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Biomedical subjects

E Rotenberg

Publications and source records attributed to E Rotenberg.

27 records · Page 2Linked to original sources

Response to frusemide in acute renal failure: dissociation of renin and diuretic responses.

Eight hypertensive children with acute post-streptococcal glomerulonephritis were given intravenous frusemide, 2 mg/kg, and the results compared with 8 similar cases not given the diuretic. Mean urine flow increased from 0.24 ml/min/m2 before frusemide to 3.63 ml/min/m2 in the 6 hours afterwards and was still 0.72 ml/min/m2 48 hours later. In contrast mean urine flow remained unchanged over 48 hours in those not given frusemide. Despite similar initial blood pressures the duration of hypertension was much shorter (mean 4.7 days) after frusemide than in the controls (mean 11.0 days) and the edema-free weight was achieved more rapidly (6.8 days compared with 13.9 days). Plasma renin activity (PRA) did not rise after frusemide in the children with acute nephritis. This was in contrast to the rapid rise seen in normal humans thus indicating a dissociation between the diuretic and renin-releasing activities of frusemide in acute nephritis. Seven children with the hemolytic-uremic syndrome or acute tubular necrosis showed no significant change in either urine flow or PRA after frusemide. Frusemide is therefore effective treatment for both hypertension and oliguria in acute nephritis. Failure of PRA to rise indicates that renin release mechanisms are abnormal in renal failure and that PRA levels need to be interpreted with caution in this condition.

Acute Kidney Injury↗

Renin release by parathyroid hormone in the dog.

Synthetic N-terminal 34 amino acid peptide of bovine parathyroid hormone (PTH) produced a consistent rise in plasma renin activity in saline-loaded dogs when given iv either as a single bolus dose of 400 U or infused steadily in lower dosage over a number of hours. Infusion of as little as 1 U/min produced a significant rise in plasma renin activity, but a greater effect was obtained with 2 U/min. Infusion of 4 U/min had no more effect than 2 U/min. In contrast to transient hypotension after rapid injection of a single large dose, blood pressure did not change significantly during the steady infusion of lower doses of PTH. These findings are compatible with the thesis that an increased distal tubular load of sodium stimulates renin release and suggest that the increased distal sodium absorption after the proximal effects of PTH may be regulated by the renin-angiotensin-aldosterone system.

Animals↗

Diphosphonate therapy in nephrocalcinosis.

4 patients with nephrocalcinosis were treated with disodium ethane 1-hydroxy-1, 1-diphosphonate (EHDP) for a period of 13 months. No clinical side-effects were observed and growth proceeded normally. Radiographic changes of osteitis fibrosa cystica developed in 1 child and bone biopsy in 2 children showed defective osteoid mineralisation. It is suggested that EHDP prevented further crystal deposition in 3 children but did not prevent non-calcium stone formation in the 4th child. In view of this and the development of histological and radiographic evidence of osteomalacia and/or secondary hyperparathyroidism in these patients the value of EHDP remains dubious. On the other hand its use may be justified when rapidly increasing calcification is expected, as for example in hyperoxaluria.

Bartter Syndrome↗

Effect of parathyroid extract on renin release in the dog.

1. A rapid increase in plasma renin activity occurred in dogs after intravenous administration of parathyroid extract. 2. This was not seen after injection of a purer parathormone preparation, or the solution used to dilute the parathyroid extract or calcitonin. 3. A vasoactive compound in parathyroid extract appears to provide the most likely explantation of this effect.

Animals↗