For a number of years I have advised students and residents to keep a notebook of topics that arise on rounds. Pick 2 topics that we discussed, then read about them for 5 minutes. Everyone has 5 minutes to read about a topic.
The idea here is that cognitive science has shown that we remember better if we both hear about a topic and read about the same topic.
Since I have embarked on this project of one medical tweet each day, I have embraced the 5 good minutes philosophy. So I will use the hashtag #5goodminutes each day, along with other tags.
Today I want to increase understanding of Type IV RTA as many students, residents and practicing physicians find this topic confusing.
Type IV RTA has other names – hyperkalemic normal gap metabolic acidosis and hyporenin/hypoaldo. Generally the pathophysiology comes starts with decreased renin production which leads to decreased aldosterone production. With decreased aldosterone production, the tubule retains potassium. The key here is hyperkalemia. That comes first and results in a normal gap acidosis. Hyperkalemia inhibits ammonia production. There are apparently several mechanisms here, but the one I understand best is that high potassium inhibits glutaminase. Ammonia production includes glutaminase acting on glutamine + H2O to produce glutamate + NH3 (ammonia).
Short aside – hypokalemia stimulates this enzyme and that explains why hypokalemia increases hyperammonemia.
The lack of ammonia means that the kidney cannot buffer our daily acid input – eventually resulting in a decreased bicarbonate.
Who gets type IV RTA? Predominantly patients with diabetic nephropathy but also several interstitial nephropathies (Sickle cell disease, Analgesic nephropathy, Lead nephropathy, Chronic pyelonephritis and Obstructive nephropathy).
Why is it so important? Given the increased prevalence of diabetic nephropathy, we see these patients most frequently. These patients generally have stage 3b or 4 CKD. Here is the other problem. Many patients have relatively decreased renin, but not quite low enough to give severe hypoaldosteronism. Imagine such a patient who has either proteinuria or systolic dysfunction (or both). They now have a strong indication for an ACE inhibitor or an ARB. So we take a patient with subclinical hyporenin and now have significant hypoaldosteronism.
Hyperkalemia in these patients becomes a major outpatient challenge to using ACE-I or ARB.
We have a new drug – patiromer (trade name Veltassa) that patients can safely take daily to excrete potassium by GI binding. The wholesale cost for patiromer (regardless of strength) is $595 per 30 packets.
I hope this short explanation helps you understand type IV RTA and also understand why nephrologists and cardiologists will be prescribing patiromer.
