Raising Urinary Citrate Lowers Calcium Oxalate and Calcium Phosphate Crystal Formation in Whole Urine

Hallson, P. C.; Rose, G.A.; Sulaiman, Shahida

doi:10.1159/000280885

Cited by 50 publications

(19 citation statements)

References 13 publications

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“…Citrate is capable of binding calcium ions to form a soluble nonionized complex, and decreases the free calcium ion activity. By decreasing free calcium, urinary saturation of both calcium oxalate and calcium phosphate crystals is reduced (8,12). Urinary citrate was significantly decreased by the vitamin B6-deficient diet in our study.…”

Section: Discussionmentioning

confidence: 99%

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload

et al. 2006

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We examined the effect of vitamin B6 deficiency on glyoxylate metabolism and hepatic alanine: glyoxylate aminotransferase (AGT) activity in rats with normal or high glyoxylate intake. Male rats were divided into four groups: a control group, a vitamin B6-free diet group, a glyoxylate water group, and a vitamin B6-free diet + glyoxylate water group. Each group was given special diet (control or vitamin B6-deficient diet) and drinking water (plain or 0.5% glyoxylate water) for 4 weeks, after which biochemical parameters and hepatic AGT mRNA level were measured. Compared with control rats, the urinary oxalate/creatinine ratio was higher in each of the other 3 groups. The urinary glycolate/creatinine ratio was also higher in the vitamin B6-free diet group and the vitamin B6-free diet + glyoxylate water group than the control group, while the urinary glycine/creatinine and citrate/creatinine ratio was lower in both groups. The hepatic AGT mRNA level was reduced in the vitamin B6-free diet group, but was increased in the glyoxylate water group than the control group. These results suggest that vitamin B6 is necessary for glyoxylate metabolism as a coenzyme of AGT. Especially in the presence of a high glyoxylate intake, vitamin B6 deficiency leads to severe hyperoxaluria and hypocituria.The majority of urinary tract stones are predominantly composed of calcium oxalate (9). Urinary oxalate plays an important role in the formation of calcium oxalate stone, and a small change of the urinary oxalate concentration has a major impact on urinary calcium oxalate saturation (15). In humans, oxalate is a metabolic end product that is excreted in the urine (18). Dietary intake of oxalate accounts for at most 15% of the oxalate excreted in the urine (11), while 50% to 60% of urinary oxalate is produced from glyoxylate by endogenous metabolism (17). Excessive synthesis of oxalate from glyoxylate is usually prevented by alanine:glyoxylate transferase (AGT).AGT is a specific vitamin B6-dependent enzyme that is found in hepatocytes, and it catalyzes transamination between glyoxylate and alanine to form pyruvate and glycine. Primary hyperoxaluria type 1 (PH1), an autosomal recessive disease resulting from AGT deficiency, is associated with a marked increase of oxalate production and urolithiasis (5). Conservative treatment of patients with PH1 involves the administration of crystallization inhibitors, a low-oxalate diet, and a high fluid intake to decrease the formation of calcium oxalate crystals.

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Section: Discussionmentioning

confidence: 99%

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload

et al. 2006

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“…Citrate is a substance that is found in urine and chelates calcium, making it unavailable for binding with oxalate and phosphate and thereby lowering urinary SS and preventing stone formation (49,50). Urinary citrate levels are highest in young children and decrease into adulthood (32,33), but relative hypocitraturia is a common finding in pediatric nephrolithiasis (22,23,28,39,40,51,52).…”

Section: Inhibitors Of Stone Formationmentioning

confidence: 99%

An Update on the Changing Epidemiology and Metabolic Risk Factors in Pediatric Kidney Stone Disease

Sas¹

2011

Clinical Journal of the American Society of Nephrology

137

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SummaryNephrolithiasis in children is a painful and costly disease that may also have detrimental long-term effects on kidney function. Recent data provide evidence that the incidence of nephrolithiasis in children is rising. Children who are white, female, and adolescent seem to have the highest risk for forming symptomatic kidney stones. Although the reasons for the rising incidence and demographic discrepancies in pediatric nephrolithiasis are not yet clear, recent investigations into urine chemistry provide clues regarding predisposing metabolic risk factors. As more data emerge regarding epidemiologic and metabolic characteristics of pediatric kidney stone formers, we hope to gain a better understanding of the causes of kidney stone disease and, ultimately, provide better strategies for stone prevention in children.

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“…Studies on hypocitraturia showed a highly variable prevalence in the single presentation, reaching 62% when associated with other disorders (14). The citrate acts on prevention of lithiasis due to its dissolving effects and by inhibiting the crystallization of calcium and uric acid salts (15). Citraturia is not directly influenced by the ingestion of alimentary citrate, but by systemic acid-basic changes produced by a certain diet.…”

Section: Commentsmentioning

confidence: 99%

Metabolic assessment in patients with urinary lithiasis

et al. 2005

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Introduction: Metabolic investigation in patients with urinary lithiasis is very important for preventing recurrence of disease. The objective of this work was to diagnose and to determine the prevalence of metabolic disorders, to assess the quality of the water consumed and volume of diuresis as potential risk factors for this pathology.Patients and Methods: We studied 182 patients older than 12 years. We included patients with history and/or imaging tests confirming at least 2 stones, with creatinine clearance ≥ 60 mL/min and negative urine culture. The protocol consisted in the collection of 2, 24-hour urine samples, for dosing Ca, P, uric acid, Na, K, Mg, Ox and Ci, glycemia and serum levels of Ca, P, Uric acid, Na, K, Cl, Mg, U and Cr, urinary pH and urinary acidification test.Results: 158 patients fulfilled the inclusion criteria. Among these, 151 (95.5%) presented metabolic changes, with 94 (62.2%) presenting isolated metabolic change and 57 (37.8%) had mixed changes. The main disorders detected were hypercalciuria (74%), hypocitraturia (37.3%), hyperoxaluria (24.1%), hypomagnesuria (21%), hyperuricosuria (20.2%), primary hyperparathyroidism (1.8%) secondary hyperparathyroidism (0.6%) and renal tubular acidosis (0.6).Conclusion: Metabolic change was diagnosed in 95.5% of patients. These results warrant the metabolic study and follow-up in patients with recurrent lithiasis in order to decrease the recurrence rate through specific treatments, modification in alimentary and behavioral habits.

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Raising Urinary Citrate Lowers Calcium Oxalate and Calcium Phosphate Crystal Formation in Whole Urine

Cited by 50 publications

References 13 publications

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload

Effect of vitamin B6 deficiency on glyoxylate metabolism in rats with or without glyoxylate overload

An Update on the Changing Epidemiology and Metabolic Risk Factors in Pediatric Kidney Stone Disease

Metabolic assessment in patients with urinary lithiasis

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