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The nucleation field of calcium oxalate crystals (CaOx) was determined in urine at 37°C, in vitro, as a function of calcium [Ca] and oxalate [Ox] concentrations, and supersaturation β defined as a multiple of the thermodynamic solubility product of CaOx monohydrate. The diagram β = f[Ox] is clearly divided into two main fields by a curve above which CaOx crystals nucleate and grow. To each [Ox], corresponds therefore a minimal β below which nucleation does not occur. There is also a critical [Ox], about 0.16 mM, below which the nucleation of calcium oxalate crystals does not occur even at very large β values. We have next plotted, on the nucleation domain of CaOx defined in vitro, the individual calculated values of β and the measured [Ox] of 66 hypercalciuric stone formers. Fifty five percent of the patients were in the zone where nucleation has a high probability. After a calcium and oxalate restricted diet of respectively 400 mg/day and 40–70 mg/day, calciuria decreased while oxaluria and supersaturation either increased, decreased, or remained stable. Such variations allow to individualize patients with high or low lithogen risk.

Among the different mechanisms involved in calcium oxalate nephrolithiasis, idiopathic hypercalciuria is well documented and is of interest for therapy (1.2.3.4.). The role of hyperoxaluria in the genesis of these stones is suggested in some studies (5.6).

The authors discuss about thirty-five personal observations of intercapillary glomerulonephritis. In twenty-five cases hematuria was the initial finding. In most cases plasma complement and immunologic parameters were normal. In three observations segmentary and focal intercapillary lesions were seen while in the remaining cases lesions were diffuse. Immunohistochemical studies allow to determine two groups of intercapillary glomerular disease : in thirty cases (85%) mesangial IgA deposits existed as seen in Berger's disease : in five cases no IgA was detected but IgM and/or C'3 was present. Twenty-eight patients were followed during an average period of twenty-eight months. In ten cases initial symptoms regressed completely. Nine patients remained unchanged with no subsequent aggravation. Two patients developed renal insufficiency with hypertension and in one case the existing disease worsened. Although no therapy seems undeniably effective, systematic antibiotics during infections bouts preceded apparent regression of disease in one third of our patients.

Plasma acetate kinetics, acid-base homeostasis and clinical tolerance were monitored in 7 patients with chronic renal failure during and after hemodialysis with standard conditions. In 6 patients, without severe clinical symptoms acetate levels became stable during the last hour of dialysis (4.86 +/- 0.44 mmol/l) and decreased according to first order kinetics (half-life (8.82 +/- 3.42 mn). Simultaneously bicarbonate levels significantly increased (p less than 0.005). At the opposite the 7th patient has been characterised by a continuous rise in acetate levels (12.3 mmol/l at the end of the dialysis), a slower elimination (half-life: 31.0 mn), a collapse of plasma bicarbonate and severe acetate intolerance. Moreover symptomatic patients were characterised by an increase of plasma levels and half-lives. Therefore it seems that during dialysis of comparable efficiency, an insufficient rate of acetate metabolism may be at the origin of a worsening of metabolic acidosis as well as an increase of acetate load, responsible for severe acetate intolerance.

95 patients with essential uncomplicated hypertension were mostly submitted to measurement of plasma renin activity, plasma volume and exchangeable sodium. According to the results of the plasma renin activity, we noted variations in blood volume and exchangeable sodium in order to determine the best possible treatment based on these data. Single treatment, based either on diuretics or beta-blockaders was rarely sufficient to bring the blood pressure down to normal. Association of these two types of drug was often very useful. Finally, a critical study of these 3 parameters was made in an economic view of investigations of the blood pressure. The plasma volume seemed to us the most useful investigation, after which came the measurement of plasma renin activity. for the exchangeable sodium seemed of little interest.

The place of diuretics in the treatment of hypertension (HT) no longer requires to be proved, but their mode of action remains uncertain. Blood volume measurements allow us to distinguish the cases of HT which are volume-dependent, and which constitute the major indication for this type of treatment. The various groups of diuretics have a specific action on the renal tubule, but may all lead to complications, which imply that their use should be rational and that biochemical follow-up should be close when they are administered for a prolonged period. Used singly, diuretics effectively suppress HT in 40 per cent of cases, and when used in association with a beta-blocker, they produce normal blood pressure in 70 per cent of cases.

It is usually accepted1,2 hat magnesium ammonium phosphate (MgNH4PO4.6H2O) nucleates and grows only from infected alkaline urines. However, crystal growth experiments carried out in pure aqueous solutions3,4 show that nucleation, growth and also phase transition of struvite into newberyite (MgHPO4.3H2O) occur easily within the acid pH range. The aim of the present study is to check whether or not alkaline infected urines are really required for the crystallization of struvite.

Our study is an attempt to determine whether, after a vasculo-renal accident (VRA) in pregnancy, renal biopsy (RB) is of interest to determining the outcome specially of blood pressure. Starting from the 201 RB we systematically performed in such patients we may conclude: first, the onset of clinical and biological troubles do not allow to postulate the existing kidney lesions. Minimal changes observed in 31 women appeared early 9 times and during the last trimester 22 times. Most of the cases observed were preeclampsia (n = 108). The clinical or biological troubles were observed 44 times within the first months of the pregnancy and in 64 patients at the end of it. A specific group isolated concerns predominant vascular lesions (n = 44). Forward troubles were observed 16 times and 28 times during the third trimester. Second: a follow up has been possible for 1 to 5 years in 145 patients. A permanent hypertension occurred out of the 80 preeclamptic women, meanwhile among the 40 women with predominant vascular lesions, 60 p. 100 developed a permanent hypertension. Thus RB provides interesting data on renal lesions revealing sometimes (n = 18) a specific nephropathy (most of them were a glomerulopathy). Furthermore predominant vascular lesions suggest hypertension to recur in later pregnancy or become permanent.

Eighteen hemodialysed patients having a plasma calcium level of 2 mmol/l or less were treated by 1-alpha-OH-D3 at a mean dose of 1.56 microgram per day for six to twelve months. Calcium levels rose significantly. The concomitant rise in phosphorus levels required large doses of aluminum hydroxide. Alkaline phosphatase and parathormone levels were significantly lowered. Seven patients had calcium levels above 2.75 mmol/l and subsequently developed metastatic calcifications. Therefore plasma calcium levels should be carefully monitored during treatment and maintained at normal levels. In twelve cases bone histomorphometric studies were done. When bone demineralization is a prominent feature, satisfactory osteoid tissue mineralization can be obtained, while bone resorption remains unchanged.

Urinary excretion of oxalate plays an important role in the formation of calcium oxalate crystals1 and stones2. Elevated oxaluria has been observed in stone-forming patients with hypercalciuria3,4. This hyperoxaluria might be explained by an increase in the intestinal absorption of calcium leading to a decrease in the intestinal concentration of calcium thereby reducing the complexation of calcium with oxalate and favouring the intestinal absorption of oxalate5.