These diuretics work in the collecting duct so they’re not very good diuretics. So what do we really utilize this drug class for?
The drug class says potassium sparing meaning it doesn’t remove potassium (it spares potassium). So what happens to blood potassium? It actually goes up because you don’t lose as much as usual! This is good for someone who is hypokalemic. Why would they be hypokalemic? Ironically, because they’re on diuretics! So this would be used together with other diuretics so they won’t become hypokalemic. There are some medications that have two diuretics in one capsule/tablet to get the beneficial effects so the patient doesn’t have to take two medications.
Relevant: Both the Thiazide diuretics and Loop diuretics cause a decrease in potassium.
Two types of potassium sparing diuretics: Direct acting and Indirect acting
Direct acting, meaning they work directly on the receptor in the collecting duct. They do block the reabsorption of sodium and water, but how well do they do it? Not very good because it’s occurring in the collecting duct of the nephron. We are primarily utilizing it for its potassium sparing purposes.
- Triamterene (Dyrenium) – p.o. – direct acting
- Amiloride (Midamor) – p.o. – direct
Indirect acting: These are competitive inhibitors of aldosterone. So let’s refresh our memory on aldosterone: Aldosterone causes sodium retention and water retention and potassium loss. Aldosterone works right around the collecting duct as well. These indirect drugs antagonize aldosterone, which causes the reverse effects of aldosterone: We lose water, sodium and retain potassium. Since it works in the collecting duct, it’s a minor amount of loss.
- Spironolactone (Aldactone) – p.o. – Indirect acting
- Eplerenone (Inspra) – p.o. – Indirect acting
Use of K+ Sparing Diuretics
Spare potassium loss of diuretics (Pharmacologically they have very minimal diuretic effect but they do decrease secretion of potassium.)
And additional uses of spironolactone (below)
Edema Associated with Liver Failure
A person with alcohol/liver disease probably has cirrhosis of the liver and can’t detoxify the blood. Albumin won’t be produced by the liver which means the individual can’t keep fluid in the blood stream and one of the symptoms of an individual that has alcohol-liver disease is abdominal fluid buildup (ascites) and they could have 20-30 liters of fluid in there. How do we get that fluid out? We could get a needle and try to drain 20-30 liters of fluid or we could use medication to pull it out.
So we need to utilize a diuretic. In this case if we use a loop diuretic, we could kill the patient because it will pull the fluid out of the blood stream when all the fluid is in the abdominal cavity. Let’s see what’s actually going on with this patient. There isn’t fluid in their blood stream, meaning the heart isn’t pumping a lot of fluid. The kidney senses there isn’t fluid coming in so it thinks there is dehydration. So the kidney is going to start up the RAA system. The kidney is going to release renin, which causes angiotensin release (the most powerful vasoconstricter) and then aldosterone (sodium/water retention). We retain the sodium and water, but there isn’t enough osmotic pressure to hold that sodium and water in, so it ends up in the abdominal cavity and that’s why the ascites just keeps getting worse and worse.
How do we stop this horrible cycle that’s causing aldosterone to keep bringing in sodium and water and ending up in the abdominal cavity?
If we antagonize aldosterone with potassium sparing diuretics such as spironolactone, we cause a sodium/water loss which could cause cardiovascular collapse BUT because it’s occurring in the collecting duct, it’s not going to be a powerful diuretic effect. If we pull in a small amount of water back into the blood stream and as long as they continue the therapy, up to a liter a day can be emptied from the abdominal area. So this will take weeks of therapy to unload that 20-30 liters.
Edema Associated with Congestive Heart Failure (CHF)
A patient has heart failure: The heart is weak and can’t pump the fluid and it ends up in the lungs and legs. The amount of perfusion going to the kidneys drops. The kidney thinks dehydration is occurring. Is a person dehydrated? Absolutely not but the kidneys think so.
So the kidneys cause the release of renin, then angiotensin 1-2 which causes vasoconstriction, putting more strain on the heart, then we release aldosterone which causes sodium/water retention which is also bad. What happens to the perfusion of the kidneys? It decreases so the kidneys think there is more dehydration which releases more renin. This is a lethal cycle and the person will be dead in 3 years if this doesn’t get corrected.
How do we stop this? We could use loop diuretics and it won’t be lethal to give them a loop diuretic but it’s NOT going to stop this cycle! One thing we could do is block aldosterone to create a sodium/water loss but it’s not going to be a great loss because potassium sparing diuretics work in the collecting ducts.
Toxicities of potassium sparing diuretics
Hyperkalemia:Â If a person is on this drug, it’s a rare day that they’re also going to be getting potassium.
Therapeutic alternatives
Foods high in potassium such as bananas.
Or potassium supplements but the risk is that if you release large amounts of potassium, ulcers can be created. Another way to reduce that risk is to give that patient liquid potassium chloride but most people can’t tolerate it because it tastes like salt so they put it in grape flavor and it tastes like grape salt so people don’t like it.
We could also give potassium intravenously: In the past there have been some really bad errors with potassium. If you’ve ever seen a vial of KaCl for injection (which is rare cause it’s not allowed on nursing floor anymore), it says it must be diluted, so you have to put it in a piggyback bag or full liter bag. Even if it’s diluted, patients complain that it’s burning and it hurts. Nurses were not diluting it properly and administering it directly and the patient would be screaming bloody murder but that wouldn’t be the problem. The problem would be when their hearts would stop in a few minutes. This is how we kill prisoners, actually (high doses of potassium). So nowadays, there’s only one place where you’ll find a vial of KaCl, and that’s in the pharmacy.
