Gastrointestinal Citrate Absorption in Nephrolithiasis

Fegan, Jeffrey; Khan, Rubina; Poindexter, John R.; Pak, Charles Y.C.

doi:10.1016/s0022-5347(17)37520-1

Cited by 43 publications

(20 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The mechanism by which K-cit reduces urinary calcium is almost certainly multifactorial. While citrate itself is readily absorbed in the intestine, 52 it decreases calcium absorption and urinary calcium excretion. 14,15 Increased urinary citrate would also bind urinary calcium, removing the calcium from the pool available for binding with phosphate or oxalate.…”

Section: Discussionmentioning

confidence: 99%

Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria

Krieger

Asplin

Frick

et al. 2015

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Potassium citrate is prescribed to decrease stone recurrence in patients with calcium nephrolithiasis. Citrate binds intestinal and urine calcium and increases urine pH. Citrate, metabolized to bicarbonate, should decrease calcium excretion by reducing bone resorption and increasing renal calcium reabsorption. However, citrate binding to intestinal calcium may increase absorption and renal excretion of both phosphate and oxalate. Thus, the effect of potassium citrate on urine calcium oxalate and calcium phosphate supersaturation and stone formation is complex and difficult to predict. To study the effects of potassium citrate on urine supersaturation and stone formation, we utilized 95th-generation inbred genetic hypercalciuric stone-forming rats. Rats were fed a fixed amount of a normal calcium (1.2%) diet supplemented with potassium citrate or potassium chloride (each 4 mmol/d) for 18 weeks. Urine was collected at 6, 12, and 18 weeks. At 18 weeks, stone formation was visualized by radiography. Urine citrate, phosphate, oxalate, and pH levels were higher and urine calcium level was lower in rats fed potassium citrate. Furthermore, calcium oxalate and calcium phosphate supersaturation were higher with potassium citrate; however, uric acid supersaturation was lower. Both groups had similar numbers of exclusively calcium phosphate stones. Thus, potassium citrate effectively raises urine citrate levels and lowers urine calcium levels; however, the increases in urine pH, oxalate, and phosphate levels lead to increased calcium oxalate and calcium phosphate supersaturation. Potassium citrate induces complex changes in urine chemistries and resultant supersaturation, which may not be beneficial in preventing calcium phosphate stone formation.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria

Krieger

Asplin

Frick

et al. 2015

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

show abstract

“…The possible mechanisms of hypocitraturia include an intrinsic renal defect (dysfunction of the Na-citrate cotransporter or disordered intracellular citrate regulation), an abnormal intestinal citrate or alkali absorption, or a normal physiologic response to a high acid-ash diet [25]. However, recent controlled studies on hypocitraturic cases have concluded that the low urine citrate in stone formers was not due to an abnormality in intestinal citrate absorption, but was probably due to a diet high in animal proteins or low in fruits and vegetables [26,27].…”

Section: Discussionmentioning

confidence: 99%

Metabolic Risk Factors in Pediatric and Adult Calcium Oxalate Urinary Stone Formers: Is There Any Difference?

et al. 2003

View full text Add to dashboard Cite

Objectives: Urolithiasis in children is recognized with an increasing frequency, while exact etiological factors remain to be determined. The aim of this study is to compare the metabolic risk factors and saturation of urine in pediatric and adult calcium oxalate (Ca-Ox) stone formers. Methods: A total of 33 pediatric (mean age: 6.8 ± 3.1 years) and 120 adult patients (mean age: 39.7 ± 5.7 years), with documented Ca-Ox urinary stone disease, underwent a comprehensive metabolic evaluation at our institution. Beside a broad serum analysis, concentrations of calcium, oxalate, magnesium, uric acid and citrate were measured in 24-hour collected urine. Saturation of urine was calculated by Marshall-Robertson’s nomograms. Results: Hypocitraturia, observed in 60.6%, and hypomagnesuria, detected in 39.4%, but not hypercalciuria, were the most common metabolic risk factors in the pediatric group. In adults, hypercalciuria still represented one of the major metabolic risk factors, detected in 44.1%, although hypocitraturia, observed in 45.8%, was the most prevalent metabolic risk factor, as it was in the pediatric group. Pediatric cases had significantly (p < 0.05) higher prevalence of hypocitraturia, hypomagnesuria and supersaturated urine when compared to adults. Metabolic abnormalities could be detected in a high percentage (82%) of primary and recurrent pediatric Ca-Ox stone formers, but not in primary adult stone formers. Conclusions: Metabolic risk factors significantly differ in pediatric and adult Ca-Ox stone formers. Hypocitraturia and hypomagnesuria seem to play a major role in stone formation, and metabolic abnormalities can be detected in a significant percentage of both primary and recurrent pediatric stone formers. Thus, a comprehensive metabolic evaluation is of utmost importance for all children with Ca-Ox stones.

show abstract

Section: Regulation Of Citrate Homeostasis By Slc13 Membersmentioning

confidence: 99%

“…Citrate absorption from nutritional sources in the small intestine seems to be mediated mainly via NaDC1 and NaDC3 [64, 65]. By this mechanism, more than 90% of an oral citrate load can be absorbed and hypocitraturia can be ameliorated [64, 66]. At physiological pH, most of serum citrate circulates in the form of triply charged citrate bound to divalent ions, such as calcium and magnesium, and is filtered freely at the glomerulus; reabsorption takes place predominantly in the proximal tubule via NaDC1 [65].…”

Section: Regulation Of Citrate Homeostasis By Slc13 Membersmentioning

confidence: 99%

The Role of Indy in Metabolic Regulation

Willmes

Birkenfeld

2013

Computational and Structural Biotechnology Journal

View full text Add to dashboard Cite

Reduced expression of the Indy (I'm Not Dead Yet) gene in D. melanogaster and C. elegans extends longevity. Indy and its mammalian homolog mINDY (Slc13a5, NaCT) are transporters of TCA cycle intermediates, mainly handling the uptake of citrate via the plasma membrane into the cytosol. Deletion of mINDY in mice leads to significant metabolic changes akin to caloric restriction, likely caused by reducing the effects of mINDY-imported citrate on fatty acid and cholesterol synthesis, glucose metabolism and ß-oxidation. This review will provide an overview on different mammalian SLC1 3 family members with a focus on mINDY (SLCl3A5) in glucose and energy metabolism and will highlight the role of mINDY as a putative therapeutic target for the treatment of obesity, non-alcoholic fatty liver disease and type 2 diabetes.

show abstract

Gastrointestinal Citrate Absorption in Nephrolithiasis

Cited by 43 publications

References 13 publications

Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria

Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria

Metabolic Risk Factors in Pediatric and Adult Calcium Oxalate Urinary Stone Formers: Is There Any Difference?

The Role of Indy in Metabolic Regulation

Contact Info

Product

Resources

About