Palatini P, Mormino P, Dorigatti F, Santonastaso M, Mos L, De Toni R, Winnicki M, Dal Follo M, Biasion T, Garavelli G, Pessina A C
Department of Clinical and Experimental Medicine, Clinica Medica 4, University of Padova, Padova, Italy.
Kidney Int. 2006 Aug;70(3):578-84. doi: 10.1038/sj.ki.5001603. Epub 2006 Jun 21.
Factors related to the development of microalbuminuria in hypertension are not well known. We did a prospective study to investigate whether glomerular hyperfiltration precedes the development of microalbuminuria in hypertension. We assessed 502 never-treated subjects screened for stage 1 hypertension without microalbuminuria at baseline and followed up for 7.8 years. Creatinine clearance was measured at entry. Urinary albumin and ambulatory blood pressure were measured at entry and during the follow-up until subjects developed sustained hypertension needing antihypertensive treatment. Subjects with hyperfiltration (creatinine clearance >150 ml/min/1.73 m2, top quintile of the distribution) were younger and heavier than the rest of the group and had a greater follow-up increase in urinary albumin than subjects with normal filtration (P<0.001). In multivariable linear regression, creatinine clearance adjusted for confounders was a strong independent predictor of final urinary albumin (P<0.001). In multivariable Cox regression, patients with hyperfiltration had an adjusted hazard ratio for the development of microalbuminuria based on at least one positive measurement of 4.0 (95% confidence interval (CI), 2.1-7.4, P<0.001) and an adjusted hazard ratio for the development of microalbuminuria based on two consecutive positive measurements of 4.4 (95% CI, 2.1-9.2, P<0.001), as compared with patients with normal filtration. Age, female gender, and 24 h systolic blood pressure were other significant predictors of microalbuminuria. In conclusion, stage 1 hypertensive subjects with glomerular hyperfiltration are at increased risk of developing microalbuminuria. Early intervention with medical therapy may be beneficial in these subjects even if their blood pressure falls below normal limits during follow-up.
高血压患者微量白蛋白尿发生发展的相关因素尚不明确。我们进行了一项前瞻性研究,以调查肾小球高滤过是否先于高血压患者微量白蛋白尿的发生。我们评估了502名基线时未经治疗的1期高血压且无微量白蛋白尿的受试者,并随访了7.8年。入组时测量肌酐清除率。入组时及随访期间测量尿白蛋白和动态血压,直至受试者出现需要降压治疗的持续性高血压。高滤过(肌酐清除率>150 ml/min/1.73 m²,分布最高五分位数)的受试者比组内其他受试者更年轻、体重更重,与正常滤过的受试者相比,其随访期间尿白蛋白增加更多(P<0.001)。在多变量线性回归中,校正混杂因素后的肌酐清除率是最终尿白蛋白的强有力独立预测因素(P<0.001)。在多变量Cox回归中,与正常滤过的患者相比,高滤过患者基于至少一次阳性测量的微量白蛋白尿发生的校正风险比为4.0(95%置信区间(CI),2.1 - 7.4,P<0.001),基于连续两次阳性测量的微量白蛋白尿发生的校正风险比为4.4(95%CI,2.1 - 9.2,P<0.001)。年龄、女性性别和24小时收缩压是微量白蛋白尿的其他重要预测因素。总之,1期肾小球高滤过的高血压受试者发生微量白蛋白尿的风险增加。即使这些受试者在随访期间血压降至正常范围以下,早期药物干预可能对他们有益。