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Biomedical subjects

J Aubia

Publications and source records attributed to J Aubia.

52 records · Page 3Linked to original sources
PubMed1985

Low incidence of hyperparathyroidism in diabetic renal failure.

The first study compared two groups on dialysis: 25 patients with diabetes mellitus and 25 matched non-diabetic patients, in relation to the presence of signs of hyperparathyroidism, to assess the reported low incidence of hyperparathyroidism in these patients. The diabetic group showed significantly lower values of PTH, Alk phosphatase, percentage of patients requiring vitamin D treatment, and less evidence of hyperparathyroidism on X-ray and in bone histomorphometry. In the second study 16 patients with chronic renal failure due to diabetic nephropathy were compared to 27 patients with the same degree of renal failure of other origin, the diabetic nephropathy group showed no increase in PTH, with falling creatinine clearance. Despite this low PTH, the phosphaturia was higher in the diabetic nephropathy group (Tm PO4/C Cr: 1.94 +/- 0.43 vs 2.5 +/- 0.68). In conclusion, patients with diabetes mellitus are less prone to develop hyperparathyroidism in progressive renal failure. This could be due to a relative increase in phosphaturia during declining function.

Diabetic Nephropathies↗
PubMed1980

Dialysis pruritus: effect of cimetidine.

The effect of oral Cimetidine compared to a classic antihistaminic and to a placebo was evaluated, under the double hypothesis of its anti-PTH and anti-pruritus action, in a population of patients recently included in Hemodialysis that were asked about the incidence and intensity of pruritus according to a scored questionnaire made for this purpose. No different efficacy of Cimetidine versus the antihistaminic classic and the placebo was observed in our study.

Cimetidine↗
PubMed1979

[Hemodialysis and complement (author's transl)].

After observing alterations in the activity of the serum complement in patients undergoing periodic hemodialysis, the authors performed a preliminary study to determine repeatedly the activity of C3, C4, and CH50 in 44 patients. They discovered a consistent drop in C3 and CH50 while C4 remained normal. An attempt to explain these findings with information from the literature offered no more than a hypothesis for further study. While the possibility of a decline in the synthesis of the complement factors cannot be disregarded, the authors believe it is much more probable that they are consumed at a rate higher than normal. Since the C4 factor does not appear to be involved, activation is probably along the alternative pathway. Defective synthesis cannot be attributed to liver disease because the latter is not always present and because there is no relationship between C3 levels and levels of albumin or the presence of hepatopathy. The literature was reviewed for data that might support the idea that the complements in these patients are activated continuously by some process in connection with dialysis, by chemical products employed for to clean the machines, by commonly administered drugs, etc. Because so few data could be found on the subject, the authors consider that is necessary to study these mechanisms and their repercussions over a longer period of time.

Acute Kidney Injury↗