Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans - Preliminary results in patients with idiopathic calcium urolithiasis

Calcium, in the form of regular food supplementation, can improve bone meta bolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these t wo aspects, ten healthy volunteers were given a conventional test meal (bre akfast; calcium content 28 mg) with or without two dosages of calcium (as c alcium-sodium citrate, CSC 1, 680 mg; CSC 2 1,360 mg), taken after an overn ight 12 h fast. To study the latter aspect, patients with idiopathic recurr ent calcium urolithiasis (ICU) received a balanced test meal of fixed compo sition, containing 1,000 mg calcium either as CSC (Mcal + CSC3; n = 6) or a s calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate abs orption; in serum, CSC increased calcitonin and suppressed parathyroid horm one, but left unchanged the markers of bone turnover, serum osteocalcin and bone alkaline phosphatase. In urine, CSC decreased bone resorption markers (collagen crosslinks) and phosphaturia increased citrate, created signs of metabolic alkalosis, and inhibited several parameters of CaOx crystallizat ion. In ICU, the CSC3 load failed to promote the crystallization of CaOx an d calcium phosphate. It was concluded that CSC supplementation of a meal: ( 1) is well tolerated by healthy subjects and ICU patients, renders calcium highly available to bone, and prevents post-prandial oxaluria from rising; and, (2) is followed by the inhibition of crystallization of renal stone fo rming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis o f renal stones would appear justified. (C) 1999 Elsevier, Paris.