1.8.5.0 Car­dio­vas­cu­lar Dis­ease and Blood Pres­sure

Hy­per­ten­sion is a strong risk fac­tor for the de­vel­op­ment and pro­gres­sion of CKD (56). An­ti­hy­per­ten­sive ther­a­py re­duces the risk of al­bu­minuria (57-60), and among pa­tients with type 1 or 2 di­a­betes with es­tab­lished CKD (eGFR <60 mL/‍min/‍1.73 m2 and UACR ≥300 mg/g Cr), ACE in­hibitor or ARB ther­a­py re­duces the risk of pro­gres­sion to ESRD (61-63). More­over, an­ti­hy­per­ten­sive ther­a­py re­duces risks of car­dio­vas­cu­lar events (57).

Blood pres­sure lev­els <140/90 mmHg are gen­er­ally rec­om­mend­ed to re­duce CVD mor­tal­i­ty and slow CKD pro­gres­sion among peo­ple with di­a­betes (60). Lower blood pres­sure tar­gets (e.g., <130/80 mmHg) may be con­sid­ered for pa­tients based on in­di­vid­u­al an­tic­i­pat­ed benefits and risks. Pa­tients with CKD are at in­creased risk of CKD pro­gres­sion (par­tic­u­larly those with al­bu­minuria) and CVD and there­fore may be suit­able in some cases for lower blood pres­sure tar­gets.

ACE in­hibitors or ARBs are the pre­ferred first-‍line agent for blood pres­sure treat­ment among pa­tients with di­a­betes, hy­per­ten­sion, eGFR <60 mL/‍min/‍1.73 m2, and UACR ≥300 mg/g Cr be­cause of their proven benefits for pre­ven­tion of CKD pro­gres­sion (61-64). In gen­er­al, ACE in­hibitors and ARBs are con­sid­ered to have sim­i­lar benefits (65,66) and risks. In the set­ting of lower lev­els of al­bu­min-‍uria (30–299 mg/g Cr), ACE in­hibitor or ARB ther­a­py has been demon­strated to re­duce pro­gres­sion to more ad­vanced al­bu­minuria (≥300 mg/g Cr) and car­dio­vas­cu­lar events but not pro­gres­sion to ESRD (64,67). While ACE in­hibitors or ARBs are often pre­scribed for al­bu­min-‍uria with­out hy­per­ten­sion, clin­i­cal tri­als have not been per­formed in this set­ting to de­ter­mine whether this im­proves renal out­comes.

Ab­sent kid­ney dis­ease, ACE in­hibitors or ARBs are use­ful to con­trol blood pres­sure but may not be su­pe­ri­or to al­ter­na­tive proven class­es of an­ti­hy­per­ten­sive ther­a­py, in­clud­ing thi­azide-‍like di­uret­ics and di­hy­dropy­ri­dine cal­ci­um chan­nel block­ers (68). In a trial of peo­ple with type 2 di­a­betes and nor­mal urine al­bu­min ex­cre­tion, an ARB re­duced or sup­pressed the de­vel­op­ment of al­bu­minuria but in­creased the rate of car­dio­vas­cu­lar events (69). In a trial of peo­ple with type 1 di­a­betes ex­hibit­ing nei­ther al­bu­minuria nor hy­per­ten­sion, ACE in­hibitors or ARBs did not pre­vent the de­vel­op­ment of di­a­bet­ic glomeru­lopa­thy as­sessed by kid­ney biop­sy (70). There­fore, ACE in­hibitors or ARBs are not rec­om­mend­ed for pa­tients with­out hy­per­ten­sion to pre­vent the de­vel­op­ment of CKD.

Two clin­i­cal tri­als stud­ied the com­bi­na­tions of ACE in­hibitors and ARBs and found no benefits on CVD or CKD, and the drug com­bi­na­tion had high­er ad­verse event rates (hy­per­kalemia and/‍or AKI) (71,72). There­fore, the com­bined use of ACE in­hibitors and ARBs should be avoid­ed.

Min­er­alo­cor­ti­coid re­cep­tor antag­o­nists (spirono­lac­tone, eplerenone, and finerenone) in com­bi­na­tion with ACE in­hibitors or ARBs re­main an area of great in­ter­est. Min­er­alo­cor­ti­coid re­cep­tor antag­o­nists are ef­fective for man­age­ment of re­sis­tant hy­per­ten­sion, have been shown to re­duce al­bu­minuria in short-‍term stud­ies of CKD, and may have ad­di­tional car­dio­vas­cu­lar benefits (73-75). There has been, how­ev­er, an in­crease in hy­per­kalemic episodes in those on dual ther­a­py, and larg­er, longer tri­als with clin­i­cal out­comes are need­ed be­fore rec­om­mend­ing such ther­a­py.