Biomedical subjects
Publications and source records attributed to P Bataille.
In this review article the various steps and local mechanisms of stone formations are summarized. Then the pathophysiology of the various risk factors namely urinary excretion of calcium, oxalate, uric acid, urine volume, urine pH and urinary inhibitors of stone formation is extensively discussed.
Between 1 January 1976 and 31 December 1986, primary glomerulonephritis was histologically diagnosed in 319 patients, living in a region of 675,000 inhabitants at the time of renal biopsy. The prevalence of primary glomerulopathy was 0.4/1000 inhabitants. The annual incidence was determined during two 5 year periods: period A (1976-1980) and period B (1981-1985): they were, respectively, 3.4 and 4.5 for 100,000 inhabitants. Berger's focal glomerulonephritis was the most common (30 p. 100) and its incidence was increasing. In contrast, membranoproliferative and acute glomerulonephritides were sharply decreased (almost disappeared), while membranous glomerulonephropathies and glomerulopathies with minimal glomerular lesions or proliferative forms with crescents increased. All primary glomerulonephritides were more prevalent in men and their frequencies increased with age. Our findings lead to the following conclusions: a) the low prevalence and incidence of primary glomerulopathies (3 times less than in other published studies) probably reflect the under medicalization of our region and the attractiveness of neighbouring metropolis, rather than a real decrease in the disease; b) the quasi- disappearance of acute and membranoproliferative glomerulonephropathies and the high incidence of IgA glomerulonephropathies suggest that their pathogenetic associations with infections sensitive to antibiotics are different; c) the increased frequency of membranous glomerulonephropathy and the glomerulopathy with minimal glomerular lesions in aged subjects is most likely due to their polymedication.
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27 patients on hemodialysis (dialysate aluminium less than 0.7 mumol/l for 2 years, and 2 mumol/l before) whose plasma Ca and PO4 were adequately controlled for already 6 months by high doses of CaCO3 alone (mean +/- SD: 9 +/- 5 g/day), were randomly divided into 2 groups, a control group (c group) which was kept on the same treatment, and a group in which CaCO3 was reduced to 3 g/day but in which plasma Ca was kept normal due to 1 alpha-OH-vitamin D3 administration (1 microgram/day at the beginning, 0.3 microgram/day after 6 months; 1 alpha group) whereas plasma phosphate was kept below 6.0 mg/dl because of Al(OH)3 (2.7-5 g/day). Initially, the 2 groups were comparable as regards the plasma concentrations of total and ionized Ca, phosphate, alkaline phosphatases, medium and C-terminal parathyroid hormone (PTH) and aluminium, but the control group had lower plasma 25-OH-vitamin D (25-OHD.) After 6 months, the same difference in plasma 25-OHD was found with comparable plasma concentrations of total and ionized calcium as well as of medium and C-terminal PTH (beta error 1%). However, plasma concentration of phosphate and the plasma Ca phosphate product, as well as the plasma aluminium were higher in the 1 alpha group whereas their PCO3H- was lower. Although the alkaline phosphatase values were not significantly different between the 2 groups, they increased only in the control group because of 1 patient who developed a vitamin-D-deficient osteomalacia (plasma 25-OHD 3 ng/ml), which was subsequently cured by physiological doses of 25-OHD3. The incidence of transient hypercalcemia (15 vs. 21 episodes) and worsening of soft tissue calcifications (3 in each group) was the same in the 2 groups.
The probability of being a stone former (PSF) was calculated in 3 groups of idiopathic calcium stone formers [with normocalciuria (NC), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH)] in 4 conditions: while on a free diet; on a calcium- and oxalate-restricted diet during 4 days; after an oxalate load, while on a 1.5-gram calcium diet, and after an oxalate load while on a calcium-restricted diet. Combined calcium and oxalate restriction significantly decreased PSF only in NC and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater during a calcium-restricted diet than during the 1.5-gram calcium diet in all groups of patients (4, 6 and 12 times greater in NC, DH and IH, respectively). These data show the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. This combined restriction is however not sufficient in idiopathic hypercalciuric patients to decrease their PSF.
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Calcium stones is responsible for 80 per cent of the stones in the upper track. It is a frequent and particularly recurrent disease and for this reason it is important to prevent its recurrence by medical treatment, dissolution of calcium stones being impossible. In the first part of this review, we have presented the theoretical basis and the clinical studies concerning conservative therapy involving high fluid intake and dietary advice on calcium and oxalate intake. Then, for the various drugs proposed for recurrence prevention we have reviewed their mechanisms of action and the controlled clinical trials concerning these drugs. Finally, the practical therapeutical choices for the management of these patients are presented according to the results of the previous metabolic evaluation.
Plasma magnesium (PMg) and urinary calcium (UCaV) and magnesium (UMgV) were measured after four days of calcium-restricted diet in 60 controls and 82 patients classified according to their calcium excretion in three groups: normo-calciuric (NCa), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH). When compared to controls, higher UMgV (4.26 +/- 0.28 mmol/d versus 3.4 +/- 0.16, p less than 0.01), lower PMg (0.79 +/- 0.01 mmol/d versus 0.84 +/- 0.01, p less than 0.05) and lower UMg/UCa ratio (0.6 +/- 0.04 versus 1.68 +/- 0.15, p less than 0.001) were observed only in IH. A significant correlation between UMgV and UCaV was found in controls, in NCa and in DH but not in IH. In conclusion, (1) the coexistence of a higher UMgV and of a lower PMg in IH suggests that there is a magnesium depletion in this group of patients; (2) since the lower UMg/UCa ratio may favour a higher propensity for calcium crystallisation and is seen only in IH, magnesium supplements may be specially indicated in this group.
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To evaluate the adequacy of simple calcium restriction for patients with idiopathic calcium stones the effect of 5 days of calcium restriction without oxalate restriction on renal excretion of calcium and oxalate, and the corresponding probability of stones were assessed in 50 controls and 48 patients. Renal excretion of calcium decreased and that of oxalate increased significantly in all groups but the importance of the changes was critically dependent upon the underlying pathophysiological condition. The probability of stones decreased only in patients with absorptive hypercalciuria type II owing to the usual excessive calcium intake and increased in those with absorptive hypercalciuria type I and renal hypercalciuria, which are associated with true hyperabsorption of calcium and represent the 2 forms of idiopathic hypercalciuria. We believe that simple calcium restriction is beneficial for patients with idiopathic calculi only when the hypercalciuria is caused by exaggerated intake of calcium, since it increases the probability of stones in patients with idiopathic hypercalciuria. Calcium restriction always is associated with an increase in oxalate excretion, suggesting that simultaneous oxalate restriction should be added in all cases to decrease the probability of stones.
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The probability of being a stone former (PSF) was calculated according to the method of Robertson in three groups of idiopathic calcium stone formers (normocalciuria (NCa), dietary hypercalciuria (DH) and idiopathic hypercalciuria (IH] during four conditions: on a free diet; on a calcium and oxalate restricted diet for four days and after an oxalate load (200 g of spinach) while on a calcium unrestricted or calcium restricted diet. Combined calciuria (Ca) and oxaluria (Ox) restriction significantly decreased PSF only in NCa and DH whereas the decrease was not significant in IH because of a concomitant significant increase in oxalate excretion. Increase of PSF with the oxalate load was significantly greater on calcium restricted than on calcium unrestricted diets in all groups of patients (4-6-12 times greater in NCa, DH and IH respectively). This shows the critical role of oxalate restriction when calcium is restricted in order to decrease the PSF. Combined restriction is not sufficient in idiopathic hypercalciuric patients to decrease their probability of stone formation.
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