More intensive BP treatment may result in a modest reduction in GFR, which is thought to be primarily due to a hemodynamic effect and may be reversible. Electrolyte abnormali- ties are also more likely during intensive BP treatment. More intensive BP lowering in patients with CKD is also supported by a BP Lowering Treatment Trialists Collaboration meta-analysis of RCTs in patients with 2. Evidence comes from AASK (The African American Study of Kidney Disease and Hypertension), 2 small trials (1 positive, 1 negative), and a meta-analysis.S9.3-3,S9.3-6,S9.3-10,S9.3-11 Albuminuria is quantified by 24-hour urine collection. A 10% to 25% increase in serum creatinine may occur in some patients with CKD as a result of ACE inhibitor therapy. 3. ARBs were shown to be noninferior to ACE inhibitors in clinical trials in the non-CKD population.S9.3-35 to 25% increase in serum creatinine may occur in some patients with CKD as a result of ARB therapy. 9.3.1. Hypertension After Renal Transplantation Recommendations for Treatment of Hypertension After Renal Transplantation References that support recommendations are summarized in Online Data Supplements 39 and 40. COR LOE Recommendations IIa SBP: B-NR 1. After kidney transplantation, it is reasonable to treat patients with hypertension to a BP goal of less than 130/80 mm Hg.S9.3.1-1 DBP: C-EO IIa B-R 2. After kidney transplantation, it is reasonable to treat patients with hypertension with a calcium antagonist on the basis of improved GFR and kidney survival.S9.3.1-2 Synopsis After kidney transplantation, hypertension is common because of preexisting kidney disease, the effects of immunosuppres- sive medications, and the presence of allograft pathology.S9.3.1-3 Transplant recipients frequently harbor multiple CVD risk fac- tors and are at high risk of CVD events. 