METABOLIC EVALUATION OF CHILDREN WITH UROLITHIASIS TO STUDY RISK FACTORS: A 1 YEAR PROSPECTIVE STUDY.

Mapping Intimacies ◽

10.36106/ijsr/7121392 ◽

2021 ◽

pp. 29-30

Author(s):

Harshawardhan V Tanwar ◽

Uttam Wadavkar

Keyword(s):

Risk Factors ◽

Prospective Study ◽

Water Intake ◽

Calcium Intake ◽

Stone Formation ◽

Urine Volume ◽

Indian Children ◽

Blood Calcium ◽

Western Literature ◽

Low Calcium

Introduction: Metabolic abnormalities are common cause of urolithiasis in pediatric age group. Children with urolithiasis are associated with considerable morbidity. By treating these abnormalities stone formation is prevented. Objectives: Prospective study to nd the metabolic risk factors of urolithiasis in children and compare them with literature. Materials and Methods: In open, prospective and observational study, 85 children were evaluated from August 2019 to June 2020. In all patients' dietary history, water intake and results of laboratory ndings were recorded. All urine samples obtained from patients were without dietary restrictions. Reference pediatric 24 hour urinary parameter was used according to western literature. Results: We investigated 85 patients with urolithiasis. Low urine volume was found in 52 patients which is comparable with previous studies indicating simple intervention as to increase water intake. Low calcium intake was found in 48 patients suggesting that low calcium intake is associated with higher incidence of urolithiasis due to increased intestinal oxalate absorption. Hypocalcaemia was found in 34 patients and 24 hour urinary abnormality was found in only 18 patients'. Both these nding does not support previous literature. Stone analysis nding does not correlate with urinary nding. Conclusions: Hypocalcaemia is major metabolic abnormality in contradiction to western literature. Low urine volume secondary to low water intake is predominant nding .There are no nomograms for urinary excretion of Calcium, uric acid, oxalate and citrate in Indian children. Keeping the optimum blood calcium level & increased uid intake can prevent stone formation in children.

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No effect of increased water intake on blood viscosity and cardiovascular risk factors

British Journal Of Nutrition ◽

10.1017/bjn20061969 ◽

2006 ◽

Vol 96 (6) ◽

pp. 993-996 ◽

Cited By ~ 8

Author(s):

Serena Tonstad ◽

Tor Ole Klemsdal ◽

Sverre Landaas ◽

Aud Høieggen

Keyword(s):

Risk Factors ◽

Water Intake ◽

Blood Viscosity ◽

Whole Blood ◽

Fluid Intake ◽

Intervention Group ◽

Urine Volume ◽

Control Group ◽

Whole Blood Viscosity ◽

Blueberry Juice

Observational data have suggested that increased water intake decreases the risk of CHD. A postulated mechanism is that increased water ingestion reduces blood viscosity. The aim of the present study was to assess the effect of increased fluid intake on blood viscosity. Men (n 67) and postmenopausal women (n 27) with one or more risk factors for CVD who reported intake of ≤ 0·5 litres water daily were randomised to a control group (n 31), an intervention group (n 32) that increased their daily water intake by 1 litre/d and an intervention group (n 31) that ingested 1 litre blueberry juice/d. All were encouraged to continue their usual diet and lifestyle. Whole-blood viscosity and blood and urine chemistries were measured by standard techniques after 2 and 4 weeks. Urine volume increased (by a median of 872 and 725 ml in the water and blueberry juice groups, respectively, v. 10 ml in the control group; P ≤ 0·002), confirming the subjects' adherence to the protocol. Urine osmolality and urinary levels of Na, K and creatinine decreased in the water and blueberry juice groups v. the controls (P < 0·05). No change was seen in whole-blood viscosity or in levels of fibrinogen, total protein, lipids, glucose, insulin, C-peptide or other chemistry and haematology variables. In conclusion, a postulated protective effect of increased water or fluid intake is not explained by a change in blood viscosity and increased fluid intake does not influence CVD risk factors in the short term.

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Racial Differences in Risk Factors for Kidney Stone Formation

Clinical Journal of the American Society of Nephrology ◽

10.2215/cjn.12671019 ◽

2020 ◽

Vol 15 (8) ◽

pp. 1166-1173

Author(s):

Anna L. Zisman ◽

Fredric L. Coe ◽

Andrew J. Cohen ◽

Christopher B. Riedinger ◽

Elaine M. Worcester

Keyword(s):

Risk Factors ◽

Stone Formation ◽

Urine Volume ◽

Free Water ◽

Post Treatment ◽

Racial Groups ◽

Urine Calcium ◽

Free Water Clearance ◽

Black Stone ◽

Stone Formers

Background and objectivesIncidence of kidney stone disease is rising. It is not known whether mechanisms of stone formation differ across racial groups. Our objective was to identify differing lithogenic risk factors across racial groups in idiopathic nephrolithiasis.Design, setting, participants, & measurementsWe conducted a retrospective cohort study evaluating metabolic risk factors in black and age-matched white idiopathic stone formers at our tertiary referral center. We compared serum and urine metabolic risk factors pre- and post-treatment across racial groups using analysis of covariance. Generalized linear modeling was used to build regression models for risk of stone formation in both groups.ResultsAmong 117 black and 172 white stone formers, urine volume was lower in black stone formers (1.4±0.8 versus 2.0±0.8 L/d, P<0.001). Urine calcium was lower in black stone formers (116±70 versus 217±115 mg/d, P<0.001). Supersaturations for calcium oxalate were similar among the groups, whereas calcium phosphate supersaturation was higher in white stone formers, and uric acid supersaturation was higher in black stone formers. Electrolyte free water clearance was significantly lower in black stone formers (207±780 versus 435±759 ml/d, P=0.02). In the subgroup of 77 black patients and 107 white patients with post-treatment evaluations, urine volume rose significantly and similarly in both groups. Urine sodium was unchanged in whites but increased in blacks by 40 mmol/d (95% confidence interval, 32 to 48 mmol/d). Electrolyte free water clearance remained lower in black stone formers (385±891 versus 706±893 ml/d, P=0.02). Post-treatment supersaturations were similar across the groups except for calcium phosphate, which improved with treatment in whites.ConclusionsBlack stone formers have lower 24-hour urine calcium excretion and urine volume. Increases in urine volume with treatment were associated with increased solute, but not free water, excretion in black stone formers.

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Effects of Mineral Composition of Drinking Water on Risk for Stone Formation and Bone Metabolism in Idiopathic Calcium Nephrolithiasis

Clinical Science ◽

10.1042/cs0910313 ◽

1996 ◽

Vol 91 (3) ◽

pp. 313-318 ◽

Cited By ~ 31

Author(s):

Martino Marangella ◽

Corrado Vitale ◽

Michele Petrarulo ◽

Lidia Rovera ◽

Franca Dutto

Keyword(s):

Drinking Water ◽

Parathyroid Hormone ◽

Bone Resorption ◽

Calcium Oxalate ◽

Calcium Intake ◽

Mineral Water ◽

Stone Formation ◽

Low Calcium ◽

High Calcium ◽

Markers Of Bone Resorption

1. To assess whether the mineral content of drinking water influences both risk of stone formation and bone metabolism in idiopathic calcium nephrolithiasis, 21 patients were switched from their usual home diets to a 10 mmol calcium, low-oxalate, protein-controlled diet, supplemented with 21 of three different types of mineral water. Drinking water added 1, 6 and 20 mmol of calcium and 0.5, 10 and 50 mmol of bicarbonate respectively to the controlled diet. 2. The three controlled study periods lasted 1 month each and were separated by a 20 day washout interval. Blood and urine chemistries, including intact parathyroid hormone, calcitriol and two markers of bone resorption, were performed at the end of each study period. The stone-forming risk was assessed by calculating urine saturation with calcium oxalate (βCaOx), calcium phosphate (βbsh) and uric acid (βUA). 3. The addition of any mineral water produced the expected increase in urine output and was associated with similar decreases in βCaOx and βUA, whereas βbsh varied marginally. These equal decreases in βCaOx, however, resulted from peculiar changes in calcium, oxalate and citrate excretion during each study period. The increase in overall calcium intake due to different drinking water induced modest increases in calcium excretion, whereas oxalate excretion tended to decrease. The changes in oxalate excretion during any one study period compared with another were significantly related to those in calcium intake. Citrate excretion was significantly higher with the high-calcium, alkaline water. 4. Parathyroid hormone, calcitriol and markers of bone resorption increased when patients were changed from the high-calcium, alkaline to the low-calcium drinking water. 5. We suggest that overall calcium intake may be tailored by supplying calcium in drinking water. Adverse effects on bone turnover with low-calcium diets can be prevented by giving high-calcium, alkaline drinking water, and the stone-forming risk can be decreased as effectively as with low-calcium drinking water.

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