Long-term potassium citrate therapy and bone mineral density in idiopathic calcium stone formers

Abstract

Several authors have described an association between idiopathic calcium (Ca) stone disease and bone mass reduction. Hypocitraturia is a frequent feature of urolithiasis, and alkaline citrate has been recommended as one of the choice treatments in this disease. Some evidence exists as to the positive effect of potassium (K) citrate therapy on bone mass. The aim of this work was the longitudinal evaluation of bone mineral density (BMD) changes in a group of Ca oxalate stone formers treated with K citrate for two years. Enrolled patients were 120; 109 subjects completed the study (51 males and 58 females). A metabolic study and distal radius BMD measurements were conducted both at baseline (BAS) and at the end of the study (END). BMD (0.451 +/- 0.081 vs 0.490 +/- 0.080 g/cm2), T-score (-1.43 +/- 1.02 vs -0.90 +/- 1.04), net gastrointestinal alkali absorption (40.37 +/- 50.57 vs 61.26 +/- 42.26 mEq/day), urinary citrate (2.53 +/- 1.15 vs 3.10 +/- 1.44 mmol/day) and K (58.93 +/- 22.28 vs 65.45 +/- 23.97 mmol/day) excretion significantly increased from BAS to END. Urinary Ca excretion remained unchanged from BAS to END (5.16 +/- 2.74 vs 5.57 +/- 2.85 mmol/ day). Our results indicate that long-term treatment with K citrate increases forearm BMD in idiopathic Ca stone formers. It seems probable that the alkali load provided by this drug reduces bone resorption by a buffering of the endogenous acid production. K citrate appears to be a further therapeutic opportunity for the management of osteoporosis in Ca stone formers.

Bone Disease in Medullary Sponge Kidney and Effect of Potassium Citrate Treatment

“…In postmenopausal women, despite no apparent acidification defect, the administration of potassium citrate at approximately the same dosage as we used induced a significant increase in urinary citrate with a parallel significant reduction in the urinary calcium and bone reabsorption markers, together with an improvement in bone mass (25). In patients with idiopathic calcium urolithiasis, treatment with potassium citrate can reverse bone loss (26,27).…”

Diet-induced acidosis and alkali supplementation

“…High-protein-fed rats supplemented with K-citrate demonstrated an increase of bone mass and bone hystomorphology compared with control animals (Zerwekh et al 2009). A prospective study carried out on 109 patients (Vescini et al 2005) affected by idiopathic kidney stone disease indicated that the increase in bone mass was related to the administration of Kcitrate for two years (bone mass density 0.451 ± 0.081 versus 0.490 ± 0.080 g/cm 2 , T-score À1.43 ± 1.02 versus À0.90 ± 1.04). The authors concluded the increased bone density was directly correlated to cessation of the demineralization process, as urinary calcium excretion rate remained unchanged.…”

Potassium citrate prevents increased osteoclastogenesis resulting from acidic conditions: Implication for the treatment of postmenopausal bone loss

“…As an alternative, supplementation with alkalizing compounds has been suggested as a tool to limit the detrimental effect of acidosis and prevent bone loss [15]. Potassium citrate (K citrate) is a potassium salt of the citric acid that is used to increase the urinary pH, thus preventing the precipitation of solutes and the formation of kidney stones [16]. However, recent findings demonstrated that lithogenic risk factors are detectable also in postmenopausal women who exhibit osteopenia, but not urolithiasis, thus reinforcing the hypothesis that potassium citrate supplementation could have beneficial effects in preventing the bone loss progression [17].…”