bumex for patient in renal failure

hodgieRN · Oct 30, 2012

Diurectics aren't necessarily contraindicated. Kidney disease has many different levels of failure. Some pt's still have the ability to produce urine even if it's very little. Think of it like this...Kidneys mainly act as a filter for proteins, electrolytes, wastes, urea, and reabsorbing water. Some pt still can pass water but lack the capabilities of filtering out larger molecules or lack both filtering and excreting water. Different areas of the nephron each have it's own capabilities (proximal tubule, the distal convoluted tubule, and the collecting tubule). The kidney's ability to reabsorb water may still work despite everything else failing. Like a leaf being unable to pass through a pool filter while water passes through.

The GFR measures the kidney's ability to filter, not necessarily it's ability to excrete water. Proteins, creatinine, myoglobin, etc, can't pass through and that is what the GFR is measuring....it's filtering properties. That is why her BUN/ creatinine is high....the kidney can't filter them out. (fyi...did you know that troponin levels are elevated in pt's with kidney failure? Cardiac enzymes levels will produce false positives b/c the kidney are actually responsible for excreting troponin, which are proteins related to heart muscle)

It sounds like your pt still has some capabilities to produce urine (water and urea). The bumex enhanced it by exaggerating water excretion. So the GFR isn't wrong b/c her BUN/ creatinine levels are high, suggesting a failure in filtering. The bumex also allowed the kidney to excrete little more electrolytes than normal. (fyi... An even better measurement of filtering is using the creatinine clearance vs the GFR.)

Another fyi... :) Your pt's hemoglobin 9.1, meaning she's anemic. Do you know why renal failure pt's are anemic? Your kidneys make something called erythropoietin. When erythropoietin is released, it signals your bone marrow to produce red blood cells. If you have kidney failure, then there no production. So, doctors prescribe Epogen to make up for it. Epogen is what cyclists use during tournaments to increase their hemoglobin production so they can have better levels of oxygenation. This is where is term "blood doping" come from. Most dialysis pt receive Epo after dialysis.

dudette10, MSN, RN · Oct 31, 2012

Cardiac enzymes levels will produce false positives b/c the kidney are actually responsible for excreting troponin, which are proteins related to heart muscle)

Overall, wonderful explanation, but I have a question about this.

How are you using the word "excreted"? Yes, kidneys "excrete" troponins in urine, but cardiac muscle is responsible for releasing troponins into serum. I thought that cardiac muscle released elevated levels of troponins in kidney failure (resulting in a a high serum troponin level on blood tests) because of the kidneys are unable to filter blood at a normal rate, therefore "backing up" fluids to the heart and causing the heart muscle to release troponins in the absence of true myocardial infacrction.

Please correct me if I misunderstood your post or I'm flat-out wrong. :)

nurse_jer · Nov 1, 2012

wow, thankyou for such a thorough answer. that makes alot of sense now. i was under the impression that GFR would control how much could be excreted. most of the renal pt's ive had with GFR in the teens didnt urinate much of anything. now i understand that it IS possible to have a low GFR and void.

thanks!

hodgieRN · Nov 1, 2012

Yes, by the word "excretion" I am referring to it being sent outside the body via the kidneys. Excretion refers to the elimination of a substance... with elimination meaning something that was created (like a substance that has been metabolized and produced specifically for elimination). That's actually a great question b/c you are going to hear a lot of terms with excretion vs. secretion. Secretion describes a substance that is released by a cell ,such as a hormone or mucous, that becomes a product for purpose. Hormones that are released from the pituitary gland are secreted...they are acting as chemical messengers for another purpose. You wouldn't say hormones are excreted from pituitary gland b/c that would mean they are being packaged for elimination. The politically correct term is secreted. Something excreted by the kidneys is urine vs something that is secreted by the kidneys is erythropoietin, calcitrol, and renin. So, the kidneys do in fact excrete troponins b/c they are eliminating it. And you are right that the heart muscle is secreting troponin ( yes, they are on their way to be excreted), but it has to go through the kidneys to actually be "excreted."

Now, If I am reading what you are saying correctly. The kidney failure, which has caused fluid overload, will cause the heart to release excess troponin, causing a false positive. Not true and here's why. Troponin (heart muscle cell) is released throughout the day in any person. You even have troponin levels right now...very low of course. And that's b/c all organs will slough cells into the bloodstream at a low rate. Your skin is constantly sloughing off cells. Your heart, lungs, mucosa, the dermal layers in your skin are all slowing, sloughing away. Meanwhile, the new germ cell layer (the base layer of skin) will eventually work it's way up and be expelled from the body. When something is injured and ischemic, those necrotic cells slough off at an astounding rate....enough to actually measure it in the lab tube. So,when someone has an MI, all those dead cells are leaving the heart in droves....thousands of cells I guessing, which results in elevated Cardiac enzymes. But fluid overload does not cause elevated (Excess) troponion. Now, if the fluid overload is so bad that fluid is congesting the heart, causing it to fail(which means the heart is being overworked aka ischemia), then that might cause an elevation. But just having fluid overload r/t of kidney failure is not supported. For argument sake, you would have to say that all pts with fluid overload would have elevated trops. Having fluid overload (edema) does not does not cause the heart to release extra troponins.

But there is something....In fluid overload, the heart can become stretched (because of everything backing up) and this will release Brain Natriuretic Peptine (BNP). BNP or BNPepetide is a biomarker that signals the stretching of the heart wall. Pt with elevated BNPs are treated as CHF pts b/c elevated BNPeptides indicate fluid overload. So, maybe that's what you were talking about. Fluid overload doesn't release troponins but it definatly releases BNP. On the other hand, troponins are released during an MI, chest compressions, chest trauma, anemia, blood loss, or even open heart surgery...... OR...... It is the normal circulating troponin (which is supposed to be excreted via the kidney) now has no where to go! And the normal everyday sloughing of troponin cells start to add up...more...and more...and more..They are sitting at the airport with their bags packed and no place to go. So, they start building up to a point, and if you took a blood sample, it would look like their Troponion levels are elevated, even though there was no cardiac event. It a false gathering of Troponions that should have flown out on the flight from the airport if it weren't for those stupid kidneys! And most dialysis pt have a troponin level of "1. or 1.3, which is a false positive." The Cardiologist will scream at you for telling him that the pts troponins levels are elevated as you mention the pts Kidney failure history. And those troponins will go down after.....once they are excreded with dialysis!

Make sense?

dudette10, MSN, RN · Nov 1, 2012

Yes, that does make sense. Thank you for that. I had the pathophysiology wrong about exactly how the troponins were elevated in kidney failure in the absence of a cardiac event.

turnforthenurse, MSN, NP · Nov 1, 2012

Excellent explanation hodgie, thank you!

OP, I have had patients with a GFR of

hodgieRN · Nov 1, 2012

No problem, glad to help! It's great that you are thinking about how processes occur in the body with cause and reaction. If you go on to be a nurse practitioner, that thought process will be the thing that guides you toward making a solid differential diagnosis. Thinking "this symptom might have resulted from this disease or event."

Angela21 · Nov 2, 2012

Jollylama, this is a good question and I'm so glad you asked it. I actually came across this post while simply searching "renal failure" because I'm currently studying this in preparation for NCLEX and have found searching for whatever I'm studying on allnurses to be a very useful way to study. This is a perfect case in point --

HodgieRN, I just wanted to say thank you so much for your very detailed but easy to understand posts. In nursing school we were told of things like "troponin" and how the levels should be checked when an MI is suspected but we were never told the why behind it. I wasn't aware that RF (and the other things you mentioned) cause the level to be elevated nor was I aware we all have some minimal level of troponin present at all times. Reading your post I found myself just delighted because it made absolutely perfect sense! I know I will never forget this now. Your explanation of the GFR and why RF patients develop anemia was also great. I had a good idea about those two but your explanation really set it clear in my mind. I really cannot properly express my gratitude to you and nurses like you that are willing to go above and beyond to help their fellow and future fellow nurses! Simply put, you guys rock! :)

Esme12, ASN, BSN, RN · Nov 2, 2012

A chronic renal failure patient in fluid overload can have an elvated troponin....the exact cause is unclear.

Many clinicians debate the usefulness of troponin and other biomarkers in patients with impaired renal function for several reasons. Often, patients admitted for non-cardiac problems will have incidentally elevated troponins. On the other hand, patients in heart failure may have positive troponins for any number of reasons, whether due to an acute ischemic myocardial insult or as a consequence of a chronic fluid-overloaded state. Some clinicians even question whether or not elevated troponins represent myocardial injury at all. In each of these cases, concomitant renal disease only further complicates the clinical picture.
Troponin (Tn) subtypes T, I, and C exist together as a protein complex bound to actin thin filaments in both skeletal and cardiac muscle. This complex regulates muscle contraction and relaxation via its interaction with actin and calcium ions released from the sarcoplasmic reticulum of the muscle cells. TnT and TnI have different isoforms in cardiac and striated muscle, which allows laboratory assays that can identify troponins specifically released from injured myocytes in the heart.
Several studies have explored the significance of elevated troponins in patients with concomitant renal disease [1-10]. Up to 80% of patients with low glomerular filtration rates (GFR), and in the absence of acute coronary syndromes or congestive heart failure, have positive values for TnT, regardless of whether or not they receive dialysis treatment. On the other hand, one large study that included more than 700 patients found the prevalence of TnI to be only 0.4-6% depending on the cut-off value chosen [3]. These results suggest that a positive TnT may represent a common and benign incidental finding in patients with impaired renal function, whereas a positive TnI occurs only in the setting of an acute coronary event. However, other studies have demonstrated consistent associations between elevated TnT and hard endpoints such as death and myocardial infarction [2,3,5,6]. Therefore, although chronic kidney disease appears to be nonspecifically associated with positive TnT values, the absolute TnT level may serve as a useful prognostic marker.
http://www.clinicalcorrelations.org/?p=1968

Cardiac troponin (cT) is released after myocardial damage. In the appropriate clinical setting, a measured elevation of cT can increase the diagnostic rate of myocardial infarction and acute coronary syndrome. Elevations of cT, however, can occur in a wide variety of other clinical situations. Failure to recognize this can lead to an over-diagnosis of myocardial infarction (MI).

I have addressed this is the past......here is a great thread with a ton of references

https://allnurses.com/emergency-nursing/elevated-troponin-renal-633135.html

Serum cardiac enzymes in patients with renal failure

hodgieRN · Nov 2, 2012

Thank you! That was really nice to hear! Again, glad to help!