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Biomedical subjects

L S Ibels

Publications and source records attributed to L S Ibels.

At least 73 records · Page 4Linked to original sources
PubMed1978

Preservation of function in experimental renal disease by dietary restriction of phosphate.

We sought to determine the importance of calcium phosphate deposition in the functional deterioration of damaged or diseased kidneys. Using the remnant-kidney model in rats, we found that dietary phosphate restriction prevented proteinuria, renal calcification, histologic changes, functional deterioration and death in uremia. Histologic examination of the remnant kidney in the nonrestricted animals showed calcium and phosphorus deposits in the cortical tubular cells, basement membranes and interstitium. A similar degree and pattern of calcification have been found in preliminary studies of human end-stage kidneys. Our results suggest that the calcification produced by the altered phosphorus metabolism present in the uremic state incites an inflammatory and fibrotic reaction leading to destruction of the remnant kidney. Phosphate restriction prevents this response in the remnant kidney. The potential applicability of these findings to other forms of experimental renal disease and to clinical uremia remains to be explored.

Animals↗
PubMed1978

Uremic hyperstannum: elevated tissue tin levels associated with uremia.

Previous work has shown that the concentration of the essential trace element tin is elevated in several tissues of dialyzed uremic patients. Analysis of 80 postmortem liver samples from controls and nondialyzed uremic and dialyzed uremic patients now shows that nondialyzed uremic patients also have abnormally high tin concentrations, averaging about three times that of controls. It is concluded that these elevated tin levels are associated with uremia rather than with dialysis. Abnormally high tin levels were also found in the kidneys of uremic patients at autopsy. This may have special importance, since tin has been shown to be a powerful inducer of heme oxygenase activity in rat kidney. The urinary excretion of tin by nondialysed uremic patients was measured and found to be normal.

Adult↗
PubMed1977

Occlusive arterial disease in uraemic and haemodialysis patients and renal transplant recipients. A study of the incidence of arterial disease and of the prevalence of risk factors implicated in the pathogenesis of arteriosclerosis.

The prevalence of clinical and sub-clinical occlusive arterial disease and of risk factors implicated in the pathogenesis of arteriosclerosis was assessed in 21 patients with chronic renal failure, 27 on maintenance haemodialysis and 51 renal allograft recipients. Clinical occlusive arterial disease was present in 27 patients, and sub-clinical arterial disease in 34. Myocardial infarction, cerebral thrombosis and lower limb arterial thrombosis had occurred only in the transplant recipients; these patients had, however, been followed for a longer period of time than the other two groups. In the allograft recipients, the cumulative incidence of any occlusive arterial disease was 416 per 1000, and that of coronary heart disease was 267 per 1000 at six years. Hypertension was present in 76 per cent of patients prior to renal replacement therapy. Following institution of definitive therapy, hypertension was of shorter duration and less common in haemodialysis patients than in renal transplant recipients. Uraemic and haemodialysis patients with occlusive arterial disease had required antihypertensive medication for significantly longer than those free of arterial disease. Transplant recipients with hypertension had a greater mean serum creatinine, were receiving a larger maintenance dosage of corticosteroids and less frequently had undergone prior bilateral nephrectomy than those transplant patients without hypertension. Serum lipid levels were elevated in 62 per cent of patients. In the uraemic and haemodialysis patients hypertriglyceridaemia was the predominant abnormality while in the transplant recipients combined hypertriglyceridaemia/hypercholesterolaemia was more frequent. Despite regular aluminium hydroxide therapy 81 per cent of uraemic and haemodialysis patients had a calcium X phosphate product higher than normal. Arterial and/or soft tissue calcification as demonstrable in 20-38 per cent of patients within each group, but could not be related to the calcium X phosphate product of radiographic evidence of hyperparathyroidism. Glucose intolerance was present in 71 per cent of the uraemic and haemodialysis patients and 33 per cent of the transplant recipients. Hyperuricaemia, cigarette smoking, obesity and a sedentary existence were also prevalent. The majority of patients had several risk factors implicated in the pathogenesis of arteriosclerosis. Occlusive arterial disease is a major problem in patients with end stage renal disease, being no less common after transplantation than with long-term maintenance dialysis. The aetiology is multifactorial.

Adult↗
PubMed1976

Renal transplantation. Effect on the ischemic heart disease of essential malignant hypertension.

In 14 of 204 consecutive cadaveric renal allograft recipients, the primary diagnosis was essential hypertension. Four patients had manifest ischemic heart disease before transplantation. Three of these patients died within 31 months of transplantation from recurrent myocardial infarction, and the fourth experienced coronary insufficiency. Cadaveric renal transplantation does not prevent the progression of coronary artery disease in patients whose renal failure was due to essential hypertension. In the presence of angina or previous myocardial infarction, these patiemts may be better treated by maintenance hemodialysis.

Adult↗
PubMed1976

Hyperlipidemia following renal transplantation.

In a series of 175 adult renal transplant patients 59% of patients had hyperlipidemia. Hyperlipidemia in these patients was characterized by both hypercholesterolemia and hypertriglyceridemia and on lipoprotein electrophoresis was demonstrated to be a mixture of types IIa, IIb and IV hyperlipoproteinemia. Serum cholesterol and triglyceride levels could both be related to the dosage of prednisone these patients received. Serum triglyceride levels could further be correlated with obesity and negatively with the duration of graft function. The latter relationship was felt to reflect the lower dose of prednisone that was administered the longer the duration of graft function. Hypertriglyceridemia was more prevalent in the 47 transplant patients who received kidneys from cadaver donors than in the 128 patients who received kidneys from related-donors. The cadaver-donor renal transplant patients, however, were receiving a larger maintenance dose of corticosteroids and had had functioning transplants for a shorter period of time. In 17 patients followed for up to 20 wks immediately following transplantation both hypercholesterolemia and hypertriglyceridemia developed within 8 wks of transplantation and persisted for the remaining 12 wks. Both serum cholesterol and triglyceride levels in this early post-transplant phase could be related to the cumulative prednisone dosage.

Adolescent↗
PubMed1975

Hyperparathyroidism after renal transplantation.

Renal transplantation reduced circulating parathyroid hormone in recipients of renal allografts. Nevertheless, biochemical and histological evidence of mild hyperparathyroidism persisted up to eight years after renal transplantation despite good graft function.

Bone and Bones↗
PubMed1975

Blood viscosity factors and occlusive arterial disease in renal transplant recipients.

29 cadaveric renal transplant recipients were assessed clinically for evidence of occlusive arterial disease prior to undergoing blood viscosity studies. Nineteen patients had manifest arterial disease (myocardial infarction, cerebral thrombosis, angina, intermittent claudication, absent peripheral pulses), while ten were free from vascular complications. Patients with arterial disease showed significant elevations of plasma viscosity (p less than 0.005), aggregation of red cells measured both at 37 and 20 degrees C (p less than 0.05), fibrinogen (p less than 0.005), serum triglyceride (p less than 0.01), serum cholesterol (p less than 0.01), erythrocyte sedimentation rate (p less than 0.02), and a significant reduction in the albumin/fibrinogen ratio (p less than 0.005) when compared with those free of disease. Two patients with no apparent vascular disease when investigated were found to have distinctly abnormal blood viscosity factors, and one subsequently developed retinal arterial thrombosis while the other suffered serious damage of the graft within 3 months of viscosity study. When all patients were considered together, significant correlations were found between viscosity of artificial thrombi or aggregation of red cells and fibrinogen level (both p less than 0.05), and serum triglyceride level (both p less than 0.05); and between rigidity of red cells and the parathyroid hormone level (p less than 0.01).

Adult↗
PubMed1975

Erythroid toxicity of azathioprin. Macrocytosis and selective marrow hypoplasis.

In a population of 70 stable renal allograft recipients receiving azathioprine, macrocytosis was present in a majority and its severity was related to azathioprine dosage. There were associated megaloblastoid marrow changes which could not be related to serum folate or vitamin B12 concentrations. Two cases of selective red cell hypoplasia in renal allograft recipients are described; in each patient, azathioprine was incriminated and the effect dose-related. These observations indicate that the erythroid effects of azathioprine may precede, and be independent of, its effects on the myeloid series.

Adult↗
PubMed1975

Studies on the nature and causes of hyperlipidaemia in uraemia, maintenance dialysis and renal transplantation.

Fasting serum triglyceride and cholesterol measurements, and lipoprotein characterization by ultracentrifugation, were performed in four groups of patients with chronic renal disease (uraemic, short- and long-term haemodialysis and renal transplant recipients) and the results compared with those obtained from age- and sex-matched control subjects. Basal insulin and growth hormone levels, and serum creatinine and albumin concentrations were measured in, and detailed dietary histories taken from patients in each group. The predominant lipid abnormalities were hypertriglyceridaemia and increased very low density lipoproteins (type IV hyperlipoproteinaemia) in both uraemic and haemodialysis patients. Following renal transplantation, a different pattern of hyperlipidaemia was found. Hypercholesterolaemia was more common and hypertriglyceridaemia less common than in the uraemic and haemodialysis group. The lipoprotein abnormalities were increased low density and/or very low density lipoproteins, with types IIa IIb and IV hyperlipoproteinaemia occurring equally frequently. In uraemic and haemodialysis patients, the proportion of carbohydrate in the diet was high, and may have played a role in the genesis of hypertriglyceridaemia. There was a positive correlation between relative body weight and serum triglyceride in the long-term dialysis group. In renal allograft recipients hypertriglyceridaemia could be attributed, at least in part, to obesity, prednisone dosage and the degree of impairment of graft function. The aetiology of hypercholesterolaemia in the transplant recipients was unclear. Neither basal insulin nor growth hormone levels were elevated in any patient group. Uraemic hypertriglyceridaemia is a clearly defined and well documented metabolic abnormality which is not corrected by dialysis. Post-transplantation hyperlipidaemia however, is a condition of variable presentation and multifactorial aetiology.

Adolescent↗
PubMed1974

Deaths from occlusive arterial disease in renal allograft recipients.

In a series of 325 recipients of cadaveric renal transplants sudden occlusive arterial disease was found to be responsible for 12% of deaths. Acute myocardial infarction (9%) occurred 25 times more than expected in the normal population and cerebral thrombosis (3%) 300 times more. The greatest loss was in the initial three-month period after transplantation. Patients with renal failure due to essential hypertension were especially at risk, accounting for six of the 12 deaths.

Adult↗