Clinical implications of abundant calcium phosphatein routinely analyzed kidney stones

Parks, Joan H.; Worcester, Elaine M.; Coe, Fredric L.; Evan, Andrew P.; Lingeman, James E.

doi:10.1111/j.1523-1755.2004.00803.x

Cited by 194 publications

(164 citation statements)

References 37 publications

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“…Some studies have shown that CaOx stones may transform into CaP stones over time, and use of citrate therapy may explain this phenomenon. 50,51 However, no definitive studies have yet proved or refuted the role of citrate in transformation of CaOx to CaP stone disease.…”

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

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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.

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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

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“…Urine pH rises progressively with increasing CaP percentage in stones (93). The mechanism of increased urinary pH in CaP SFs is unknown.…”

Section: High Urine Ph As a Main Risk Factor For Cap Stonesmentioning

confidence: 99%

Kidney stone disease

Coe

Evan

Worcester

2005

Journal of Clinical Investigation

681

527

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About 5% of American women and 12% of men will develop a kidney stone at some time in their life, and prevalence has been rising in both sexes. Approximately 80% of stones are composed of calcium oxalate (CaOx) and calcium phosphate (CaP); 10% of struvite (magnesium ammonium phosphate produced during infection with bacteria that possess the enzyme urease), 9% of uric acid (UA); and the remaining 1% are composed of cystine or ammonium acid urate or are diagnosed as drug-related stones. Stones ultimately arise because of an unwanted phase change of these substances from liquid to solid state. Here we focus on the mechanisms of pathogenesis involved in CaOx, CaP, UA, and cystine stone formation, including recent developments in our understanding of related changes in human kidney tissue and of underlying genetic causes, in addition to current therapeutics.

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“…Some data suggest that calcium phosphate stones have increased in prevalence. If true, the reasons are uncertain and have been attributed to treatment with citrate supplements (see below) or adverse effects of extracorporeal shockwave lithotripsy (3,4). Lithotripsy has been hypothesized to lead to defective urinary acidification, but this effect is highly speculative.…”

Section: Overview Of Calcium Phosphate Stonesmentioning

confidence: 99%

A Woman with Recurrent Calcium Phosphate Kidney Stones

Goldfarb

2012

Clinical Journal of the American Society of Nephrology

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SummaryKidney stones composed predominantly (50% or more) of calcium phosphate constitute up to 10% of all stones and 15%-20% of calcium stones, 80% of which are composed of calcium oxalate. Calcium phosphate is a minor component of up to 30% of calcium oxalate stones as well. The cause of calcium phosphate stones is often obscure but most often related to a high urine pH. Some patients with calcium phosphate stones may have incomplete renal tubular acidosis. Others have distal renal tubular acidosis characterized by hyperchloremic acidosis, hypocitraturia, and high urine pH. The use of carbonic anhydrase inhibitors such as acetazolamide, topiramate, and zonisamide leads to a similar picture. Treatment options to specifically prevent calcium phosphate stone recurrence have not been tested in clinical trials. Increases in urine volume and restriction of sodium intake to limit calcium excretion are important. Citrate supplementation is probably effective, although the concomitant increase in urine pH may increase calcium phosphate supersaturation and partially offset the inhibition of crystallization resulting from the increased urine citrate excretion and the alkali-associated reduction in urine calcium excretion. Thiazides lower urine calcium excretion and may help ensure the safety of citrate supplementation.

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Clinical implications of abundant calcium phosphatein routinely analyzed kidney stones

Abstract: Stone CaP% has risen for three decades. CaP SF, particularly with brushite stones, receive more ESWL treatments than CaOx SF, not explained by stone number or duration of stone disease. Urine supersaturations explain the high CaP%. High CaP% does not hamper medical stone prevention.

Cited by 194 publications

References 37 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

Kidney stone disease

A Woman with Recurrent Calcium Phosphate Kidney Stones

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