"#69: CKD (Chronic Kidney Disease) Prescribing Do's and Don'ts" - Help From The Curbsiders

As I always remind my occasional visitors, these posts are just my study notes. The Search And Categories Functions of the blog allow me to easily access any of the topics I have studied and reviewed. And so for the topic of today’s post you should just go to #69: CKD Prescribing Do’s and Don’ts with @kidney_boy, Joel Topf NOVEMBER 27, 2017 By MATTHEW WATTO, MD and listen to the podcast and review the outstanding show notes.

I’ve embedded the outstanding podcast below:

What follows are excerpts from #69 CKD Prescribing Do’s and Don’ts:

Clinical Pearls:

Many medications cause serious issues in patients with chronic kidney disease (CKD).
Bactrim (trimethoprim-sulfamethoxazole) was associated with 3 excess cardiac deaths per 1,000 prescriptions presumably due to hyperkalemia (i.e. patients with CKD at risk)
Bactrim blocks K+ secretion in renal tubule: blocks ENaC channels in distal nephron causinghyperkalemia (acts like amiloride)
Bactrim also competes with creatinine secretion so may cause a benign rise in serum creatinine
Patients with CKD depend on prostaglandins for vasodilation of afferent arterioles and renal blood flow. NSAIDs block prostaglandin activity and can cause acute kidney injury. Risk is high in patient taking an NSAID + ACE inhibitor (ACE-I) + diuretic (or if volume depleted)!
KDIGO Guidelines recommend avoiding NSAIDS in patients with CKD, but the evidence suggests that risk of NSAID use in CKD patients is pretty low:
- The Male Physician Study showed no elevation in serum creatinine with consistent NSAID use
- The PRECISION Trial also showed only ~1% risk of kidney events in CKD patients with daily high-dose NSAIDs
- We’d avoid in CKD 4. Consider cautious use in CKD 2-3.
“Strong” observational data demonstrates a link between proton pump inhibitors and CKD. Mechanism unclear, but theories include recurrent acute interstitial nephritis(AIN)/acute kidney injury (AKI), chronic hypomagnesemia, and interference with the potentially renoprotective alkaline tide phenomenon (Toth-Manikowski, S and Gram M Kidney Int Reports May 2017)
With ACE-inhibitors (e.g. lisinopril): Expect a rise in serum creatinine. If the creatinine bump > 30%, stop ACE-I therapy. An increase in creatinine after ACE-I may show greatest risk of mortality(though it unclear what would happen if the patients with bumps were not on ACE-I)
Contrast-induced kidney injury (CIN) may be overestimated in literature. The AMACING trial shows that pre-hydration does not reduce kidney injury in those exposed to contrast. True CIN likely much more rare than commonly thought!
Metformin is OK to use until estimated GFR is under 30 ml/min
ACE-Is demonstrate a significant reduction in progression of chronic kidney disease and reduction in proteinuria per the RENAAL and IDNT trials. Less patients had doubling of serum Cr, and progression to end-stage renal disease (ESRD). Mortality benefit was NOT observed.
Spironolactone and non-DHP calcium channel blockers (verapamil, diltiazem) can reduce proteinuria but have not been shown to improve clinical outcomes in CKD (source UpToDate).
Canagliflozin and empagliflozin (SGLT2-inhibitors): shown to decrease mortality albuminuria, and loss of renal function among patients type 2 diabetes at high cardiovascular risk in the CANVAS andEMPA-REG studies. View Dr. Topf’s video summary of the studies or read his blogpost on Precious Bodily Fluids