Decreased sebum excretion in chronic renal failure.
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Biomedical subjects
Publications and source records attributed to D N Kerr.
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The effects of intravenous iron, with and without androgens, was studied in a group of 39 patients treated by regular haemodialysis, almost all of whom had normal serum iron concentrations. Intravenous iron 1-2 g every 4 months produced a significant rise in haemoglobin from 6.3 to 7.9 g/dl in 17 female patients with their kidneys in situ (p less than 0.001). In a group of 13 male subjects intravenous iron plus testosterone produced a similar rise in haemoglobin from 6.9 to 8.6 g/dl (p less than 0.001). Nine nephrectomised patients showed no significant response to iron and androgens. There were no fatalities and no serious side effects in 500 courses of intravenous iron.
The radiological findings in the skeletal surveys of 70 patients receiving long-term haemodialysis for chronic renal failure have been correlated with histological findings in a specimen obtained by biopsy of the iliac crest. Many significant associations were found, and the ones presented are those thought to be most useful in the interpretation of the radiological abnormalities. The main conclusions are that fractures and severe medullary rarefaction appear to be most commonly the result of osteomalacia; subperiosteal erosions are associated with the more severe grades of osteitis fibrosa; cortical striations and sclerosis are associated with an increased amount of osteoid, and sclerosis is diagnosed more frequently by radiological means than by iliac-crest biopsy.
Two regular hemodialysis patients were assessed before, during and after therapy for 8 1/2 months with 1alpha-hydroxycholecalciferol (1alphaOHD3). The first patient (F.S.), treated with 2 mug daily, improved considerably with complete resolution of histological osteomalacia (O.M.), reduction in osteitis fibrosa (O.F.) and healing of Looser zones. The second patient (T.Y.), who was treated at the same time with a combination of phenobarbitone and phenytoin, showed no improvement while taking 3 mug of 1alphaOHD3 daily. It is suggested that hepatic microsomal enzyme inducing drugs antagonize the action of 1alphaOHD3 by interfering with its subsequent hepatic 25-hydroxylation.
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Five patients with haemodialysis bone disease were treated with 1 to 1.5 mug of 1,25 (OH)2D3 daily for periods ranging from 6 -8 months. There was a significant improvement in calcium absorption but no troublesome hypercalcaemia was encountered. Secondary hyperparathyroidism improved, both histologically and radiologically, and there was a fall in serum PTH and return of serum alkaline phosphatase to within normal limits. There was also improvement in the patients' mineralisation status, but this change was slower and less marked. Muscle power improved significantly, both clinically and electromyographically.
Measurement of serum lipids in 75 patients on regular haemodialysis showed that they had a higher mean serum triglyceride level than normal subjects. Cholesterol levels were not significantly different. Amongst haemodialysis patients men had higher serum triglycerides than women and women had higher cholesterol levels than men, a situation analogous to that found in normal subjects. In men, serum triglycerides correlated with percent body fat and treatment with Sustanon 250(R) intramuscularly weekly caused a significant rise.
Undried cellulose gel film manufactured by British Cellophane Ltd (BCL) has been evaluated in vivo and in vitro. Results obtained indicate that undried cellulose gel film is superior in terms of ultrafiltration and middle molecular clearance to the widely used Cuprophan membrane and comparable with the Rhône Poulenc AN69 Acrylopolynitrile membrane for middle molecular clearance. The gel film is suitable for use with conventional dialysis equipment and in terms of residual blood volume, leak rate and pyrogenicity is indistinguishable from cuprophan.
Two groups of patients treated by short (Milan) and long (Newcastle) haemodialysis were compared for incidence of symptoms and biochemical control. Short dialysis corrected urea and creatinine as well but control of potassium and phosphate were similar. The only apparent penalties to be paid by short dialysis patients were a higher incidence of itching, tingling or numbness, impairment of vibratory sense and difficulty in controlling blood pressure. The short dialysis group had higher haemoglobin and less dyspnoea, muscle weakness and dizziness after dialysis.
Muscle weakness and tenderness together with a rise in serum creatine kinase (C.K.) were noted in five uraemic patients treated with 1-2 g of clofibrate ('Atromid-S') daily. Excessive accumulation of both total and free serum chlorophenoxyisobutyric acid (C.P.I.B.), the active circulating metabolite after clofibrate therapy, was found in three patients in whom it was sought. It is suggested that chronic renal failure should be regarded as a contraindication to the use of clofibrate for the treatment of any coexisting hyperlipidaemia. If such therapy is contemplated it must be cautiously instituted at low dosage and the patient monitored by regular assessment of serum C.K. and levels of both total and free C.P.I.B.
Plasma immunoreactive beta-melanocyte stimulating hormone (beta-MSH) concentrations were greatly increased in patients with chronic renal failure. There was no correlation between the severity of the renal failure or the degree of pigmentation and the plasma beta-MSH levels.
A radiofibrinogen catabolism study performed on 40 patients with glomerulonephritis has shown increased fibrinogen catabolism in active immune-complex disorders.
Regular haemodialysis with the Kiil dialyser for 8-10 h three times a week is the present standard of adequate dialysis. In 100 patients treated by this regime there was no positive correlation between plasma urea and creatinine before or after dialysis and any of the symptoms of which these patients still complained. There are no grounds for believing that a further increase in dialysis would relieve residual symptoms. However, any reduction in current standards of dialysis should be justified by prolonged clinical trial of large groups of patients before they are accepted as equivalent in view of the infrequency of some uraemic manifestations such as pericarditis. The implications of the middle molecular hypothesis are discussed.
A study of serum proteins in patients on regular hemodialysis has shown that many have low serum transferrin levels but near normal serum albumin and normal or raised pre-albumin levels. Hemoglobin values were related to transferrin levels. Low transferrin levels also occurred in patients with advanced osteitis fibrosa. Deficient protein intake seems the likely explanation. Measurement of pre-albumin does not reflect low protein intake in chronic renal failure; reasons for this discussed.
Until recently all disposable dialyzers have had a poorer overall performance than the best non-disposable dialyzer, the Meltec multipoint. The three disposables considered here (Gambro Lundia Nova, Cordis HFAK 4 and Rhone Poulenc RP 5) all have clearance of small molecules close to or, for the HFAK 4, just above that of the multipoint though their middle molecular clearance is not quite as good as the multipoint. The HFAK 4 has a better basal ultranfiltration rate but a poorer maximum ultrafiltration capacity. The RP 5 has a higher residual blood volume than the multipoint. In other respects the dialyzers are almost interchangeable and are reasonable alternatives to the multipoint in those centers which can afford single use disposable dialyzers.
Serial histological studies in patients after successful renal transplantation indicate that with restoration of adequate renal function osteomalacia invariably improves with symptomatic relief in bone pain. Histological changes of osteitis fibrosa resolve more slowly and radiological changes may persist longer, occasionally in the absence of confirmatory histological evidence of secondary hyperparathyroidism. For accurate and sensitive follow-up a combination of biochemistry, histology and radiology is desirable.
Cyclophosphamide was administered orally, in a dose just sufficient to depress the white-cell count to 3000-4000 per mm3 (mean 1.5 mg/kg/day), to 27 patients with proliferative glomerulonephritis for 12 months; 26 patients acted as controls. Cyclophosphamide conferred no benefit as judged by mortality, morbidity, renal function (serum creatinine and creatinine clearance) or proteinuria. The side effects of cyclophosphamide included permanent amenorrhoea in five of seven menstruating women. Since no controlled trial has yet shown that any immuno-suppressive drug benefits proliferative glomerulonephritis we question whether such drugs should be administered in this disease except in the course of planned prospective trials.
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