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PubMed1978

Antacid-induced osteomalacia and nephrolithiasis.

A 36-year-old woman suffered from bone pain, muscle weakness, and renal stones after prolonged ingestion of antacids for esophageal reflux. Investigation disclosed hypophosphatemia, hypercalciuria, and osteomalacia by bone biopsy. All symptoms and abnormal laboratory findings reversed with a regimen of oral phosphate supplementation and cessation of antacid intake.

Adult↗
PubMed1978

Kinetics of early time calcium oxalate nephrolithiasis.

This paper examines the kinetics of calcium deposition in rat kidneys after an intraperitoneal sodium oxalate injection. From the results we conclude that only a limited portion of tubular surface is available for adsorption of calcium oxalate crystals, that adsorpption of calcium oxalate crystals onto tubular epithelium is a process of greater than first order with regard to the dose, and that the washout of retained particles from the tubules is a first-order process as related to time. Also, we conclude that in these animals, which were subjected to a large oxalate challenge, the deposition of calcium oxalate crystals is virtually all intratubular.

Animals↗
PubMed1983

[Idiopathic calcium nephrolithiasis: therapeutic aspects].

The 75% of the renal stone formers have a so-called idiopathic calcium urolithiasis. The majority of these patients, however, do have a detectable biochemical disorder such as hypercalciuria, hyperuricosuria or hyperoxaluria. A high fluid intake unequivocally represents the first step in the therapeutic approach to these patients. Nevertheless, the detection of any type of biochemical disturbance is of great importance since the addition of a specific therapy will then become possible. Patients with absorptive idiopathic hypercalciuria will be advised to decrease their intake of dairy products as a function of the degree of calcium hyperabsorption, and simultaneously the major dietary sources of oxalate such as chocolate, spinach, rhubarb and asparagus will be eliminated; neutral orthophosphates (3-4 times 500 mg/d) or a thiazide, resp. an analogue as chlorthalidone (50 mg/d) are reasonable alternatives. Renal idiopathic hypercalciuria should be treated, according to the authors, with chlorthalidone (50 mg/d), with or without allopurinol (300 mg/d) depending on the presence of concomitant hyperuricosuria. Patients with dietary idiopathic hypercalciuria should be advised to better equilibrate the various components of their dietary intake. Finally, patients with isolated idiopathic hyperuricosuria whose disease would remain active despite a high fluid intake should receive allopurinol (300 mg/d). The treatment of isolated idiopathic hyperoxaluria is not yet well established. Two main arguments favor this so to say "tailored" approach to the idiopathic stone former: first, some metabolic disturbances are causally related to a particularly active and severe urolithiasis, whereas others are less so; second, the lack of efficacy of some types of treatment appears more and more to be due to insufficient screening of the patients before starting a given treatment.

Calcium↗