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Loss of anionic charge of the glomerular basement membrane is one of the contributing factors in the development of albuminuria in diabetic individuals. Decreased anionic charge is associated with increased urinary heparan sulphate excretion. There isn't enough data concerning this issue in nondiabetic hypertensive patients.
The aim of this study is to determine the relationship between microalbuminuria and urinary heparan sulphate excretion in essential hypertensive patients.
Sixty hypertensive patients, 30 microalbuminuric and 30 normoalbuminuric enrolled in the study group. The control group contained 30 healty individuals. All subjects had been evaluated for urinary infections and urolithiasis. A 24 hour urine sample collected used for measurement of urinary creatinin, albumin and heparan sulphate excretion. Mean age of three groups were similar. Also mean duration of hypertension were similar between normoalbuminuric and microalbuminuric patients 6.2±1.5, 6.3±1.8 years respectively. Urinary excretion rates in control, normoalbuminuric and microalbuminuric groups were 14.3±1.5, 16.4±1.4 ,67±17 mg/day respectively. Heparan sulphate excretion rates were 332.6±193,671.2±310,4058±1078 mg/day respectively. Urinary heparan sulphate excretion was markedly increased in microalbuminuric patients compared with normal and normoalbuminuric hypertensive subjects (p<0.001).Heparan sulphate excretion was not correlated with albuminuria or duration of hypertension.
As a result urinary heparan sulphate excretion is increased in hypertensive patients. This confirms that urinary loss of glycosaminoglycans may be involved in the pathogenesis of hypertensive microalbuminuria.