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

• Published in: Biomedicine & pharmacotherapy 1999-06, Vol.53 (5), p.264-273
• Main Authors: Herrmann, U., Schwille, P.O., Schmiedl, A., Fan, J., Manoharan, M.
• Format: Article
• Language: English
• Subjects: acute oral load; Adult; Biological and medical sciences; Biological Availability; Blood Gas Analysis; Calcium - metabolism; Calcium Citrate - adverse effects; Calcium Citrate - pharmacokinetics; Calcium Citrate - therapeutic use; Calcium Oxalate - urine; calcium oxalate crystallization; calcium sodium citrate; Drug toxicity and drugs side effects treatment; Female; General and cellular metabolism. Vitamins; Homeostasis - drug effects; Humans; intestinal absorption; Male; Medical sciences; Middle Aged; mineral homeostasis; Minerals - metabolism; Oxalates - metabolism; Pharmacology. Drug treatments; renal stone patients; Toxicity: urogenital system; Urinary Calculi - blood; Urinary Calculi - drug therapy; volunteers
• ISSN: 0753-3322; 1950-6007
• DOI: 10.1016/S0753-3322(99)80097-3

Calcium, in the form of regular food supplementation, can improve bone metabolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these two aspects, ten healthy volunteers were given a conventional test meal (breakfast; calcium content 28 mg) with or without two dosages of calcium (as calcium-sodium citrate, CSC 1,680 mg; CSC 2 1,360 mg), taken after an overnight 12 h fast. To study the latter aspect, patients with idiopathic recurrent calcium urolithiasis (ICU) received a balanced test meal of fixed composition, containing 1,000 mg calcium either as CSC (Meal + CSC3; n = 6) or as calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate absorption; in serum, CSC increased calcitonin and suppressed parathyroid hormone, 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 crystallization. In ICU, the CSC3 load failed to promote the crystallization of CaOx and 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 forming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis of renal stones would appear justified.