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Biomedical subjects

M K Chan

Publications and source records attributed to M K Chan.

At least 145 records · Page 8Linked to original sources
PubMed1984

Pathogenic roles of post-heparin lipases in lipid abnormalities in hemodialysis patients.

The relative roles of hepatic lipase and lipoprotein lipase in the pathogenesis of uremic lipid abnormalities were studied in 92 hemodialysis patients. Fasting serum cholesterol, triglyceride, and HDL-cholesterol concentrations were measured. Plasma lipoprotein electrophoretic patterns were determined in all patients. Hepatic lipase and lipoprotein lipase activities were selectively measured in post-heparin plasma in 59 patients. Hemodialysis patients had higher serum triglyceride and lower HDL-cholesterol concentrations than did their age and sex-matched control subjects. Both hepatic and lipoprotein lipase activities were reduced in hemodialysis patients. An inverse relation between lipoprotein lipase activities and serum triglyceride concentrations emerged. Lipoprotein lipase activities correlated with in vivo post-heparin fractional clearance rates of Intralipid. A positive correlation between lipoprotein lipase activities and HDL-cholesterol concentrations probably reflected impaired catabolism of triglyceride-rich lipoproteins being responsible for the low HDL-cholesterol concentrations. Hemodialysis patients (41.3%) had an abnormal lipoprotein (the 'mid-band'). While hepatic lipase activities did not correlate with any parameters of lipid metabolism, patients with 'low' hepatic lipase activities had a significantly higher prevalence of 'mid-bands' than did those with 'normal' activities. No evidence was developed to prove that the 'mid-band' lipoproteins were remnant particles.

Adolescent↗
PubMed1984

Post-heparin hepatic and lipoprotein lipase activities in nephrotic syndrome.

Lipid metabolism was studied in 18 patients with nephrotic syndrome due to various glomerulonephritides. Nephrotic patients had hypercholesterolemia with or without hypertriglyceridemia. The mean serum high-density lipoprotein cholesterol concentration was not significantly reduced in nephrotic patients. Hepatic lipase and lipoprotein lipase activities were measured selectively in post-heparin plasma from all 18 patients using a substrate-specific method. The mean lipoprotein lipase activity in nephrotic patients was markedly reduced while the mean hepatic lipase activity was not significantly different from that of controls. Lipoprotein lipase activities correlated inversely with serum triglyceride concentrations, but positively with in vivo post-heparin fractional clearance rates of Intralipid and with serum high-density lipoprotein concentrations. Nephrotic serum inhibited lipoprotein lipase activity in normal subjects. The percentage inhibition, however, did not correlate with the degree of hypertriglyceridemia. A relatively weak inverse correlation was shown to exist between plasma albumin concentration and hepatic lipase activities.

Adolescent↗
PubMed1984

Captopril in hypertension after renal transplantation.

Eight hypertensive renal allograft recipients who had received captopril are presented. Captopril in a maximal daily dose of 250 mg enabled the withdrawal of large doses of beta-blocking agents and vasodilators. Blood pressure was satisfactorily controlled in all except one. No adverse side effects were observed other than the 'first dose' effect which resulted in transient anuria in one patient. Captopril appears to be a useful agent in the management of severe hypertension after renal transplantation.

Adolescent↗
PubMed1984

Effects of propranolol and hemodialysis on the response of glucose, insulin, C-peptide and cyclic AMP to glucagon challenge.

Hypoglycemia is frequently reported in hemodialysis patients on propranolol. We studied the influence of propranolol on carbohydrate metabolism in sixteen hemodialysis patients (eight on propranolol and eight not) with pre-dialysis oral glucose tolerance tests (OGTT) and pre- and post-dialysis glucagon tests. Propranolol was shown to have significant suppressive effect on the insulin response during OGTT. With glucagon challenge pre- and post-dialysis, despite a similar cAMP response, patients on propranolol had significantly lower glucose response than those not receiving propranolol and it is postulated that this is due to post-receptor post-cAMP inhibition of hepatic glycogenolysis. Moreover, while the glucose response in patients not on propranolol significantly increased after dialysis, no significant change was found in patients on propranolol. The significantly higher C-peptide, insulin and cAMP responses to glucagon challenge in the hemodialysis patients as compared to normal controls may be due to delayed clearance of glucagon, and the further increased responses after dialysis may be due to the removal of a dialyzable factor suppressing these responses.

Adult↗
PubMed1982

Lipid nephrotoxicity in chronic progressive glomerular and tubulo-interstitial disease.

It is hypothesised that chronic progressive kidney disease may be mediated by abnormalities of lipid metabolism. A series of self-perpetuating secondary events follows an initial glomerular injury. Increased glomerular basement membrane permeability leads to loss of lipoprotein lipase activators, resulting in hyperlipidaemia. Circulating low-density lipoprotein binds with glycosaminoglycans in the glomerular basement membrane and increases its permeability. Filtered lipoprotein accumulates in mesangial cells and stimulates them to proliferate and produce excess basement membrane material. The proximal tubular cells metabolise some of the filtered lipoprotein and the remainder are altered on passage down the nephron. Luminal apoprotein precipitates, initiating or aggravating tubulo-interstitial disease, if the intraluminal pH is close to the isoelectric point of the apoprotein. The hypothesis offers new approaches to the study of chronic progressive kidney disease by proposing a major pathogenetic role for lipid abnormalities.

Apoproteins↗
PubMed1982

Plasma LCAT activities in renal allograft recipients.

Plasma LCAT activities were measured in 51 renal allograft recipients as well in 18 patients before and after successful renal transplantation. The mean plasma LCAT activity of the 51 patients did not differ significantly from that of 27 normal subjects. When the patients were separated into two groups according to whether they had normal or impaired renal function, there was no significant difference in their mean LCAT activities. Plasma LCAT activities correlated significantly with total cholesterol and total triglyceride concentrations. The sequential study demonstrates that the low plasma LCAT activities in uraemic patients rose towards normal after successful transplantation. At the same time, total cholesterol and HDL-cholesterol concentrations also increased. The increase in LCAT activity after renal transplantation is due to increased concentrations of the enzyme and probably reflects increased turnover of triglyceride-rich lipoproteins.

Adult↗
PubMed1982

Plasma lecithin-cholesterol acyltransferase activities in uraemic patients.

Plasma lecithin-cholesterol acyltransferase (LCAT) activity was measured in 43 haemodialysis and 15 peritoneal dialysis (CAPD) patients. LCAT activities in both groups of patients were significantly lower than those of normal subjects and did not correlate with any of the other biochemical parameters studied. The effect of intravenous administration of 100 U/kg of heparin on LCAT activity was examined in 21 haemodialysis patients and 19 normal subjects. Heparin inhibited LCAT activity by increasing plasma free fatty acid concentrations. LCAT remained inhibited throughout a dialysis session and returned towards pre-dialysis levels an hour after haemodialysis was discontinued. The cause of the low LCAT activities in the patients was not certain, but did not appear to be due to the presence of inhibitors in the uraemic plasma. The significance of these findings is discussed.

Adult↗
PubMed1982

Response patterns to DL-carnitine in patients on maintenance haemodialysis.

10 hypertriglyceridaemic hemodialysis patients were given dl-carnitine, 600 mg daily, for 8 weeks and then 1.2 g daily for 12 weeks. Serum total cholesterol, total triglyceride, high-density lipoprotein cholesterol and plasma free fatty acid (FFA), glucose, and immunoreactive insulin concentrations were measured at regular intervals during the treatment. Intravenous fat tolerance tests were performed in 9 patients. Plasma FFA concentrations fell and the post-heparin fractional clearance rate of Intralipid increased significantly after all-carnitine administration. While overall no clear-cut effect of dl-carnitine on serum lipids was found, two patterns of response to dl-carnitine could be distinguished: the 'paradoxic' response with a rise in serum triglyceride concentrations and the dual response to two different dosages of dl-carnitine.

Adult↗
PubMed1982

Hyperlipidemia in patients on maintenance hemo- and peritoneal dialysis: the relative pathogenetic roles of triglyceride production and triglyceride removal.

A study was undertaken in 76 patients on maintenance hemodialysis and 26 patients on maintenance peritoneal dialysis to elucidate the pathogenesis of hyperlipidemia in these patients. A high prevalence of hypertriglyceridemia and low concentrations of high density lipoprotein cholesterol was found. Hemodialysis patients had low or normal total cholesterol concentrations which were significantly lower than those on peritoneal dialysis. The length of treatment did not affect the prevalence of the lipid abnormalities. Both pre- and post-heparin fractional clearance rates of Intralipid were markedly reduced in both groups of dialysis patients and were correlated inversely with serum triglyceride concentrations. However, when compared with normal subjects with similar fractional clearance rates of Intralipid, both groups of dialysis patients had higher serum triglyceride concentrations, probably reflecting increased triglyceride production. Serum triglyceride concentrations in both groups of dialysis patients were positively correlated with plasma immunoreactive insulin levels. Furthermore, a significant inverse correlation was observed between plasma immunoreactive insulin levels and post-heparin fractional clearance rates of intralipid. It was concluded that insulin resistance probably caused the defective triglyceride removal, and that both decreased removal and increased production of triglycerides contributed to the hyperlipidemia in dialysis patients.

Adult↗