scholarly journals Calcium and Vitamin D Supplementation and Their Association with Kidney Stone Disease: A Narrative Review

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4363
Author(s):  
Matteo Bargagli ◽  
Pietro Manuel Ferraro ◽  
Matteo Vittori ◽  
Gianmarco Lombardi ◽  
Giovanni Gambaro ◽  
...  
Keyword(s):  
Vitamin D ◽  
Kidney Stone ◽  
Stone Formation ◽  
Vitamin D Supplementation ◽  
Stone Disease ◽  
Normal Body Mass Index ◽  
Calcium Excretion ◽  
Kidney Stone Disease ◽  
Low Calcium Diet ◽  
Stone Formers

Kidney stone disease is a multifactorial condition influenced by both genetic predisposition and environmental factors such as lifestyle and dietary habits. Although different monogenic polymorphisms have been proposed as playing a causal role for calcium nephrolithiasis, the prevalence of these mutations in the general population and their complete pathogenetic pathway is yet to be determined. General dietary advice for kidney stone formers includes elevated fluid intake, dietary restriction of sodium and animal proteins, avoidance of a low calcium diet, maintenance of a normal body mass index, and elevated intake of vegetables and fibers. Thus, balanced calcium consumption protects against the risk for kidney stones by reducing intestinal oxalate availability and its urinary excretion. However, calcium supplementation given between meals might increase urinary calcium excretion without the beneficial effect on oxalate. In kidney stone formers, circulating active vitamin D has been found to be increased, whereas higher plasma 25-hydroxycholecalciferol seems to be present only in hypercalciuric patients. The association between nutritional vitamin D supplements and the risk for stone formation is currently not completely understood. However, taken together, available evidence might suggest that vitamin D administration worsens the risk for stone formation in patients predisposed to hypercalciuria. In this review, we analyzed and discussed available literature on the effect of calcium and vitamin D supplementation on the risk for kidney stone formation.

scholarly journals Genetic variants of calcium and vitamin D metabolism in kidney stone disease

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Sarah A. Howles ◽  
Akira Wiberg ◽  
Michelle Goldsworthy ◽  
Asha L. Bayliss ◽  
Anna K. Gluck ◽  
...  
Keyword(s):  
Vitamin D ◽  
Kidney Stone ◽  
Association Studies ◽  
Vitamin D Supplementation ◽  
Stone Disease ◽  
Calcium Excretion ◽  
Genome Wide Association Studies ◽  
Vitamin D Metabolism ◽  
Kidney Stone Disease

AbstractKidney stone disease (nephrolithiasis) is a major clinical and economic health burden with a heritability of ~45–60%. We present genome-wide association studies in British and Japanese populations and a trans-ethnic meta-analysis that include 12,123 cases and 417,378 controls, and identify 20 nephrolithiasis-associated loci, seven of which are previously unreported. A CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of only nephrolithiasis patients, the CYP24A1-associated locus correlates with serum calcium concentration and a number of nephrolithiasis episodes while the DGKD-associated locus correlates with urinary calcium excretion. In vitro, DGKD knockdown impairs CaSR-signal transduction, an effect rectified with the calcimimetic cinacalcet. Our findings indicate that studies of genotype-guided precision-medicine approaches, including withholding vitamin D supplementation and targeting vitamin D activation or CaSR-signaling pathways in patients with recurrent kidney stones, are warranted.

scholarly journals Genetic variants of calcium and vitamin D metabolism in kidney stone disease

2019 ◽  
Author(s):  
Sarah A. Howles ◽  
Akira Wiberg ◽  
Michelle Goldsworthy ◽  
Asha L. Bayliss ◽  
Emily Grout ◽  
...  
Keyword(s):  
Vitamin D ◽  
Genetic Variants ◽  
Kidney Stone ◽  
Association Studies ◽  
Stone Disease ◽  
Calcium Excretion ◽  
Genome Wide Association Studies ◽  
Vitamin D Metabolism ◽  
Kidney Stone Disease

Kidney stone disease (nephrolithiasis) is a major clinical and economic health burden1,2 with a heritability of ~45-60%3. To identify genetic variants associated with nephrolithiasis we performed genome-wide association studies (GWAS) and meta-analysis in British and Japanese populations, including 12,123 nephrolithiasis cases and 416,928 controls. Twenty loci associated with nephrolithiasis were identified, ten of which are novel. A novel CYP24A1 locus is predicted to affect vitamin D metabolism and five loci, DGKD, DGKH, WDR72, GPIC1, and BCR, are predicted to influence calcium-sensing receptor (CaSR) signaling. In a validation cohort of nephrolithiasis patients the CYP24A1-associated locus correlated with serum calcium concentration and number of kidney stone episodes, and the DGKD-associated locus correlated with urinary calcium excretion. Moreover, DGKD knockdown impaired CaSR-signal transduction in vitro, an effect that was rectifiable with the calcimimetic cinacalcet. Our findings indicate that genotyping may inform risk of incident kidney stone disease prior to vitamin D supplementation and facilitate precision-medicine approaches, by targeting CaSR-signaling or vitamin D activation pathways in patients with recurrent kidney stones.

scholarly journals Nutrition and Kidney Stone Disease

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1917
Author(s):  
Roswitha Siener
Keyword(s):  
Kidney Stone ◽  
Fluid Intake ◽  
Stone Formation ◽  
Urinary Stone ◽  
Stone Disease ◽  
Urinary Stones ◽  
Dietary Therapy ◽  
Effective Prevention ◽  
Kidney Stone Disease ◽  
Nutrition And Diet

The prevalence of kidney stone disease is increasing worldwide. The recurrence rate of urinary stones is estimated to be up to 50%. Nephrolithiasis is associated with increased risk of chronic and end stage kidney disease. Diet composition is considered to play a crucial role in urinary stone formation. There is strong evidence that an inadequate fluid intake is the major dietary risk factor for urolithiasis. While the benefit of high fluid intake has been confirmed, the effect of different beverages, such as tap water, mineral water, fruit juices, soft drinks, tea and coffee, are debated. Other nutritional factors, including dietary protein, carbohydrates, oxalate, calcium and sodium chloride can also modulate the urinary risk profile and contribute to the risk of kidney stone formation. The assessment of nutritional risk factors is an essential component in the specific dietary therapy of kidney stone patients. An appropriate dietary intervention can contribute to the effective prevention of recurrent stones and reduce the burden of invasive surgical procedures for the treatment of urinary stone disease. This narrative review has intended to provide a comprehensive and updated overview on the role of nutrition and diet in kidney stone disease.

Vitamin D and kidney stone disease

2013 ◽  
Vol 22 (4) ◽  
pp. 383-389 ◽  
Author(s):  
Jie Tang ◽  
Michel B. Chonchol
Keyword(s):  
Vitamin D ◽  
Kidney Stone ◽  
Stone Disease ◽  
Kidney Stone Disease

scholarly journals A test of the hypothesis that the collecting duct calcium-sensing receptor limits rise of urine calcium molarity in hypercalciuric calcium kidney stone formers

2009 ◽  
Vol 297 (4) ◽  
pp. F1017-F1023 ◽  
Author(s):  
Kristin J. Bergsland ◽  
Fredric L. Coe ◽  
Daniel L. Gillen ◽  
Elaine M. Worcester
Keyword(s):  
Water Conservation ◽  
Kidney Stone ◽  
Stone Formation ◽  
Collecting Duct ◽  
Urine Volume ◽  
Calcium Excretion ◽  
Calcium Sensing Receptor ◽  
Urine Calcium ◽  
Calcium Sensing ◽  
Stone Formers

The process of kidney stone formation depends on an imbalance between excretion of water and insoluble stone-forming salts, leading to high concentrations that supersaturate urine and inner medullary collecting duct (IMCD) fluid. For common calcium-containing stones, a critical mechanism that has been proposed for integrating water and calcium salt excretions is activation of the cell surface calcium-sensing receptor (CaSR) on the apical membranes of IMCD cells. High deliveries of calcium into the IMCD would be predicted to activate CaSR, leading to reduced membrane abundance of aquaporin-2, thereby limiting water conservation and protecting against stone formation. We have tested this hypothesis in 16 idiopathic hypercalciuric calcium stone formers and 14 matched normal men and women in the General Clinical Research Center. Subjects were fed identical diets; we collected 14 urine samples at 1-h intervals during a single study day, and one sample overnight. Hypercalciuria did not increase urine volume, so urine calcium molarity and supersaturation with respect to calcium oxalate and calcium phosphate rose proportionately to calcium excretion. Thus CaSR modulation of urine volume via IMCD CaSR activation does not appear to be an important mechanism of protection against stone formation. The overnight period, one of maximal water conservation, was a time of maximal stone risk and perhaps a target of specific clinical intervention.

scholarly journals P0175DETERMINANTS OF RENAL PAPILLARY APPEARANCE IN RENAL STONE FORMERS: AN IN-DEPTH EXAMINATION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Matteo Bargagli ◽  
Rossella De Leonardis ◽  
Mauro Ragonese ◽  
Angelo Totaro ◽  
Francesco Pinto ◽  
...  
Keyword(s):  
Kidney Stones ◽  
Kidney Stone ◽  
Medical Condition ◽  
Stone Formation ◽  
Blood Parameters ◽  
Stone Disease ◽  
Stone Composition ◽  
Stone Recurrence ◽  
Stone Formers

Abstract Background and Aims Nephrolithiasis is a medical condition characterized by high prevalence among the general population both in Europe and in the U.S. and it is responsible for high costs reaching up to $10 billion per year. It is associated with specific comorbidities such as obesity, arterial hypertension, diabetes mellitus, metabolic syndrome and chronic kidney disease. Kidney stones development is believed to start either from Randall’s plaques or from stone plugs. Both these lesions can be seen on renal papillary surfaces, but what promotes the formation of plaques and plugs is not entirely understood. The aim of this study is to investigate the association between the urinary metabolic milieu and a published endoscopic papillary evaluation score (PPLA). We also evaluated the correlation of PPLA score with kidney stone recurrence during follow-up. Method We prospectively enrolled 31 stone forming patients who undergone retrograde intrarenal surgery procedures. Visual inspection of the accessible renal papillae was performed in order to calculate the PPLA score based on the appearance of ductal plugging, surface pitting, loss of papillary contour and Randall’s plaque extension. Demographic information, blood samples, 24h urine collections and kidney stone events during follow-up were collected. Stone composition was analyzed using infrared-spectroscopy. Relative urinary supersaturations (RSS) for calcium oxalate (CaOx), calcium phosphate (CaPi) and uric acid (UA) were calculated using the Equil2 software. PPLA score > 3 was defined as high. Results Median follow-up period was 11 (min/max 5, 34) months. PPLA score was inversely correlated with BMI (rho = −0.39, p = 0.035) and history of recurrent kidney stones (median PPLA 5.0 vs 2.5, p = 0.029), these results were confirmed when PPLA was considered as a categorical variable (median BMI 27 vs 24, recurrent stone disease 12 vs 62%, p= 0.006). Furthermore, high PPLA score was associated with lower odds of new kidney stone events during follow-up (OR 0.154, 95% confidence interval 0.024, 0.998, p = 0.05). No significant correlations were found between PPLA score, stone composition, blood parameters, 24h urine solute excretions and RSS for CaOx, CaPi and UA. Conclusion Different papillary abnormalities seem to be linked to specific mechanisms of stone formation. Although data regarding PPLA score are inconsistent, it may be a valid asset for both medical and surgical management of nephrolithiasis. Larger, long-term prospective clinical studies need to be conducted to assess the validity of PPLA score system in evaluating risk of stone recurrence.

scholarly journals Proteomics of Crystal–Cell Interactions: A Model for Kidney Stone Research

Cells ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 1076 ◽  
Author(s):  
Thongboonkerd
Keyword(s):  
Kidney Stone ◽  
Current Knowledge ◽  
Stone Formation ◽  
Public Health Problem ◽  
Stone Disease ◽  
Cell Interactions ◽  
Global Public Health ◽  
Proteomics Data ◽  
Kidney Stone Disease ◽  
Crystal Cell

Nephrolithiasis/urolithiasis (i.e., kidney stone disease) remains a global public health problem with increasing incidence/prevalence. The most common chemical composition of kidney stones is calcium oxalate that initiates stone formation by crystallization, crystal growth, crystal aggregation, crystal–cell adhesion, and crystal invasion through extracellular matrix in renal interstitium. Among these processes, crystal–cell interactions (defined as “the phenomena in which the cell is altered by any means of effects from the crystal that adheres onto cellular surface or is internalized into the cell, accompanying with changes of the crystal, e.g., growth, adhesive capability, degradation, etc., induced by the cell”) are very important for crystal retention in the kidney. During the past 12 years, proteomics has been extensively applied to kidney stone research aiming for better understanding of the pathogenic mechanisms of kidney stone formation. This article provides an overview of the current knowledge in this field and summarizes the data obtained from all the studies that applied proteomics to the investigations of crystal–cell interactions that subsequently led to functional studies to address the significant impact or functional roles of the expression proteomics data in the pathogenesis of kidney stone disease.

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