HD and ACE-I and K

[Farcus]

Clin Pharmacist here with a question for nephrologists or anyone who can chime in, today i had a pt on my floor with K of 7s, standard reversal put through and pt is esrd w/ ihd mwf, on admission K was 5 and pt on home dose lisinopril 40mg daily restarted. Being the pharmacist, I gave the md a call regarding the pt's K and ace-i and md called back and told me due to moa of hyperkalemia ace-i in esrd hd pt usually is not an issue? pt on ace-i,bb,and clonidine for htn, though no dhp-ccbs. Now I know there are a lot of data on ace-i/arb for residual renal function/cv benefit what not but I have never heard of this rationale in particular by this particular nephrolgoist, I understand hyperK 2/2 to aldosterone so how does this have to do with esrd pt with hd and hyperK? Did a quick pubmed search and indeed there are some LIMITED studies out there saying k shouldn't be an issue "http://ndt.oxfordjournals.org/content/22/4/1150.full" although everything I been taught/literature/seen suggest it can cause hyperkalemia. I hope someone can explain this to me. thanks! any literature would be much appreciated since i mostly find it can cause hyperK.

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[nephappl]

ACEIs and ESRD: For you to develop hyperkalemia by using ACEIs you need functioning kidneys able to retain potassium induced by the decrease in aldosterone. Patient with ESRD and no functionally anaphric can not retain K, if you have residual function you can certainly have. Thing is hemodialysis is extremely effective removing K so the only factor affecting K balance is potassium intake and acid base status which is taken care of by the bicarbonate you put in the dialysate. We use them a lot in HD patients as for most of them angiotensin is a significant factor in patient's hypertension.
Potassium supplementation is an issue as dialysis is the only way to get rid of potassium , also you can change the K concentration in the dialysate to take patient's K level where you want it to be. In peritoneal dialysis many patients need K supplementation as normally PD solutions are K free so K is dialyzed.
So in summary Can ACEIs induced hyperkalemia in ESRD pts?Yes if you have residual kidney function however the effect is completely overcome by the hemodialysis treatment that makes it irrelevant in clinical parctice

 

[CptNemo]

The bowel plays a role.

Patients with ESRD have a >3-fold increased secretory capacity for potassium via their bowel compared to ppl with normal renal function. Part of this process is regulated by aldosterone, as the bowel is responsive to aldosterone. The old-school physiologists/nephrologist bring this up from time to time.

http://www.ncbi.nlm.nih.gov/pubmed/15772943
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1552657/

Is this clinicially relevant? Most of the time, probably not because, as mentioned above: HD/PD takes off enough or if it doesn't, the K bath is adjusted so that it does; but if someone is already prone to hyperkalemia, ACE-inhibitors will reduce their K losses (via the GI tract), even if they are anuric. So it would not be unreasonable to hold them in the setting of ESRD + hyperkalemia.

 

[Farcus]

Thanks for the information nephappl and cptnemo. So I guess what you guys are basically saying is that since you have ESRD (assuming none to near to none residual function) it would be physiologically impossible given ace-i moa on hyperK is due to suppression of aldosterone but there would not be much effect on K accumulation since the we're assuming most of the nephrons and mr-receptor are none functioning. Furthermore, if there is some residual function and some K accumulation, this is at least partially offset by significant >3x increase in secretion of K via GI and also regardless of residual function, offset by HD extraction. I guess i just didn't make the connection that you need functioning kidney to have K accumulation from low aldosterone.