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Biomedical subjects

R G Henderson

Publications and source records attributed to R G Henderson.

At least 37 records · Page 2Linked to original sources
PubMed1981

'Nephrotoxicity' and metabolic acidosis in transplant patients on cyclosporin A.

Renal function, as represented by serum creatinine and creatinine clearance, 18 to 24 months after renal transplantation was studied in 21 patients receiving Cyclosporin A and compared with that of 25 patients on corticosteroids and azathioprine. Although renal function at six months post transplantation was significantly poorer in those patients on Cyclosporin A compared with those on conventional therapy, it did not deteriorate with time. No significant alteration in renal function was observed in five hepatic transplant recipients on Cyclosporin A after three months. Lower serum bicarbonate was observed more frequently in those renal transplant recipients on Cyclosporin A than in those on conventional therapy, reflecting possible tubular damage.

Acidosis↗
PubMed1979

Cyclosporin A initially as the only immunosuppressant in 34 recipients of cadaveric organs: 32 kidneys, 2 pancreases, and 2 livers.

34 patients treated with cyclosporin A received 36 cadaveric organ allografts (32 kidneys, 2 pancreases, and 2 livers), 26 kidneys are still supporting life, 3 after more than a year; the pancreases and livers are also functioning. 20 patients are not receiving steroids, and 15 of these have not had any additional immunosuppressive agents. In these patients infectious complications have not been severe, but a gastroduodenal lymphoma has developed in 1 patient. 6 patients were given 'Cytimum' (a cyclophosphamide derivative) and steroids in addition to cyclosporin A: 5 of these died of infections and 1 also had a lymphoma. 11 patients received additional steroids: 1 of these died from septicaemia and lymphoma. Nephrotoxicity can be avoided by perioperative hydration and forced diuresis. Cyclosporin A is effective on its own and is a very potent immunosuppressive drug. Additional immunosuppressive agents may lead to severe complications.

Adult↗
PubMed1979

Variation in plasma prednisolone concentrations in renal transplant recipients given enteric-coated prednisolone.

Renal transplant recipients receiving intermittent haemodialysis and kept under normal ward conditions showed appreciable differences in plasma prednisolone concentrations after therapeutic doses of enteric-coated prednisolone tablets. This gross day-to-day variation occurred irrespective of the dosage used. Breakfast given before prednisolone tended to reduce the rate of absorption of the drug, the effect being quantitatively most pronounced with large doses. Haemodialysis had no apparent effect on the elimination of prednisolone from plasma. Such erratic blood concentrations of prednisolone as observed in these patients, possibly resulting from variable absorption, may be potentially hazardous. Hence use of enteric-coated tablets in renal transplant recipients should be viewed with caution.

Adolescent↗
PubMed1979

Severe acidosis from acetazolamide in a diabetic patient.

An insulin-dependent diabetic patient with nephropathy developed severe acidosis after treatment with acetazolamide for glaucoma. A renal tubular abnormality may have allowed the usually self-limiting acidosis of acetazolamide to progress. It is suggested that the plasma electrolytes of patients at risk should be monitored.

Acetazolamide↗
PubMed1979

Treatment of renal bone disease with 1 alpha-hydroxylated derivatives of vitamin D3. Clinical, biochemical, radiographic and histological responses.

Forty patients with severe bone disease and chronic renal failure were treated with 1 alpha-hydroxycholecalciferol (1 alpha-OHD3) or 1,25-dihydroxycholecalciferol (1,25(OH)2D3) for 7--49 months (total = 738 patient months). There were symptomatic, biochemical and radiographic improvements in the majority of patients (greater than 70 per cent). Paired bone biopsies, taken before and during treatment in 26 patients, showed no change in bone matrix area, whereas matrix area decreased in a control group of 26 patients over the same period. There were small but consistent decreases in bone marrow fibrosis and in bone cell (osteoblast and osteoclast) counts in treated patients but not in controls. However, the proportion of patients who showed histological 'cure', in the sense of complete reversal of marrow fibrosis or excess osteoid was no greater in the treated than in the control group...

Adolescent↗
PubMed1978

The position of the nutrient foramen in the growing tibia and femur of the rat.

In rats of 40, 49 and 59 days of age the positions of the femoral and tibial nutrient foramina were determined by direct measurement, using a travelling microscope. The femoral nutrient foramen remained constant in position with increasing age, whereas the tibial nutrient foramen moved relatively nearer to the distal end of the shaft. In the case of the femur this can be accounted for entirely by differences in growth rates at the epiphyseal plates of the femur compensating for the disproportion in the distances of the foramen from the two plates. In the tibia, however, extension of the extremely oblique nutrient canal as the bone increases in girth is also involved. Bone remodelling in the vicinity of the canal is not necessary to explain the results.

Animals↗
PubMed1977

Correlation of clinical, biochemical and skeletal responses to 1alpha-hydroxyvitamin D3 in renal bone disease.

Thirty-five patients with bone disease and chronic renal failure (twenty-four on maintenance haemodialysis) were treated for 7--39 months with 1alpha-hydroxyvitamin D3, 2--2.5 microgram daily by mouth. Symptoms (bone pain and muscle weakness) and radiographic appearances improved and plasma alkaline phosphatase returned to normal in the majority of patients (87, 76 and 75% respectively). In contrast, histological appearances in bone improved in only 46% twenty-three patients from whom paired biopsies were available, and this change was not greatly different from that seen in a comparable group of untreated patients. Significant correlations were noted in individual patients between the changes in symptoms, X-rays, plasma alkaline phosphatase and immunoreactive parathyroid hormone and these, in turn, were related to histological changes in bone, although these latter changes were often small. It is concluded that 1alpha-hydroxyvitamin D3 is a useful new drug in the treatment of renal bone disease, but that the evaluation of the response depends critically on the method of assessment used.

Adolescent↗
PubMed1977

Renal osteodystrophy in nondialysed adolescents. Long-term treatment with 1alpha-hydroxycholecalciferol.

The effects of small oral doses (1-2 microgram/day) of 1alpha-hydroxycholecalciferol, given for 1 to 2 years, have been examined in four nondialysed adolescents with chronic renal failure and bone disease. Treatment increased calcium retention and plasma calcium, and decreased plasma levels of alkaline phosphatase, hydroxyproline, and immunoreactive parathyroid hormone. X-ray abnormalities of bone regressed, and 2 patients underwent successful surgical correction of knock-knees; bone histology in these 2 was normal at the time of operation. 2 patients developed hypercalcaemia which promptly reversed when 1alpha-hydroxycholecalciferol was withdrawn. In one patient treatment was initially successful, but later there was biochemical, radiographic, and histological evidence of relapse. Long-term treatment of such patients with 1alpha-hydroxycholecalciferol may be effective and facilitate the surgical correction of deformities, but this is not invariable. Toxic effects are similar to those of vitamin D itself, but are more readily reversible.

Adolescent↗
PubMed1975

The effect of 1,25-dihydroxycholecalciferol on renal tubular reabsorption of phosphate, intestinal absorption of calcium and bone histology in hypophosphataemic renal tubular rickets.

1. 1,25-Dihydroxycholecalciferol (1,25-(OH)2-D3) was given at a dose of 5-0 nmol (2-1 mug) daily by mouth for 4-12 days to three patients with hypophosphataemic (type I), vitamin D-resistant rickets. 2. 1,25-(OH)2-D3 increased intestinal absorption and urinary excretion of calcium without significant effect on the renal handling of phosphate or its plasma concentration. 3. It is concluded that in this type of vitamin D-resistant rickets the renal phosphate abnormality is unlikely to be due to diminished endogenous production of 1,25-(OH)2-D3. 4. The difference between this condition and other hypophosphataemic states is discussed.

Bone and Bones↗