One of the standard pieces of advice I give patients regarding chronic kidney disease is to avoid NSAIDs. However, not infrequently, patients have co-morbidities that demand NSAIDs. This usually triggers a conversation with my patients where I describe how ibuprofen can cause acute renal failure (I just took care of a new patient who developed RIFLE stage: Failure from a couple of doses of Mobic on top of stepped up ibuprofen use). I then explain that we extrapolate from the acute renal failure that NSAIDs are probably not beneficial in CKD and are likely harmful.
What about chronic renal dysfunction following long-term NSAID intake? In today’s medical environment, the evidence is weak. Prospective cohort studies in the Physicians’ Health Study (Rexrode et al, JAMA 2001) and the Nurses’ Health Study (Curhan et al, Arch Int Med 2004) failed to show an association between even high levels of cumulative lifetime NSAID intake and decrease in renal function.
My concern about these studies is the effect, we physicians have on the outcomes. Telling kidney patients to avoid ibuprofen and other NSAIDs is standard fare in CKD care. I’m sure these patients tend to use less ibuprofen and more acetaminophen, just as liver patients probably do the opposite. So educated patients with CKD will avoid NSAIDs but regardless of NSAID intake they will have a much higher progression to kidney related endpoints than their peers without a diagnosis of CKD. The epidemiologist sees a large cohort of acetaminophen users (my CKD patients) ending up with renal failure and sees that people with CKD use very little ibuprofen and may infere that acetaminophen causes kidney failure and ibuprofen is protective.
These are the type of questions that CRIC should be able to answer.