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Biomedical subjects

A Ulmann

Publications and source records attributed to A Ulmann.

At least 109 records · Page 6Linked to original sources

[Medical treatment of calcium nephrolithiasis (author's transl)].

Calcium calculi are by far the most frequent of urinary stones. In many cases their formation is enhanced by lithogenetic abnormalities, including idiopathic calciuria. The basis of the treatment is to promote diuresis by absorbing for an indefinite period a mineral water containing less than 100 mg/l of calcium. There is no evidence that drugs reducing calciuria (thiazides, phosphorus) or uraturia (allopurinol) are effective, and they should be reserved to cases of rapidly progressive lithiasis. A long-term strategy for the prevention of lithiasis is discussed.

Calcium↗

Effects of weight and glucose ingestion on urinary calcium and phosphate excretion: implications for calcium urolithiasis.

Renal handling of phosphate and calcium was studied in 17 hypercalciuric stone-formers, 6 normocalciuric stone-formers and 10 normal subjects before (fasting state) and 45 and 75 min after the ingestion of 100 g glucose. The ratio of fasting urinary calcium to creatinine (UCa/creat) was higher in hypercalciuric than in normocalciuric stone-formers or controls. A positive correlation was found between weight index and fasting UCa/creat for all subjects studied (r = 0.36; P less than 0.05). A negative correlation was apparent between the weight index and the fasting renal threshold phosphate concentration (TmP/GFR) (r = 0.40; P less than 0.02), the latter parameter being slightly but insignificantly lower in hypercalciuric stone-formers than in controls. After glucose ingestion. UCa/creat rose significantly in all groups. The maximal rise in UCa/creat was also positively correlated with the weight index for all patients ( r = 0.42; P less than 0.02), and 75 min after glucose ingestion, TmP/GFR decreased in all groups, dropping to a significantly lower level in the hypercalciuric patients than in the controls. No correlation was apparent between the weight index and the magnitude of the reduction in TmP/GFR. Plasma 1, 25-dihydroxyvitamin D3 and immunoreactive parathyroid hormone were measured before glucose ingestion and were not correlated either with each other or with plasma phosphorus, TmP/GFR, or UCa/creat before or after glucose ingestion. These results imply that weight is a determining factor in the renal handling of calcium and phosphorus. Such findings might be of importance to the clinical investigation and management of calcium stone-formers.

Adult↗

Enzymic measurement of urinary pyrophosphate with a centrifugal analyzer.

We describe a simple, rapid, and fully automated technique for measuring urinary pyrophosphates with a centrifugal analyzer (the ENI GEMSAEC). This technique depends on the enzymic magnesium-dependent reaction with UDPG pyrophosphorylase (UTP: alpha-D-glucose-1-phosphate uridylyl transferase, EC 2.7.7.9) and spectrophotometry of the NADPH formed in a combined system of phosphorylation and reduction. Many samples of urine can be analyzed quickly without pretreatment, with high sensitivity (1.3 mA/mumol of substrate) and good reproducibility. The mean within-run coefficient of variation for a 50 mumol/L pyrophosphate solution was 1.4%. We determined the optimum enzyme and magnesium concentrations necessary for use in a 4-min reaction. Because there is no inhibitory effect of chloride and phosphate ions, pyrophosphate can be measured directly in urine, without prior extraction. With this technique, the mean value (and SD) for urinary pyrophosphate excretion by 30 healthy subjects was 39.3 (SD 17.2) mumol/24 h.

Autoanalysis↗

Early effects of 1 alpha,25-dihydroxy-vitamin D3 on phosphate absorption. A role for alkaline phosphatase?

Using ex vivo perfused intestinal loop from vitamin D-deficient rats, we studied the lumen-to-vein transport of 32Pi in intestines perfused intraluminally with [gamma-32P] ATP, [alpha-32P] ATP or 32Pi, and infused through their vascular connections with either 1,25(OH)2D3 (6nM) or ethanol vehicle. For intestines perfused with [gamma-32P] ATP in which the gamma-32P is easily liberated by alkaline phosphatase, 1,25(OH)2D3 infusion resulted in a significant and early (15 min) increase in net lumen-to-vein 32Pi transport. Pretreatment of rats with levamisole, an inhibitor of alkaline phosphatase, partially inhibited such 32Pi transport. For intestines infused with [alpha-32P] ATP, the lumen-to-vein transport of 32Pi did not differ in 1,25(OH)2D3-treated and in control intestines. For intestines perfused with 32Pi, 1,25(OH)2D3 infusion resulted in an early (15 min) increase in lumen-to-vein transport of 32Pi. It is concluded that 1,25(OH)2D3 rapidly stimulates intestinal Pi transport both directly and also by increasing inorganic phosphate content inside the intestinal lumen. The latter effect probably involves 1,25(OH)2D3-stimulated alkaline phosphatase activation.

Adenosine Triphosphate↗

[Vitamin D metabolites in a new case of drug-induced hypercalcemia (author's transl)].

The authors report on a new case of severe hypercalcaemia induced by prolonged oral treatment with high doses of vitamin D2. (6 mg/day for 9 months). Blood calcium level did not return to normal until 6 months after the drug was discontinued. The plasma concentration of 25 (OH) D was more than three times the normal value and remained very high throughout the observation period. The plasma concentration of 24, 25 (OH)2 D was slightly raised during treatment but became normal after 15 days, while that of 1,25 (OH)2 D, the active form of vitamin D, remained normal throughout, suggesting that the pathogenesis of vitamin D-induced hypercalcaemia is probably complex.

25-Hydroxyvitamin D 2↗

[Isolated dissection of the renal artery. A rare cause of arterial hypertension (author's transl)].

During aetiological investigation of recently developed hypertension in a 31-year-old man, isolated dissection of the upper branch of the right renal artery was discovered. Injection, after sodium depletion, of saralasin, a competitive angiotensin II inhibitor, resulted in significant fall of the mean arterial pressure. During sodium depletion, the plasma renin activity was higher in the right renal artery (17.8 ng/ml/h) than in the left artery (9.4 ng/ml/h) and the infra-renal portion of the inferior vena cava (8.7 ng/ml/h). These figures suggested that surgical treatment of the dissection would have beneficial effects on blood pressure. Six months after resection of the pathological arterial segment and replacement by a graft from the internal saphenous vein, blood pressure had spontaneously returned to normal levels.

Adult↗

[Measurement of plasma 1,25 dihydrovitamin D. Normal and pathological values in adults (author's transl)].

Plasma levels of 1,25 dihydrovitamin D (1,25 (OH)2D) were measured in normal subjects and in patients with various diseases, using a radiocompetition method. Mean values of 89 +/- 58 pmol/l (1 s.d.) were found in normal adults, irrespective of sex. Plasma 1,25 (OH)2D values were high in 12/31 patients with lithiasis and hypercalciuria, in 1/7 patients with lithiasis and normal calciuria and in 2/4 patients with idiopathic parathyroid adenoma; they were normal in 2 patients with essential hypoparathyroidism. 1,25(OH)2D was undetectable in 5 patients with chronic renal failure, low in 7 and normal in 4. Following successful kidney transplantation (serum creatinine less than 120 mumol/l) one-half of the patients had normal values and the other half high values.

Calcitriol↗

Changes in plasma 1,25 and 24,25-dihydroxyvitamin D after renal transplantation in children.

The purpose of this investigation is to analyze changes in plasma 1,25-(OH)2D and 24,25-(OH)2D after successful renal transplantation in 20 children and young adults. Studies were performed on 8 subjects between the 1st and 10th month and on 12 others between the 20th and 30th to 36th month. Samples were assayed for plasma and urinary calcium, inorganic phosphate, creatinine, plasma bicarbonate, immunoreactive parathyroid hormone, 25-(OH)D, 24,25-(OH)2D, and 1,25-(OH)2D concentrations. Results showed the following: (1) All subjects had normal or high plasma levels of dihydroxyvitamin D metabolites. (2) In subjects with normal GFR's there was a significant inverse correlation between plasma 1,25-(OH)2D concentrations and tubular reabsorption of phosphorus. (3) These correlations were not found in subjects with subnormal creatinine clearances (50 to 100 ml/min/1.73 m2) even though plasma 1,25-(OH)2D concentrations in these subjects were similar to those with normal creatinine clearances. (4) In subjects with subnormal creatinine clearances, an increase in plasma 1,25-(OH)2D concentrations to very high levels was observed during the first months following renal transplantation.

24,25-Dihydroxyvitamin D 3↗

Human parathyroid gland adenylate cyclase activity: inhibition by 24,25-dihydroxycholecalciferol in vitro.

1. Plasma membranes were prepared from parathyroid adenomas in patients with primary hyperparathyroidism and from hyperplastic glands obtained from patients with chronic renal insufficiency. The basal and isoproterenol- or sodium fluoride-stimulated adenylate cyclase activities were measured in membranes in the presence of several vitamin D3 metabolites. 2. 24,25-Dihydroxycholecalciferol (10 and 1000 pmol/l) decreased isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in membranes prepared from parathyroid glands. 1,25-Dihydroxycholecalciferol (1000 pmol/l) inhibited the isoproterenol-stimulated adenylate cyclase activity. 25-Hydroxycholecalciferol and vitamin D3 had no effect on adenylate cyclase activities. Basal adenylate cyclase activity was not affected by any of th vitamin D3 metabolites tested. 3. These results indicate that 24,25-dihydroxycholecalciferol inhibits the isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in parathyroid tissues. Such an inhibition could explain the very rapid decrease in parathyroid hormone secretion after 24,25-dihydroxycholecalciferol administration that has been previously reported.

24,25-Dihydroxyvitamin D 3↗

[Compared metabolic effects of phosphorus or hydrochlorothiazide therapy in hypercalciuric stone-formers (author's transl)].

The hypocalciuric effect of phosphorus or hydrochlorothiazide therapy was evaluated in 26 hypercalciuric stone-formers after 2 to 4 months and 8 to 12 months treatment. After 2 to 4 months, a significant decrease of the urinary calcium to creatinine ratio was noted only in a group of 7 patients receiving phosphorus supplementation (1500 mg/day). The decrease was transient however, since in 5 of these patients, the calcium to creatinine ratio was found to be at pretreatment levels when the patients were reinvestigated after 8 to 12 months on phosphorus. In contrast, in 8 patients receiving hydrochlorothiazide (50 mg/day) during 8 to 12 months, this ratio was significantly lower (P less than 0.01) than before treatment. A group of patients maintained on high water intake alone for 8 to 12 months served as a control and no modification in calcium excretion was observed. This study indicates that long-term treatment with hydrochlorothiazide is more efficient in lowering urinary calcium excretion than phosphorus therapy.

Calcium↗

Renal parathyroid hormone-dependent adenylate cyclase in vitamin D-deficient rats. Inhibition by hydroxylated vitamin D3 metabolites.

The adenylate cyclase activation by bovine synthetic parathyroid hormone (bPTH) (1-34) was studied in vitro in kidney plasma membranes from D-deficient (D-Mb) or normal (D+Mb) rats. In D-Mb, the apparent affinity of parathyroid hormone (PTH) for membranes (170 +/- 30 nM) was significantly higher than that measured in D+Mb (55 +/- 5 nM). The maximum velocity of the PTH-stimulated adenylate cyclase was significantly higher in D+Mb than in D-Mb (163.0 +/- 13.7 and 93.4 +/- 6.7 pmol of cAMP/mg of protein/min, respectively). The action of vitamin D metabolites on the adenylate cyclase stimulation by PTH was then studied in vitro in D-Mb and D+Mb. In D-Mb, 25-hydroxyvitamin D3, 24,25-, and 1, 25-dihydroxyvitamin D3 significantly inhibited cAMP production in the presence of 0.87 microM of bPTH. Vitamin D3 had no effect. Maximal inhibition (86%) was observed for 1,25-dihydroxyvitamin D3. 1,25-Dihydroxyvitamin D3 decreased the maximum velocity of PTH-stimulated adenylate cyclase but did not modify the bPTH apparent affinity for D-Mb. The vitamin D3 metabolites tested did not modify the cyclase stimulation by isoproterenol, sodium fluoride, or 5'-guanylylimidodiphosphate. The presence of 1,25-dihydroxyvitamin D3 or 25-hydroxyvitamin D3 did not increase the (Na-K)-ATPase or the phosphodiesterase activities. In the presence of 1,25-dihydroxyvitamin D3 and bPTH, the apparent affinity of ATP for the catalytic moiety was not modified. The maximum velocity was decreased. These results suggest an in vitro interaction between hydroxylated vitamin D metabolites and kidney membranes PTH receptor.

24,25-Dihydroxyvitamin D 3↗

[An unrecognised cause of hypercalcaemia: hypercalcaemia-hyocalcluria syndrome].

A 32-year-old man with insulin-dependent diabetes secondary to chronic calcifying pancreatitis of alcoholic origin in whom hypocalciuria (22 to 88 mg/24 hours) was discovered by chance, renal function being normal. Plasma phosphate levels were between 25 and 35 mg/l and the level of parathyroid hormone was at the upper limit of normal. Cervicotomy led to the discovery of three parathyroid glands which were removed. Their weight was increased and their histological appearance normal. The fourth parathyroid was not seen. Hypercalcaemia and hypocalciuria were found during the operation and persis 3 years after, with none of the usual causes being found. This patient has a certain number of characteristics reminiscent of familial hypercalcaemia-hypocalciuria syndrome: high plasma calcium levels associated with low calciuria despite normal renal function and a plasma parathyroid level normal in most cases. The physiopathology of this syndrome remains unknown. Its course is benign, without renal complications. Partial parathyroidectomy is ineffective.

Adult↗

Plasma vitamin D metabolites in a patient with sporadic hypophosphataemic osteomalacia (adult-onset type).

Sporadic hypophosphataemic osteomalacia (adult-onset type) was demonstrated in a 40-year-old man on the basis of severe osteomalacia, hypophosphataemia, hyperphosphaturia and glycinuria. Plasma immunoreactive parathyroid hormone (iPTH) concentration was 9.3 ng prot./ml (normal range: 4-8 ng prot./ml). Plasma 25-hydroxy-vitamin D and 24,25-dihydroxy-vitamin D concentrations were 11 and 2.4 ng/ml respectively. Basal 1 alpha,25-dihydroxy-vitamin D concentrations were slightly elevated (116 and 96 pg/ml) and increased to 240 pg/ml after 3 days on a low-phosphorus diet. The patient was put on oral treatment with 25-hydroxycholecalciferol (100 microgram per day) and phosphorus (1500 mg per day). On the 4th month on treatment, a clinical improvement was apparent. Plasma 25(OH)D was 44 ng/ml, plasma 1,25(OH)2D was 256 pg/ml. However, plasma phosphorus remained low (0.77 mmol/l). On the 9th month of treatment a radiological improvement was evident despite a persistent hypophosphataemia (0.68 mmol/l). These facts suggest in our patient the existence of a vitamin D-independent renal phosphorus leak.

Adult↗