ACE inhib & diuretics in the setting of AKI

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sthy

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Hi every one,

When do we need to hold ACE inhib in the setting of abnormal kidney function test?

How about diuretics? For K-sparing diuretics, I think when Cr is >1.5. But, does this apply to other diuretics too like loop diuretics?

Which kidney function test is normally good to look for to hold these med. I am asking this becouse sometimes Cr, Cr clearance are normal and only BUN or GFR becomes abnormal.

Thank you

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Hi every one,

When do we need to hold ACE inhib in the setting of abnormal kidney function test?

How about diuretics? For K-sparing diuretics, I think when Cr is >1.5. But, does this apply to other diuretics too like loop diuretics?

Which kidney function test is normally good to look for to hold these med. I am asking this becouse sometimes Cr, Cr clearance are normal and only BUN or GFR becomes abnormal.

Thank you

Depends on if we're talking an acute kidney injury or mere chronic renal disease.

In the setting of acute kidney injury we hold the ace-i to prevent any further loss of blood flow to the rest of kidney proper, and hopefully stave of ATN or prevent a worsening of ATN.

In the setting of chronic renal disease, the ace-i is your go to BP med, especially in the diabetic population.

And diuretics . . . the thiazide diuretics, except for metolazone, don't really work once GFR drops below like 30-40 in the chronic renal state. However, furosemide (and it's cousins torsemide and bumetanide) will work on whatever is left and often when you start running into GFRs <20 you like to add it on it give the beans a little boost. You obviously hold these (*initially) in the acute kidney injury setting to see how things settle out. Giving thiazide and loop diuretics together outside of the in-patient setting is generally considered a bad idea. Your other diuretics are generally a "bad" idea, though can be used, but the electrolyte problems they may cause is much more unpredictable in the CKD patient.

The thing to remember about the calculated GFR is that it's only real utility is in the chronic kidney disease state. I know, I know, the in-patient pharamacists dose all their meds off of a spot GFR, but you need to think about what is actually going on. If you clamped BOTH renal arteries what would your immediate effective GFR be? Zero, right? Assuming you have an initial Cr of 1.0, what would be your new measured Cr immediately after clamping? I'd be 1.0. And 24 hours later probably 2.0 . . . but the whole time there has been ZERO flow through any glomeruli . . .

The beans, dey fun!
 
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