Citrate inhibits growth of residual fragments in an in vitro model of calcium oxalate renal stones

Chow, Ka Ming; Dixon, J.S.; Gilpin, S. A.; Kavanagh, John P.; Rao, P. N.

doi:10.1111/j.1523-1755.2004.00566.x

Cited by 50 publications

(33 citation statements)

References 30 publications

(39 reference statements)

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“…Citrate in the urine chelates with calcium and forms a soluble complex, thus reducing calcium ion activity and CaOx SS (39). Citrate can also adhere to the surface of CaOx crystals to prevent crystal nucleation and aggregation (6). Citrate supplementation is a general treatment in patients with kidney stones.…”

Section: Discussionmentioning

confidence: 99%

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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Ethylene glycol (EG)-induced hyperoxaluria is the most commonly employed experimental regimen as an animal model of calcium oxalate (CaOx) stone formation. The variant sensitivity to CaOx among different rat strains has not been fully explored, although the Wistar rat is known to accumulate more CaOx in kidney tissue after low-dose EG exposure than in the Fischer 344 (F344) rats. Supersaturation of CaOx in tubular fluid contributes to the amount of CaOx crystal formation in the kidney. We hypothesized that the urinary supersaturation of CaOx in Wistar rats is higher than that of F344 rats, thereby allowing for greater CaOx crystal deposition in the Wistar rat. Age-matched male Wistar and F344 rats were treated with 0.75% EG or drinking water for 8 wk. Twenty-four-hour urine was collected at 0, 2, 4, 6, and 8 wk for analysis of key electrolytes to calculate the CaOx supersaturation. Plasma oxalate level was also measured. Our data confirmed the different sensitivity to renal toxicity from EG between the two rat strains (Wistar > F344). After EG treatment, the plasma oxalate level and urine oxalate excretion were markedly greater in the Wistar rats than in the F344 rats, while urine calcium was slightly decreased in Wistars. Thus, the CaOx supersaturation in urine of Wistar rats was higher, which led to a greater crystal deposition in kidney in Wistar rats. These studies suggest that during EG treatment, changes in urine electrolytes and in CaOx supersaturation occur to a greater extent in the Wistar rat, in agreement with its greater sensitivity to EG toxicity.

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Section: Discussionmentioning

confidence: 99%

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

McMartin²

2009

American Journal of Physiology-Renal Physiology

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“…In our retrospective analysis we included patients with low citrate excretion (<1.67 mmol/24-h), defining hypocitraturia [15], having undergone a renal acidification capacity test. Subjects with urinary bacterial contamination (≥10 5 colonies/mL) or incomplete 24-hour urinary collection [16] were not included in the study because of the risk of falsely low urinary citrate excretion.…”

Section: Methodsmentioning

confidence: 99%

Signification of distal urinary acidification defects in hypocitraturic patients

et al. 2017

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Background and objectivesHypocitraturia has been associated with metabolic acidosis and mineral disorders. The aim of this study was to investigate the occurrence of urinary acidification defects underlying hypocitraturia.Materials and methodsThis retrospective observational study included 67 patients (32 men), aged 40.7±15.1 years with hypocitraturia (<1.67 mmol/24-h) and nephrolithiasis, nephrocalcinosis, and/or bone demineralization, referred to our center from 2000 to 2015. We aimed to assess renal distal acidification capacity, prevalence and mechanisms of urinary acidification defects. Patients with low baseline plasma HCO3- (<22 mmol/L) were studied by bicarbonate loading or furosemide/fludrocortisone tests. Patients with normal baseline plasma HCO3- had an ammonium-chloride challenge test. A normal response was a decrease in urinary pH <5.3 and an increase in urinary NH4+ ≥33 μmol/min and defined idiopathic hypocitraturia.ResultsEleven patients (16.4%) had low HCO3- and overt distal acidification defect. Three had a mutation in the gene encoding AE1, 4 had Gougerot-Sjögren syndrome and no cause was found in the remaining 4 cases. Fifty-six patients (83.6%) had normal HCO3-; of those, 33 (58.9%) had idiopathic hypocitraturia. Among the 23 (41%) remaining patients, 12 were unable to increase urinary NH4+ excretion (among them, 8 were able to decrease urinary pH and 4 were not) whereas 11 were able to increase urinary NH4+ excretion but unable to decrease urinary pH. These 11 patients had higher fasting urinary calcium, reflecting bone resorption, than the other 12 patients: median 0.41 [0.24–0.47] vs. 0.22 [0.08–0.37] mmol/mmol creatinine (P = 0.04).ConclusionsPatients with hypocitraturia and normal plasma HCO3- frequently show a latent acidification defect that can be further dissected into one of several subtypes based on urinary pH and NH4+ response to the acid load. Those patients with impaired urine acidification capacity but preserved NH4+ excretion exhibit particularly high calciuria and should be identified to optimize nephrolithiasis prevention.

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“…Crystal inhibitors are protein crystal inhibitors (uropontin, nephrocalcin), glycosaminoglycans, citrate, and pyrophosphate. At the present time, citrate is the only naturally occurring inhibitor that is routinely measured in urine [3,13].…”

Section: Physicochemical Factorsmentioning

confidence: 99%

“…In the United States, the prevalence of kidney stones has increased over the past 30 years, and the risk among white persons is approximately three times than among black persons. Nearly 90% of stones in men and 70% in women contain calcium, most commonly as calcium oxalate with variable amounts of calcium phosphate [2,3]. Once a person forms a calcium-containing stone, another stone will generally develop in less than 7 years, with a decreasing time interval to future stone events.…”

Section: Introductionmentioning

confidence: 98%

Calcium Nephrolithiasis

Brener

Winchester

Bergman

2011

Clinic Rev Bone Miner Metab

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Nephrolithiasis is a major cause of morbidity involving the urinary tract. The prevalence of this disease in the United States increased from 3.8% in the 1970s to 5.2% in the 1990s. There were nearly 2 million physician office visits for nephrolithiasis in 2000, and estimated annual costs totaled $2 billion. About 80% of stones are composed of calcium oxalate with variable amounts of calcium phosphate. New information has become available on the clinical presentation, epidemiologic risk factors, evaluative approach, and outcome of various therapeutic strategies. In this report, we will review the epidemiology and mechanisms of calcium kidney stones formation and outline management aimed at preventing recurrences. Improved awareness and education in both the general population and among health care providers about these modifiable risk factors has the potential to improve general health and decrease morbidity and mortality secondary to renal stone disease.

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Citrate inhibits growth of residual fragments in an in vitro model of calcium oxalate renal stones

Abstract: Citrate inhibited stone growth in this laboratory model. This was true both in defined media and with addition of UMM. This adds to evidence justifying the use of alkaline citrate in calcium oxalate nephrolithiasis.

Cited by 50 publications

References 30 publications

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Strain differences in urinary factors that promote calcium oxalate crystal formation in the kidneys of ethylene glycol-treated rats

Signification of distal urinary acidification defects in hypocitraturic patients

Calcium Nephrolithiasis

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