Re: Serum creatinine elevation after renin-angiotensin system blockade and long term cardiorenal risks: cohort study
Schmidt et al’s article uses a large population sample to try and inform practitioners’ response to the rise in creatinine seen in a proportion of patients following initiation of angiotensin inhibition/blockade. Their data exposes a number of areas of poor prescribing practice, but unfortunately does not really help clinicians with their decision making process.
More than 29,000 patients were taking NSAIDs when the ACE-I/A2RB was initiated, a drug interaction that is pathophysiologically known to increase the likelihood of a deterioration in kidney function and is contraindicated. Nearly 12,000 were taking a loop or potassium sparing diuretic, which increases the risk of a deterioration in renal function and of hyperkalaemia, and implies the presence of significant co-morbidity.
While there was an increase in the early relative risk of ESKD, the absolute risk of ESKD is low compared to the absolute risk of cardiac events and death. The authors state that the data were restricted to patients that continued to use an ACE-I/A2RB. Given that the major theorised benefit of these drugs in non-proteinuric renal disease is reduction in cardiovascular events and overall mortality, and not reduction in ESKD events, we do not know whether or not the outcomes in this study are actually favourable; i.e. continued use reduced these event rates. What happens to those where the medication is discontinued? The primary finding of the study appears to be that a rise in creatinine (of any level) identifies a very high risk group, presumably due to their abnormal vascular response. We still don’t know what we should then do with these patients once we have identified them.
Competing interests: No competing interests