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Biomedical subjects

A Rapoport

Publications and source records attributed to A Rapoport.

At least 109 records · Page 6Linked to original sources
PubMed1975

Excretion of inhibitors of calcification in urine. Part I. Findings in control subjects and patients with renal stones.

The total excretion of inhibitors of in vitro calcification was measured (in inhibiting units per day) in 24-hour urine samples of 11 control subjects and 20 patients with renal calculi. A semiquantitative method incorporating the rachitic rat cartilage technique was used. In both groups there was a significant positive correlation between the number of inhibiting units per day and the daily urine volume. The mean number of inhibiting units per day was significantly (P smaller than 0.05) higher in the stone patients than in the controls. However, the stone-formers had significantly larger (P smaller than 0.01) 24-hour urine volumes. When corrections were made for urine volume there was no significant difference between the two groups. These data suggest that the underlying abnormality responsible for renal stone formation is not a persistent decrease in the total concentration of urinary inhibitors of calcification.

Adult↗
PubMed1975

Excretion of inhibitors of calcification in urine Part II. Findings in patients with chronic renal failure.

By means of a semiquantitative method incorporating the rachitic rat cartilage technique, the total urinary inhibitory activity with respect to calcification was compared in 11 control subjects and 20 patients with renal failure. The patients had significantly lower mean values of inhibiting units per day than did the control subjects. Both groups showed a significant positive correlation between the number of inhibiting units per day and urine volume. When urine volume was taken into account in the comparison, the numbers of inhibiting units for patients continued to be lower than the numbers for controls. These findings are consistent with the hypothesis that the increase of inhibitory activity observed in uremic serum is secondary to a decrease in excretion of the responsible factor (or factors) in the urine, and that the factor (or factors) in serum responsible for the inhibition are identical to those in the urine.

Adult↗
PubMed1974

Contrasting effect of hemodialysis and peritoneal dialysis on the inhibition of in vitro calcification by uremic serum.

Our findings support the earlier observation of Yendt, Connor and Howard that uremic serum inhibits the calcification of rachitic rat cartilage in vitro. We also confirmed their studies showing that this inhibition is not the consequence of increased levels of serum magnesium or blood urea. In addition, we have shown that aqueous solutions of creatinine and uric acid in concentrations up to 20 mg./100 ml. do not cause any inhibition.Hemodialysis of uremic patients does not change the inhibitory activity of their blood. In contrast, after 24 hours of peritoneal dialysis, the blood of most patients does not inhibit calcification.The inhibitory activity of uremic serum, observed in vitro, may be important in the pathogenesis of osteomalacia in patients with renal failure. Failure of hemodialysis to alter this activity may contribute to the progression of renal osteodystrophy in patients on maintenance hemodialysis.

Adolescent↗
PubMed1971

Plasma calcitonin in renal osteodystrophy.

Whether calcitonin plays a significant role in the pathogenesis of renal osteodystrophy is not known. Plasma calcitonin-like activity (CLA) was measured by means of an extraction procedure and bioassay in 17 patients with chronic renal failure. Recent bone biopsy data were available for 11 patients. Plasma CLA was found to be in the normal range in the patients studied. There was a positive and strong correlation between plasma calcium and plasma CLA. Chronic dialysis and renal transplantation had no significant effect on plasma CLA. The severity and type of bone lesions did not correlate with plasma CLA. Although plasma calcitonin in chronic renal failure does not appear to be directly related to renal osteodystrophy, normal mobilization of calcitonin may protect the skeleton to some degree from the high levels of parathyroid hormone usually present in such patients.

Adult↗