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Intensive Blood Pressure Control in Autosomal Dominant Polycystic Kidney Disease-How Safe Is It?-Reply.

Intensive Blood Pressure Control in Autosomal Dominant Polycystic Kidney Disease— How Safe Is It? To the Editor Maintaining optimal blood pressure in patients without diabetes with chronic kidney disease (CKD) has always been controversial. In a systematic review and metaanalysis published in a recent issue of JAMA Internal Medicine, Tsai et al1 assessed the clinical data of 8127 patients; they focused on detecting an association between intensive blood pressure control and renal outcomes in patients without diabetes with CKD. Consequently, no significant difference in major renal outcomes was found between intensive (<130/80 mm Hg) and standard BP control (<140/90 mm Hg) groups during a median follow-up of 3.3 years. Nevertheless, nonblack patients or those with higher levels of proteinuria were found to benefit from the intensive BP-lowering strategy. Interestingly, patients with polycystic kidney disease (ADPKD) were also included in this study.1 Very few studies have been conducted on the hypertension control in the population of patients with ADPKD. Schrier et al,2 in a study conducted on 558 patients ages 15 to 49 years and in their early CKD stages, assigned the groups to either standard (120/70130/80 mm Hg) or low (95/60-110/75 mm Hg) blood pressure target groups. Authors found that maintaining rigorous BP control in young healthy hypertensive patients with ADPKD with relatively preserved kidney function at earlier stages of the disease is associated with a slower increase in total kidney volume, greater reduction in urinary albumin excretion, and a greater decline in the left ventricular mass index. However, no further renal benefits such as improved renal function was observed following low BP target strategy. Unlike patients with CKD with other underlying mechanisms, intensive blood pressure lowering should be practiced more cautiously in patients with ADPKD. Given that there is bilateral intrarenal ischemia in ADPKD due to the compression effect of the cyst, these patients are potentially vulnerable to acute renal perfusion changes following initiation of RAAS blockers particularly in those with severer renal insufficiency and massive cystic diseases. RAAS (renin-angiotensin-aldosterone system) blockers might impair the already-compromised perfusion of the intact normal renal parenchyma which is compensated by the elevated systemic pressure. Hence, administration of RAAS blockers should be performed more vigilantly in patients with ADPKD.