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Biomedical subjects

J G Ledingham

Publications and source records attributed to J G Ledingham.

At least 145 records · Page 8Linked to original sources
PubMed1972

Effects of haemodialysis on bone in chronic renal failure.

Quantitative histological studies have been done on 80 sequential bone biopsies taken at yearly intervals from 37 patients with chronic renal failure on long-term haemodialysis treatment. Twenty-three patients were studied at the start of dialysis, and in about half the bone was abnormal. During dialysis mean osteoid area and the maximum number of unmineralized osteoid lamellae increased, and mineralized bone area decreased. The loss of bone during dialysis was also reflected in reduction of the width of individual trabeculae. These trends were less obvious in patients already established on dialysis at the time of the initial biopsy. The course of osteitis fibrosa appeared to be unaffected by dialysis.

Adult↗
PubMed1971

Comparative double-blind trial of cephalexin and ampicillin in treatment of urinary infections.

Cephalexin was compared with ampicillin in the treatment of urinary tract infections by a random double-blind technique. Both drugs were found to be equally effective. In 21 out of 31 patients treated with cephalexin and in 20 out of 31 treated with ampicillin the urine was sterile three weeks after starting therapy. The bacteriological findings at one and eight weeks were also similar in both groups. No serious adverse reactions were attributable to cephalexin, which seemed to be tolerated rather better than ampicillin.

Adult↗
PubMed1970

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects.

The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen. Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion. The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis. In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure. The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance. These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an intrarenal action of potassium ions to modify renin release. Potassium might modify renin secretion directly by acting on the juxtaglomerular cells or by a change in its tubular reabsorption or secretion. The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport.

Adult↗