Effects of Dietary Nutrients Upon Urinary Excretion of Calcium, Uric Acid and Citrate in Renal Stone Formers

1994 ◽  
pp. 434-434
Author(s):  
I. P. Heilberg ◽  
L. A. Martini ◽  
L. Cuppari ◽  
S. A. Draibe ◽  
N. Schor
Keyword(s):  
Uric Acid ◽  
Urinary Excretion ◽  
Renal Stone ◽  
Stone Formers ◽  
Dietary Nutrients

Correlation of Urinary Excretion of Glycosaminoglycans and Uric Acid in Healthy Adults and in Renal Stone Formers

Urolithiasis ◽  
1989 ◽  
pp. 251-251
Author(s):  
H. Sidhu ◽  
A. K. Hemal ◽  
S. Vaidyanathan ◽  
S. K. Thind ◽  
R. Nath
Keyword(s):  
Uric Acid ◽  
Urinary Excretion ◽  
Renal Stone ◽  
Healthy Adults ◽  
Stone Formers

Abnormal Urate Transport in Erythrocytes of Patients with Idiopathic Calcium Nephrolithiasis: A Possible Link with Hyperuricosuria

1993 ◽  
Vol 85 (1) ◽  
pp. 41-44 ◽  
Author(s):  
Giovanni Gambaro ◽  
Massimo Vincenti ◽  
Francesco Marchini ◽  
Angela D'Angelo ◽  
Bruno Baggio
Keyword(s):  
Uric Acid ◽  
Urinary Excretion ◽  
Calcium Oxalate ◽  
Metabolic Disorder ◽  
Renal Stone ◽  
Heparan Sulphate ◽  
Anion Transport ◽  
Stone Disease ◽  
Urate Transport ◽  
Stone Formers

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.

scholarly journals Dietary treatment of urinary risk factors for renal stone formation. A review of CLU Working Group

2015 ◽  
Vol 87 (2) ◽  
pp. 105 ◽  
Author(s):  
Domenico Prezioso ◽  
Pasquale Strazzullo ◽  
Tullio Lotti ◽  
Giampaolo Bianchi ◽  
Loris Borghi ◽  
...  
Keyword(s):  
Risk Factors ◽  
Urinary Excretion ◽  
Renal Stone ◽  
Sodium Intake ◽  
Stone Formation ◽  
Urinary Stone ◽  
Fruit And Vegetables ◽  
Calcium Excretion ◽  
Urinary Oxalate ◽  
Stone Formers

Objective: Diet interventions may reduce the risk of urinary stone formation and its recurrence, but there is no conclusive consensus in the literature regarding the effectiveness of dietary interventions and recommendations about specific diets for patients with urinary calculi. The aim of this study was to review the studies reporting the effects of different dietary interventions for the modification of urinary risk factors in patients with urinary stone disease. Materials and Methods: A systematic search of the Pubmed database literature up to July 1, 2014 for studies on dietary treatment of urinary risk factors for urinary stone formation was conducted according to a methodology developed a priori. Studies were screened by titles and abstracts for eligibility. Data were extracted using a standardized form and the quality of evidence was assessed. Results: Evidence from the selected studies were used to form evidencebased guideline statements. In the absence of sufficient evidence, additional statements were developed as expert opinions. Conclusions: General measures: Each patient with nephrolithiasis should undertake appropriate evaluation according to the knowledge of the calculus composition. Regardless of the underlying cause of the stone disease, a mainstay of conservative management is the forced increase in fluid intake to achieve a daily urine output of 2 liters. Hypercalciuria: Dietary calcium restriction is not recommended for stone formers with nephrolithiasis. Diets with a calcium content ≥ 1 g/day (and low protein-low sodium) could be protective against the risk of stone formation in hypercalciuric stone forming adults. Moderate dietary salt restriction is useful in limiting urinary calcium excretion and thus may be helpful for primary and secondary prevention of nephrolithiasis. A low-normal protein intake decrease calciuria and could be useful in stone prevention and preservation of bone mass. Omega-3 fatty acids and bran of different origin decreases calciuria, but their impact on the urinary stone risk profile is uncertain. Sports beverage do not affect the urinary stone risk profile. Hyperoxaluria: A diet low in oxalate and/or a calcium intake normal to high (800-1200 mg/day for adults) reduce the urinary excretion of oxalate, conversely a diet rich in oxalates and/or a diet low in calcium increase urinary oxalate. A restriction in protein intake may reduce the urinary excretion of oxalate although a vegetarian diet may lead to an increase in urinary oxalate. Adding bran to a diet low in oxalate cancels its effect of reducing urinary oxalate. Conversely, the addition of supplements of fruit and vegetables to a mixed diet does not involve an increased excretion of oxalate in the urine. The intake of pyridoxine reduces the excretion of oxalate. Hyperuricosuria: In patients with renal calcium stones the decrease of the urinary excretion of uric acid after restriction of dietary protein and purine is suggested although not clearly demonstrated. Hypocitraturia: The administration of alkaline-citrates salts is recommended for the medical treatment of renal stone-formers with hypocitraturia, although compliance to this treatment is limited by gastrointestinal side effects and costs. Increased intake of fruit and vegetables (excluding those with high oxalate content) increases citrate excretion and involves a significant protection against the risk of stone formation. Citrus (lemons, oranges, grapefruit, and lime) and non citrus fruits (melon) are natural sources of dietary citrate, and several studies have shown the potential of these fruits and/or their juices in raising urine citrate levels. Children: There are enought basis to advice an adequate fluid intake also in children. Moderate dietary salt restriction and implementation of potassium intake are useful in limiting urinary calcium excretion whereas dietary calcium restriction is not recommended for children with nephrolithiasis. It seems reasonable to advice a balanced consumption of fruit and vegetables and a low consumption of chocolate and cola according to general nutritional guidelines, although no studies have assessed in pediatric stone formers the effect of fruit and vegetables supplementation on urinary citrate and the effects of chocolate and cola restriction on urinary oxalate in pediatric stone formers. Despite the low level of scientific evidence, a low-protein (< 20 g/day) low-salt (< 2 g/day) diet with high hydration (> 3 liters/day) is strongly advised in children with cystinuria. Elderly: In older patients dietary counseling for renal stone prevention has to consider some particular aspects of aging. A restriction of sodium intake in association with a higher intake of potassium, magnesium and citrate is advisable in order to reduce urinary risk factors for stone formation but also to prevent the loss of bone mass and the incidence of hypertension, although more hemodynamic sensitivity to sodium intake and decreased renal function of the elderly have to be considered. A diet rich in calcium (1200 mg/day) is useful to maintain skeletal wellness and to prevent kidney stones although an higher supplementation could involve an increase of risk for both the formation of kidney stones and cardiovascular diseases. A lower content of animal protein in association to an higher intake of plant products decrease the acid load and the excretion of uric acid has no particular contraindications in the elderly patients, although overall nutritional status has to be preserved.

Comparative Study of 24-Hour Urinary Excretion of Glycosaminoglycans by Renal Stone Formers and Healthy Adults

1989 ◽  
Vol 16 (1) ◽  
pp. 45-47 ◽  
Author(s):  
H. Sidhu ◽  
A.K. Hemal ◽  
S.K. Thind ◽  
R. Nath ◽  
S. Vaidyanathan
Keyword(s):  
Comparative Study ◽  
Urinary Excretion ◽  
Renal Stone ◽  
Healthy Adults ◽  
Stone Formers

scholarly journals Circadian Periodicity of Circulating Plasma Lipid Peroxides, Uric Acid and Ascorbic Acid in Renal Stone Formers

2016 ◽  
Vol 32 (2) ◽  
pp. 220-224 ◽  
Author(s):  
Rajeev Singh Kushwaha ◽  
R. C. Gupta ◽  
J. P. Sharma ◽  
Sumita Sharma ◽  
Raj Kumar Singh ◽  
...  
Keyword(s):  
Ascorbic Acid ◽  
Uric Acid ◽  
Renal Stone ◽  
Plasma Lipid ◽  
Lipid Peroxides ◽  
Circadian Periodicity ◽  
Stone Formers

scholarly journals Excretion of urine extracellular vesicles bearing markers of activated immune cells and calcium/phosphorus physiology differ between calcium kidney stone formers and non-stone formers

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Jiqing Zhang ◽  
Sanjay Kumar ◽  
Muthuvel Jayachandran ◽  
Loren P. Herrera Hernandez ◽  
Stanley Wang ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Calcium Oxalate ◽  
Extracellular Vesicles ◽  
Immune Cells ◽  
Kidney Stone ◽  
Fibroblast Growth Factor 23 ◽  
Pathogenic Mechanisms ◽  
Phosphorus Excretion ◽  
Stone Formers ◽  
Calcium Phosphorus

Abstract Backgrounds: Previous studies have demonstrated that excretion of urinary extracellular vesicles (EVs) from different nephron segments differs between kidney stone formers and non-stone formers (NSFs), and could reflect pathogenic mechanisms of urinary stone disease. In this study we quantified selected populations of specific urinary EVs carrying protein markers of immune cells and calcium/phosphorus physiology in calcium oxalate stone formers (CSFs) compared to non-stone formers (NSFs). Methods Biobanked urine samples from CSFs (n = 24) undergoing stone removal surgery and age- and sex- matched NSFs (n = 21) were studied. Urinary EVs carrying proteins related to renal calcium/phosphorus physiology (phosphorus transporters (PiT1 and PiT2), Klotho, and fibroblast growth factor 23 (FGF23); markers associated with EV generation (anoctamin-4 (ANO4) and Huntington interacting protein 1 (HIP1)), and markers shed from activated immune cells were quantified by standardized and published method of digital flow cytometry. Results Urine excretion of calcium, oxalate, phosphorus, and calcium oxalate supersaturation (SS) were significantly higher in CSFs compared to NSFs (P < 0.05). Urinary excretion of EVs with markers of total leukocytes (CD45), neutrophils (CD15), macrophages (CD68), Klotho, FGF23, PiT1, PiT2, and ANO4 were each markedly lower in CSFs than NSFs (P < 0.05) whereas excretion of those with markers of monocytes (CD14), T-Lymphocytes (CD3), B-Lymphocytes (CD19), plasma cells (CD138 plus CD319 positive) were not different between the groups. Urinary excretion of EVs expressing PiT1 and PiT2 negatively (P < 0.05) correlated with urinary phosphorus excretion, whereas excretion of EVs expressing FGF23 negatively (P < 0.05) correlated with both urinary calcium and phosphorus excretion. Urinary EVs with markers of HIP1 and ANO4 correlated negatively (P < 0.05) with clinical stone events and basement membrane calcifications on papillary tip biopsies. Conclusions Urinary excretion of EVs derived from specific types of activated immune cells and EVs with proteins related to calcium/phosphorus regulation differed between CSFs and NSFs. Further validation of these and other populations of urinary EVs in larger cohort could identify biomarkers that elucidate novel pathogenic mechanisms of calcium stone formation in specific subsets of patients.

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