The purpose of this study was to assess the role of urine α1-microglobulin as a marker of hypertension-induced renal damage compared to the gold-standard markers (estimated glomerular filtration rate, eGFR; urine albumin and urine albumin-to-creatinine ratio, ACR). Its response on different BP-lowering drugs was also studied.Design and method:
Sixty never-treated hypertensives (65.0% males, 46.9 years, 141.4/94.0 mmHg) were randomized to an angiotensin receptor blocker (ARB)- or non-dihydropyridine calcium channel blocker (CCB)-based regimen. Patients with diabetes, established cardiovascular or renal disease were excluded. Blood samples and 24-hour urine were analyzed at baseline and 6 months after pharmaceutical blood pressure (BP) normalization. Serum creatinine was measured and eGFR was calculated. Urine albumin, creatinine, and α1-microglobulin were measured and ACR was calculated.Results:
Minor changes (p = NS) in eGFR were noted during follow-up in both groups (from 111.0 to 108.4 and from 111.3 to 114.0 ml/min/1.73 m2 in the ARB and CCB group, respectively). 24-hour urine indices were all significantly improved (P < 0.01) with ARB (albumin from 19.4 to 8.2 mg/l, ACR from 21.5 to 10.0 mg/g, α1-microglobulin from 5.06 to 3.64 mg/l) but not (P = NS) with CCB treatment (albumin from 15.6 to 13.9 mg/l, ACR from 17.6 to 17.1 mg/g, α1-microglobulin from 4.94 to 4.79 mg/l). These differences between groups remained significant (P < 0.05) after adjusting for office heart rate (HR) and BP. Alpha-1-microglobulin was significantly correlated (P < 0.05) to albumin and ACR both at baseline (r = 0.283 and 0.299, respectively) and at the end of follow-up (r = 0.432 and 0.465, respectively) but not (P = NS) to eGFR. It was also significantly related (P < 0.05) to cardiovascular risk scores (Framingham and HeartScore) both at baseline (r = 0.264 and 0.436, respectively) and at the end of follow-up (r = 0.308 and 0.472, respectively).Conclusions:
Urine α1-microglobulin emerges as a potentially valuable marker of hypertension-induced renal impairment. Its kinetics and its response to treatment appears similar to that of albumin. ARBs emerge as superior to non-dihydropyridine CCBs at improving its excretion in urine, independently of HR/BP control.