Renal Resistive Index and Urinary N-acetyl-?-glucosaminidase as Predictors of Early Renal Involvement in Patients WithEssential Hypertension

Abstract

Background: The long-standing essential hypertension causes renal injury. N-acetyl-β-glucosaminidase (NAG) was considered as an indicator of the functional status of the renal tubules. The resistive index (RI), measured at the level of the interlobar arteries, is thought to reflect downstream vascular impedence and therefore, has been suggested as a measure of renal arterial stiffness. The aim of this study was to investigate whether changes in renal function assessed by urinary N-acetyl-β-glucosaminidase (NAG) and proteinurea are present in hypertensive patients with normal serum creatinine and the association of these changes with renal vascular resistance assessed by ultrasound Doppler. Methods: The study enrolled 78 patients with essential hypertension and 57 age-and sex-matched normotensive subjects. BMI, creatinine, creatinine clearance, uric acid, lipid profile, total proteins, NAG and creatinine in urine were assessed. RI was evaluated by ultrasound Doppler of the interlobar arteries. Results: Hypertensive patients had significantly higher urinary excreted NAG, total urinary proteins and RI than controls. RI was significantly correlated with age, systolic blood pressure, hyperten-sion duration, total proteins, total cholesterol, excreted NAG and creatinine clearance. In multivariate analysis RI was significantly and independently influenced by NAG and creatinine clearance. Conclusions: Early glomerular and tubular dysfunctions precede the overt changes in serum creatinine and glomerular filtration rate in hypertensive patients. Resistive index is increased along with these abnormalities. So, it should be regarded as a marker of early renal and systemic vascular damage and could help identify hypertensive patients for whom more aggressive preventive and therapeutic measures are advisable.

Early markers of obesity-related renal injury in childhood

“…Mousa and co-workers demonstrated that the level of urinary NAG excretion was significantly increased in hypertensive patients compared with normotensive subjects. The upregulated urinary NAG excretion statistically correlated with patient age, serum uric acid, and duration of hypertension [17]. Zhang et al tracked the progression of nephropathy in hypertensive and obese SHROB rats versus control hypertensive SHR-lean rats.…”