Key result
Withdrawing RAAS blockade in CKD with progressive AKI is linked to ~27% lower serum creatinine.
Why the study?
Reports on renal and cardiovascular outcomes after discontinuing RAAS blockade in advanced CKD have been discordant, prompting longer-term evaluation of AKI reversal following RAAS blockade withdrawal.
Does elective withdrawal of long-term RAAS blockade improve kidney function in CKD patients with new-onset inexplicable progressive AKI?
Cohort (n=71)
No
Does elective withdrawal of long-term RAAS blockade improve kidney function in CKD patients with new-onset inexplicable progressive AKI?
Elective withdrawal of long-term RAAS blockade in CKD patients with inexplicable progressive AKI may lead to significant and sustainable improvement in renal function without increasing mortality.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for RAAS withdrawal in CKD with progressive AKI; randomized trials needed before clinical adoption.
Background: RAAS blockade is renoprotective for both diabetic and non-diabetic CKD. There have been discordant reports on renal and cardiovascular outcomes following RAAS blockade discontinuation in advanced CKD. To the contrary, a few prospective cohort studies have demonstrated reversal of otherwise inexplicable AKI in patients after discontinuation of RAAS blockade. This is a 4-year report of such a cohort. Methods: Prospective Cohort Analysis, enrolled between February 2018 – 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 as defined by a > 25% increase in baseline serum creatinine. Results: By February 2022, 12 patients had died, and 8 patients were on hemodialysis for ESRD. The remaining 51 patients, with a baseline serum creatinine of 1.30 ± 0.42 (0.66–2.70) mg/dL, have been followed up for 706 (40-1478) days. Peak serum creatinine at study entry was 2.17 ± 1.06 (1.1–8.3) mg/dL, n = 51, P < 0.0001, t = 6.4872, df = 135. Serum creatinine, 48 months later, was 1.58 ± 0.54 (0.84–3.3) mg/dL, n = 50, p < 0.0001, t = 5.1805, df = 119. Death in 7 of 8 (87.5%) patients were from non-renal causes; most deaths occurred despite improved kidney function. Conclusion: Elective withdrawal of long-term RAAS blockade in CKD patients with new-onset progressive yet otherwise inexplicable AKI results in significant sustainable renal salvage. Such self-selected patients generally exhibit improved renal outcomes without increased mortality. This is consistent with late-onset renal failure from angiotensin blockade (LORFFAB), first described in 2005 from the Mayo Clinic Health System in Northwestern Wisconsin.
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Macaulay Amechi (2022) conducted a cohort in Chronic kidney disease with new-onset progressive acute kidney injury (n=71). Elective withdrawal of long-term RAAS blockade vs. Peak serum creatinine at study entry was evaluated on Serum creatinine at 48 months (p=<0.0001). Elective withdrawal of long-term RAAS blockade in CKD patients with new-onset progressive AKI resulted in significant sustainable renal salvage, with serum creatinine decreasing from a peak of /dL to /dL at 48 months.
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