoting the formation of monosodium urate or uric acid crystals, which either act as seed crystals for calcium oxalate or adsorb normally occurring macromolecular inhibitors of calcium oxalate crystallization. Both mechanisms require that hyperuricosuria cause excessive supersaturation of the urine, but this has not yet been studied under conditions of normal lifestyle. We have measured the saturation with respect to sodium hydrogen urate and the concentration of undissociated uric acid in the urine samples of 67 patients with calcium nephrolithiasis, who had idiopathic hypercalciuria, hyperuricosuria, both, or neither disorder. Patients with hyperuricosuria excreted urine that was supersaturated with respect to monosodium urate or undissociated uric acid more frequently than did other stone formers or normal subjects, and are therefore at a greater risk of forming a solid phase of monosodium urate or uric acid. Treatment measures that lowered uric acid excretion also lowered urine saturation, and this may be the reason that such treatment tends to prevent calcium stone recurrence.

Adolescent↗
PubMed2004

Idiopathic congenital nonobstructive nephrolithiasis: a case report and review.

We describe a case of congenital nephrolithiasis, which presented with hematuria at birth. No etiopathological factor could be determined for renal stone formation despite extensive investigation. There was a family history of renal stones in both maternal and paternal grandparents and of microscopic hematuria in the mother. There was no associated urinary flow obstruction and the hematuria remitted spontaneously. The infant was treated conservatively. The follow-up studies revealed persistence of renal stone but no hematuria. This case can be considered as idiopathic, or an early presentation of one of the rare genetic disorders associated with renal stones. Congenital nonobstructive nephrolithiasis has not been reported previously and should be considered as a cause of hematuria during this age.

Hematuria↗
PubMed1990

Glycosaminoglycan content, oxalate self-exchange and protein phosphorylation in erythrocytes of patients with 'idiopathic' calcium oxalate nephrolithiasis.

1. This study was performed to test the hypothesis that glycosaminoglycans may play an important role in the observed abnormalities in oxalate flux seen in patients with calcium oxalate nephrolithiasis. 2. Oxalate flux rate, erythrocyte membrane glycosaminoglycan content, membrane protein phosphorylation and effect of heparan sulphate on erythrocyte oxalate flux in vitro were studied in control subjects and patients with calcium oxalate nephrolithiasis. 3. In comparison with control subjects, renal stone-formers showed a significantly higher oxalate self-exchange, a lower erythrocyte membrane glycosaminoglycan content and a higher membrane phosphorylation rate. In stone-formers, erythrocyte glycosaminoglycan content correlated inversely with both oxalate flux rate and protein phosphorylation. In vitro, heparan sulphate promoted a significant fall in the rate of oxalate self-exchange. 4. These findings support the hypothesis that a lower erythrocyte membrane content of glycosaminoglycans enhances membrane protein phosphorylation, leading to an increased rate of transmembrane oxalate flux.

Adult↗
PubMed1993

Abnormal urate transport in erythrocytes of patients with idiopathic calcium nephrolithiasis: a possible link with hyperuricosuria.

1. The demonstration of an inheritable anomaly of erythrocyte oxalate transport in 'primary' calcium nephrolithiasis suggested that this disease might be a generalized metabolic disorder characterized by a defect in cellular anion transport. 2. To determine whether this anomaly is restricted to oxalate alone, we studied erythrocyte transmembrane urate self-exchange in calcium-oxalate renal stone formers in whom urinary excretion of uric acid is frequently increased. 3. Abnormal urate self-exchange was found in 30% of the patients. The urate self-exchange rate constant was correlated with 24 h urinary excretion of uric acid; the erythrocyte anomaly was also associated with the frequency of hyperuricosuria and a more intense disease activity. Transmembrane urate self-exchange was inhibited by stilbene and heparan sulphate. Morphazinamide administration did not reduce urinary urate excretion in patients with abnormal urate erythrocyte self-exchange. 4. These findings suggest that hyperuricosuria during calcium-oxalate renal stone disease might be due to a cellular defect in urate transport, and further support the hypothesis that idiopathic nephrolithiasis is a metabolic disorder characterized by a defect in cellular anion transport.

Biological Transport↗