The effects of citrate on hydroxyapatite induced calcium oxalate crystallization and on the formation of calcium phosphate crystals

Berg, C.; Tiselius, H.-G.

doi:10.1007/bf00256245

Cited by 31 publications

(14 citation statements)

References 12 publications

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“…This may reflect an increase in urine crystal inhibitory activity due to the higher urinary citrate concentration. 66 Further studies are necessary to determine whether the provision of K-cit to GHS rats fed hydroxyproline, which causes them to form only CaOx stones, would affect urinary supersaturation or stone formation.…”

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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“…Apparently the presence of dissolving calcium-phosphate particles enhances the formation of calcium oxalate crystals [45,83]. It has been shown before that several calcium-phosphate materials can act as a heterogeneous nucleator of calcium oxalate [8,58,59,62]. This heterogeneous nucleation is pH dependent [83].…”

Section: Intratubular Crystal Nucleation Experimentsmentioning

confidence: 99%

Intratubular crystallization events

Kok¹

1997

World J Urol

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Can urolithiasis start as an intratubular event? Under severe hyperoxaluric conditions in animal models at least crystal formation can. Recently models have been presented that assess the chances of crystal formation under more normal conditions. These models describe changes in fluid composition as this passes through the nephron, these conditions being simulated in in vitro experiments. It appears that under naturally occurring intratubular conditions calcium-salt crystallization takes place within the time tubular fluid normally spends in the nephron. Precipitation starts with a calcium-phosphate phase under conditions found in the thin lambs. This crystalline phase then (partly) dissolves when collecting duct conditions are used, thereby inducing formation of calcium oxalates. Under these conditions the latter increase in size by way of crystal growth and agglomeration. Large particle formation and cell adhesion can eventually result in particle retention and subsequent stone formation. Viewing urolithiasis as originally an intratubular event has consequences for in vitro experiments and treatments, which are discussed in this paper.

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“…In addition to the reduced ion activity of calcium, citrate has inhibitory influences on the growth of CaOx on crystals of CaOx (26)(27)(28)(29)(30), CaOx on crystals of CaP (5,31,32) and CaP on crystals of CaP (33,34). The inhibitory influence of citrate on CaP and CaOx crystal aggregation might be particularly important (10,14).…”

Section: Discussionmentioning

confidence: 99%

Long-term Follow-up of Stone Formers Treated with a Low Dose of Sodium Potassium Citrate

Jendle-Bengten

Tiselius

2000

Scandinavian Journal of Urology and Nephrology

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We evaluated the clinical efficacy of long-term preventive treatment with a single evening dose of alkaline citrate. Information was collected from the files of 52 recurrent stone formers prescribed a daily intake of 3.75-5 g of sodium potassium citrate (SPC; 14-18 mmol of citrate). The annual and cumulative rates of stone formation and the rate of recurrence were compared before and during the treatment. A comparison was also made between the patients with (Group R) and without (Group NR) recurrent stone formation during treatment in terms of urine composition and previous history of the disease. For all patients who started the treatment, the number of stones was smaller during treatment (period tT) than during a period of the same length immediately before treatment (period tB), but greater than the number formed during a corresponding period immediately after the diagnosis (period tA). Via questionnaire we found low treatment compliance, with only 62% of the patients reporting consistent taking of their medication (Group T). The patients in Group T had a smaller cumulated number of stones during period tT than that during periods tA and tB, but the Kaplan-Meier curve of the fraction of patients remaining stone-free during treatment was almost identical to that recorded in 446 recurrent stone formers without medical treatment. No significant differences were recorded in terms of relevant pretreatment urinary risk factors between Groups T(R) and T(NR), but numerically higher values of calcium oxalate (CaOx) supersaturation and calcium/citrate quotients were observed in Group T(R). When 9 patients with a daily intake of SPC and a citrate excretion below 2.5 mmol/day were compared with 16 hypocitraturic patients only given drinking advice, the cumulated percentages of patients without recurrent stone formation in the 2 groups after 3 years were 44% and 48%, respectively. Although the number of patients in this study was small, our results indicate poor long-term protection from recurrent calcium stone formation when a single evening dose of only 3.75-5 g of SPC was taken. The rate of stone formation was apparently slightly reduced, but the fraction of patients free of recurrence was no different from that in patients without medical treatment.

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The effects of citrate on hydroxyapatite induced calcium oxalate crystallization and on the formation of calcium phosphate crystals

Cited by 31 publications

References 12 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

Intratubular crystallization events

Long-term Follow-up of Stone Formers Treated with a Low Dose of Sodium Potassium Citrate

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