ACEI/ARBs dilate the efferent arterioles which is renal protective in long run. However, they should be held in acute kidney injury (AKI) to allow compensation and increased clearance. I am not sure if they should be held in a patient with rhabdo that has mildly impaired renal function. A brief literature search and UpToDate search did not give a clear answer.
It would seem that keeping ACEI/ARB might be helpful (avoid increased pressure on glomerulous when toxin is present) but I could also see allowing arteriole construction might help maintain renal function. Anyone studied this, know of research or have evidence based thoughts? Could be a nice clinical study...
ACEI/ARBs should be avoided in the situations of advanced CKD, AKI, intravascular volume depletion (dehydration status) which might be highly associated with rhabdomyolysis. I believe that ACEI/ARBs have to be discontinued when severe rhabdomyolysis occurs.
Yes ACEI /ARBs should be discontinued in the clinical situation mentioned
should be discontinue with AKI with or without intravascular volume dysregulation
As per other answers, believe ACEi should not be used in this setting.
Thank you for your answers. My inclination is also the hold the ACEI/ARB temporarily in a patient (with normal to mildly impaired renal function) who has rhabdo in addition to standard treatment. There seems to be a paucity of research on the topic so making an evidence-based decision is difficult.
I can see a potential theoretical benefit to both continuing and holding in this situation. (Percieved benefit from continuing would be to maintain less pressure on glomerulus at the same time as heme pigment levels are highest, potentially preventing AKI by lessening tubular accumulation and injury). Obviously, volume replacement should be the primary treatment.
What was the indication for ACEI/ARB in this patient? What was the baseline creatinine in this patient ?. The decision to stop these drugs in AKI ( of any etiology ) is based on evidence based medicine & you are fully justified in stopping them . ACEI/ARB , NSAIDS & Nephrotoxic antibiotics are the common drug combinations which can cause AKI in situations such as hypovolemia & sepsis . Withdrawal of these drugs or avoiding them improves renal function in early stages of AKI ( stage 1 or 2 ).
Thomas
I think if AKI is at all an issue, it would be prudent to withhold ACEi/ ARB until the acute kidney injury and its significant risk factors (rhabdomyolysis in this case) settles.
Although ACEi/ ARB have a useful long term Reno-protective effect in many CKD patients (particularly those with proteinuria or signicant albuminuria) the short term impact of its affect efferent arteriolar vasodilatation is almost always a drop in intra-glomerular pressure- something that can be desirable in the long term in slowing CKD progression in proteinuric disease, but in the short term, is almost always associated with a variable (and generally reversible) drop in GFR.
That short term drop is not something you want added into the mix during any AKI episode or its assessment- even if it is something we accept after recovery, in a stable patient- for whom we might want to maximise and reap the long term benefits of renin angiotensin modulation.
In any AKI settings it is better to avoid ACEI / ARB, so that the renal dysfunction can recover. Once there is recovery then it is good to restart them.
ACE inhibitor should be avoided in rhabdomyloysis as a cause of AKI, as ACE inhibitor may worse GFR, beside risk of severe huperkalemia.
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