Background Renin-angiotensin-aldosterone (RAAS) blockade is acclaimed, by consensus, to be renoprotective in both diabetic and non-diabetic chronic kidney disease (CKD). Contradictory reports exist regarding renal and cardiovascular outcomes after stopping RAAS blockade in advanced CKD. A few prospective, non-randomized, cohort studies have demonstrated improvement in kidney function after discontinuation of RAAS blockade. In this study, we investigated renal and mortality outcomes following the elective withdrawal of RAAS blockade after otherwise inexplicable acute kidney injury (AKI). Methodology We conducted a retrospective cohort analysis of patients enrolled between February 2018 and May 2021. Kidney function was monitored after elective withdrawal of long-term RAAS blockade in CKD patients presenting with new-onset otherwise inexplicable progressive AKI, defined by a >25% increase in baseline serum creatinine. Results In total, 71 patients, 69 Caucasians, one African American, and one Hispanic, were included in the study, with a male-to-female ratio of 42:29, and a mean age of 69.4 (37-95) years. Through February 2022, 12 patients had died, with eight remaining on hemodialysis for end-stage renal disease. Of the remaining 51 patients followed for 706 (40-1,478) days, baseline serum creatinine was 1.30 ± 0.42 (0.66-2.70) mg/dL, peak enrollment serum creatinine was 2.17 ± 1.06 (1.1-8.3) mg/dL (n = 51, p < 0.0001, t = 6.4872, df = 135), and serum creatinine after four years was 1.58 ± 0.54 (0.84-3.3) mg/dL (n = 50, p < 0.0001, t = 5.1805, df = 119). Death in 11 of 12 (91%) patients was from non-renal causes, and most deaths occurred despite improved kidney function. Conclusions Our results demonstrate clearly improved renal outcomes in most patients following the elective withdrawal of long-term RAAS blockade in CKD patients with new-onset progressive yet otherwise inexplicable AKI without increased cardiovascular mortality.
Keywords: acute kidney injury; chronic kidney disease (ckd); commitment bias; late-onset renal failure from angiotensin blockade; raas inhibitors.
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