1. Seventeen healthy controls and 63 patients with idiopathic calcium stone disease of the urinary tract were investigated for urinary calcium and oxalate excretion and for [14C]oxalate intestinal absorption. 2. Under comparable controlled dietary intake a significant increase in calcium excretion as found in patients with stone disease. Oxalate excretion and [14C]oxalate intestinal absorption were mildly but not significantly increased. When patients with stone disease were subdivided into normocalciuric and hypercalciuric subjects, oxalate excretion and [14C]oxalate absorption were significantly increased in the latter. There was a significant direct relationship between calcium excretion and both oxalate excretion and [14C]oxalate absorption. 3. [14C]Oxalate absorption increased significantly in 22 stone-formers when dietary calcium was changed from normal to low. 4. The kinetics of [14C]oxalate intestinal absorption showed that the main difference between normocalciuric and hypercalciuric subjects occurred within the first 6 h after the oxalate-labelled meal. 5. These results confirm that mild hyperoxaluria is a frequent feature of idiopathic calcium stone disease even when patients and controls are studied under controlled dietary conditions. Our data are consistent with the hypothesis that hyperoxaluria is secondary to calcium hyperabsorption and is upper intestinal in origin.
Antral somatostatin- and gastrin-producing cells (D and G cells) were studied in a group of patients with chronic renal failure (CRF) in comparison with a control group. Gastric acid secretion and serum gastrin, phosphate, and parathormone (PTH) levels were also evaluated in every patient. The group with CRF showed a mild increase both in G- and in D-cell denisty. In this group serum phosphate and PTH levels were higher than normal, showing hyperparathyroidism in every patient. A direct correlation was found between G-cell density and parathyroid function in patients with CRF. Hyperparathyroidism, therefore, seems to play a role in the mechanism of increased serum gastrin levels in CRF.
The Authors present their results on the intestinal absorption and renal handling of oxalate in normal subjects.The major hyperoxaluric syndromes -primary hyperoxaluria (hOx) , enteric hOx and mild hOx in idiopathic stone disease -are discussed. The results of studies in 20 enteric hyperoxaluric patients and 161 idiopathic calcium oxalate stone formers are reported, with special reference to the pathogenesis and treatment of these syndromes.Oxalic acid (Ox) is a strong organic acid (P~l= 1.2; P~2= 4.27) whose clinical importance derives from the very low solubility in biological fluids of its calcium salts, so that Ox is present in about 80% of the human urinary calculi. At the physiological urinary pH, Ox is virtually all in the dissociated form. Calcium oxalate (CaOx) solubility does not vary significantly from pH 5 through 7K sp , th CaOx H20 = 2.5 x 10-9 mo1 2 (T = 37° C) (8) Ksp , th CaOx 2H20 = 5.0 x 10-9 mo1 2 (T = 37° C) (3).
M. Pavone-Macaluso et al. (eds.), Advances in Nephrourology
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