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CLINICAL STATEMENTS AND GUIDELINES September 16, 2025 Circulation. 2025;152:e114–e218. DOI: 10.1161/CIR.0000000000001356 e164 Synopsis The prevalence of hypertension is 67% to 92% among people with CKD. CKD is an important risk factor for CVD, and the coexistence of hypertension and CKD further increases the risk of CVD events. Despite this risk, a majority of people with CKD have uncontrolled BP.6 As demonstrated in SPRINT, intensive BP treat ment (mean achieved SBP 121 mm Hg) versus stan dard treatment (mean achieved SBP 136 mm Hg) reduced the risk of CVD, including among those with CKD.1 The recommendation in this guideline is for a treatment goal SBP <130 mm Hg and balances the benefits of intensive BP lowering with risks of adverse events.7 An ACEi or an ARB is recommended for ini tial treatment of hypertension in CKD due to long-term kidney and CVD benefits in people with moderate or severe albuminuria (≥30 mg/g) and may be consid ered for those with lower level albuminuria (<30 mg/g) based on expert opinion.4,5,8–12 These recommendations refer to people with nondialysis-requiring CKD given limited data in patients receiving chronic hemodialysis or peritoneal dialysis. ACEi or ARB is also appropriate for less-severe CKD (stage 1 or 2) when moderate or severe albuminuria is present. Recommendation-Specific Supportive Text 1 SPRINT data demonstrated adults with CKD and hypertension can be effectively and safely treated to SBP <130 mm Hg.1 Additionally, meta-analyses have shown benefit of treating SBP <130 mm Hg versus higher SBP targets. An analysis of CKD patients from 4 trials found that an SBP target of <130 mm Hg (versus <140 mm Hg) decreased all-cause mor tality.2 A meta-analysis of the CKD subsets from 18 trials reported that more-intensive SBP (mean SBP 132 mm Hg) versus less-intensive SBP (mean SBP 140 mm Hg) control resulted in 14% reduction in allcause mortality.3 While <120 mm Hg is more effec tive at preventing CVD events,3 meta-analyses of trial data support an SBP <130 mm Hg to balance the benefits of intensive BP-lowering with the risks of adverse events.7 2 There is robust evidence to support ACEi or ARB as first-line antihypertensive therapy in CKD for CVD benefits.4,5,8–12 The evidence to support kidney benefit is strongest when albuminuria is moder ate or severe (>30 mg/g), with consideration for using ACEi or ARB with mild albuminuria based on expert opinion. ACEi or ARB reduce intraglomeru lar pressure, which may cause a transient decrease, or dip, in eGFR up to 30%. This short-term decline in eGFR is not associated with decreased longterm outcomes and should not prompt discon tinuation of the ACEi or ARB.13–15 Electrolytes should be rechecked 2 to 4 weeks after initiating or intensifying ACEi or ARB dosage, monitoring for hyperkalemia or a decline in eGFR of >30%, which may require reducing or holding the agent temporarily or additional evaluation. ACEi or ARB can be continued in people with eGFR <30 mL/ min/1.73 m2 as an RCT found that discontinuation was not associated with a significant difference in long-term decrease in eGFR.16 The combined use of an ACEi and an ARB should be avoided because of increased harm, as discussed further in Section 5.2.8 (“Electrolyte Imbalances”).12,17,18 5.3.8.1 Hypertension After Kidney Transplantation Synopsis Hypertension is common after kidney transplantation because of pre-existing kidney disease, effects of im munosuppressive medications, and presence of allograft pathology.1–3 One study reported high prevalence of masked hypertension in kidney transplant recipients,4 who frequently have multiple risk factors that increase the risk of CVD events. Hypertension may accelerate kidney function decline and increase the risk for CVD and mortality.2,5 Immunosuppression may contribute to the risk of hypertension in organ transplant recipi ents (including kidney and other organs). Calcineurin inhibitor-based immunosuppression regimens are as sociated with a high (70% to 90%) prevalence of hy pertension.3 There are no robust trials in post-transplant patients comparing different BP targets or drug choices. A systematic review did not find that any BP-lowering medication class reduced the risk of graft loss, with drawal because of adverse events, death, cardiovascular outcomes, or kidney outcomes compared with placebo/ other drug classes.6 One trial of 188 kidney transplant recipients randomized patients to spironolactone versus placebo for 3 years and found no difference in kidney function or proteinuria.7 Overall, there is insufficient evi dence to support specific recommendations on BP tar gets or recommended agents for kidney transplant re cipients. 5.3.9 Cerebrovascular Disease Synopsis Stroke is a major cause of death, disability, and demen tia.1 Due to its heterogeneous causes and hemodynamic consequences, the management of BP in adults with stroke is complex and challenging. To accommodate the variety of important issues pertaining to BP management in the stroke patient, treatment recommendations require recognition of stroke acuity, stroke type, and therapeu tic objectives. Future studies should focus on identifying more precise BP targets, accounting for stroke etiology, personalized cerebrovascular hemodynamics, and appro priate antihypertensive agents. Downloaded from http://ahajournals.org by on October 7, 2026