Abstract

The pathophysiological mechanisms resulting in hyperlipidaemia in albuminuric insulin-dependent diabetic patients are largely unknown. Increased non-specific hepatic protein synthesis as a response to urinary protein loss, has been proposed. However in that case it is unexplained why the plasma concentration of the high density lipoprotein (HDL) subfraction, in contrast to all other lipoprotein subfractions, is normal or even reduced in albuminuric patients. We studied the urinary excretion of HDL-cholesterol in 26 insulin-dependent diabetic patients matched according to sex and age into three groups. I: normal urinary albumin excretion (< 30 mg 24 h-1; n = 8); II: incipient nephropathy (urinary albumin excretion in the range of 30-300 mg 24 h-1; n = 7); and III: clinical nephropathy (urinary albumin excretion > 300 mg 24 h-1; n = 11). Eight normal subjects served as controls. Lipoproteins in urine were separated by ultracentrifugation, and the daily urinary loss of HDL-cholesterol was 1.30 mumol (0.83-2.21) (median and range) in controls, 1.27 mumol (0.56-2.59) in group I, 1.39 mumol (0.55-1.97) in group II and 4.02 mumol (1.33-42.12) in group III (p < 0.01). More than 95% of cholesterol in urine was found in the HDL-fraction. The plasma concentrations of total cholesterol, very low density lipoprotein cholesterol, low density lipoprotein cholesterol and triglyceride were 21-94% higher in patients with clinical nephropathy compared with normal controls and group I.(ABSTRACT TRUNCATED AT 250 WORDS)

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