S-Kreat Elevations After Starting Angiotensin-Renin Blockade Signal High Risk.

[Argirios Argiriou]

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SUMMARY AND COMMENT | GENERAL MEDICINE

April 25, 2017

Serum Creatinine Elevations After Starting Angiotensin-Renin Blockade Signal High Risk.

Paul S. Mueller, MD, MPH, FACP Reviewing Schmidt M et al., BMJ 2017 Mar 9; 356:j791

Patients whose levels rose after starting angiotensin-converting–enzyme inhibitors or angiotensin-receptor had worse outcomes.

National Kidney Foundation guidelines recommend stopping angiotensin-converting–enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) if serum creatinine increases by ≥30% after starting treatment. However, the rationale for this 30% threshold is unclear. In this cohort study of 122,000 U.K. adults, researchers assessed outcomes associated with rises in serum creatinine concentrations during the first 2 months after beginning ACE inhibitor or ARB treatment.

About 2100 patients (1.7%) had serum creatinine increases of ≥30% after starting treatment. Compared with patients in whom creatinine increased by <30%, those with larger increases were more likely to die (adjusted incident rate ratio, 1.84) or to develop end-stage kidney disease (IRR, 3.43), heart failure (IRR, 1.37), or myocardial infarction (IRR, 1.46) during about 10 years of follow-up. Moreover, dose-response relations between serum creatinine and these outcomes were observed even when creatinine rose by 10% to 19% or 20% to 29% following ACE inhibitor or ARB initiation.

Comment

In this real-world study, which was subject to residual confounding, any increase in serum creatinine after starting ACE inhibitor or ARB treatment was associated with higher risks for death, end-stage kidney disease, heart failure, and myocardial infarction — with no distinct cutoff at 30%. Whether ACE inhibitors or ARBs directly cause adverse outcomes or just unmask underlying pathophysiology are unknown. Nonetheless, patients with increases in serum creatinine after starting these drugs should be recognized as a high-risk group and monitored closely.

Editor Disclosures at Time of Publication

Disclosures for Paul S. Mueller, MD, MPH, FACP at time of publication

Consultant / advisory board

Boston Scientific (Patient Safety Advisory Board)

Editorial boards

Medical Knowledge Self-Assessment Program (MKSAP 17 General Internal Medicine Committee); MKSAP 17 General Internal Medicine (author/contributor)

Leadership positions in professional societies

American Osler Society (Vice President)

Citation(s):

Schmidt M et al. Serum creatinine elevation after renin-angiotensin system blockade and long term cardiorenal risks: Cohort study. BMJ 2017 Mar 9; 356:j791. (Δεν είναι ορατοί οι σύνδεσμοι (links). Εγγραφή ή Είσοδος)

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[schumifer]

χμμμ  δε θυμάμαι να έβαλα ασθενή σε ΑΜΕΑ/σαρτάνη και να μην του ανέβηκε έστω και ελάχιστα η κρεατινίνη...

[GirousisN]

Schematic illustration of settings wherein angiotensin-converting enzyme (ACE) inhibitor therapy may worsen renal function. Conditions causing renal hypoperfusion include systemic hypotension, high-grade renal artery stenosis, extracellular fluid volume contraction (simplified as "dehydration" in the Figure), and administration of vasoconstrictor agents (non-steroidal anti-inflammatory drugs or cyclosporine, not shown), and congestive heart failure. These conditions typically increase renin secretion and angiotensin-II production. Angiotensin-II constricts the efferent arteriole to a greater extent than the afferent arteriole, such that glomerular hydrostatic pressure and glomerular filtration rate (GFR) can be maintained despite hypoperfusion. When these conditions occur in ACE-inhibitor treated patients, angiotensin-II formation and effect are diminished, and GFR may decrease. Adapted with permission from Circulation. 2001;104:1985-1991.[13]

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