HALT-PKD

这个子项目是许多利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 假设肾素血管紧张素醛固酮轴系统（RAAS）的激活和高血压在囊性肾病的结构进展和ADPKD的肾功能丧失中发挥重要和独立的作用。这项研究有两个部分。研究A的假设是，在患有高血压或正常高血压且肾功能相对保留（GFR> 60 mL/min/1.73 m ²）的ADPKD个体中，与ACE-I单药治疗相比，使用ACE-I/ARB联合治疗多水平阻断RAAS将延迟囊性疾病的进展，与标准对照相比，低血压目标将延迟进展。 研究B的假设是，在伴有中度肾功能不全（GFR 30 - 60 mL/min/1.73）的高血压ADPKD个体中，与ACE-I单药治疗相比，使用ACE-I/AR B联合治疗强化阻断RAAS将减缓肾功能下降，与标准血压控制（收缩压120 - 130 mmHg和舒张压70 - 80 mmHg）无关。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Activation of the Renin Angiotensin Aldosterone Axis System (RAAS) and hypertension are hypothesized to play important and independent roles in the structural progression of cystic renal disease and in the loss of renal function in ADPKD. There are two pieces to this study. The hypothesis for Study A is that in ADPKD individuals with hypertension or high-normal blood pressure and relatively preserved renal function (GFR>60mL/min/1.73m¿), multi-level blockade of the RAAS using combination ACE-I/ARB therapy will delay progression of cystic disease compared to ACE-I monotherapy, and a low blood pressure goal will delay progression as compared with standard control. The hypothesis for Study B is that in hypertensive ADPKD individuals with moderate renal insufficiency (GFR 30-60 mL/min/1.73¿), intensive blockade of the RAAS using combination ACE-I/ARB therapy will slow the decline in kidney function over ACE-I monotherapy, independent of standard blood pressure control (systolic 120-130 and diastolic 70-80 mm Hg).