Blog entry by Meguid El Nahas
A number of publications have recently linked AKI to the development or progression of CKD.
In the November issue of cJASN:
Thakar et al as well as an editorial on the topic highlight this important issue.
Thakar and colleagues report the increased incidence of CKD in elderly diabetics who develop one or more episodes of AKI.
This publication along with another 5 reviewed in the editorial by Bydash and Ishani stress teh association between AKI and CKD.
In the Thankar et al paper, elderly diabetics with CKD3 and significant proteinuria were at the highest risk.
I ask myself, what do T2DM, with CKD and heavy proteinuria have in common?
The answer is the "Elephant in the Room" that everybody chooses to ignore... INHIBITION OF THE RAAS!!!
So I suspect that these older diabetics with CKD3 ar eall on the dreaded ACE inhibitors, ARBs or a combination of both when in reality they have significant underlying atherosclerosis, CAD as well as peripheral vascular disease; also most likely to be suffering from atherosclerotic renovascular disease and ischemic nephropathy.
I therefore urge the authors of these publications to examine the medication these patients are on and the relationship between RAAS inhibitors and the development of AKI/CKD.
Also, I urge Nephrologists to spare their older patients with T2DM and atherosclerotic manifestations (that most have) the use of inhibitors of the renin angiotensin aldosterone system (RAAS). These are often immediately detrimental to these patients kidney function. They may also accelerate the decline of kidney function as shown many years ago by Suissa and colleagues in Canada and by Onuigbo and colleagues in the US.
BUT also, they may constitute an added risk to elderly patients who have an AKI insult thus further compromising their acute insult and further compromising their pre-existent CKD.