CLINICAL TRIAL: HALT-PKD

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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 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 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).