[Complement and alpha l-antitrypsin after renal transplantation].
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Biomedical subjects
Publications and source records attributed to J Hodler.
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The clinical, biochemical and radiological signs of uremic osteopathy in 25 patients dialyzed at the dialyzing unit of the Medical Policlinic of the University of Berne are described. Comparison, mainly of radiologic signs, with the published experience of other centers shows a relatively high frequency of nonsymptomatic osteopenia and metastatic and vascular calcifications in our patients, even though their serum calcium and phosphorous concentrations were kept relatively normal. The frequencies of radiologic alterations in other dialyzing units reported in the literature differ widely from one center to another; this may be due to different technology, but even more to varying evaluation of the findings by different radiologists.
1. In a retrospective study the serum concentrations of calcium and phosphate and the activity of serum alkaline phosphatase in 54 epileptic patients treated by a variety of antiepileptic drugs (group A) were compared with those in 54 non-epileptic control patients (group B). Group B was chosen by computer to assign to each epileptic one control patient of identical sex and age. Patients affected by kidney or liver diseases were excluded from the study. 2. The data showed significantly lower calcium and phosphate concentrations and a higher activity of alkaline phosphatase in group A. Serum phosphate, but not calcium, was inversely correlated to the activity of serum alkaline phosphatase. 3. A minority of the epileptic patients were treated either by diphenylhydantoin or phenobarbital. The serum calcium tended to be lower under the former drug. The combined intake of both drugs produced no further hypocalcemic effect.
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The examples of tubular proteinuria, postobstructive diuresis, tubular function in terminal renal failure and the hereditary defects of tubular transport mechanisms are used to demonstrate the difficulty in elucidating defects of renal membrane transports in man. She is caused by the impossibility of applying the appropriate techniques to evaluate membrane functions in man and by the complexity of human disease. The rapidly growing knowledge of physiologic membrane functions in the kidney should however enable some progress in the field of human pathophysiology in a not too remote future.
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