So here's what I know - Nephrotic syndrome is characterized by the TRIAD: hyperproteinuria, hypoalbuminemia, and hyperlipidemia. It leaves the patient with edema(usally periorbital....maybe ascites), decreased cardiac output secondary to hypovolemia, and hypotension. Someone please help explain why I would give an ACE-Inhibitor to a patient with HYPOVOLEMIA AND HYPOTENSION. Exact dose in my notes is 12.5 mg p.o. bid. Thanks!
Oct 26, '08
The edema caused by this can lead to pleural effusion. An ACE inibitor slows production of the hormone leading to they body's retaining fluid.
You can have hypotension without hypovolemia.
Last edit by SuesquatchRN on Oct 26, '08
Oct 28, '08
while studying for my acute renal failure exam, I read something about how angiotensin II actually causes renal arteriole vasoconstriction. This was according to my critical care textbook by Sole. Perhaps one of the cellular benefits of ACEI w/ nephrotic syndrome is preventing renal hypoxia and necrosis secondary to ineffective renal perfusion r/t renal arteriole vasoconstriction?
i have read contrasting info about protein restriction versus protein therapy. I think in some cases protein is restricted to prevent osmotic diuresis and further damage to the kidneys, or to prevent the protein from moving into spaces already affected by increased capillary permeabiltiy, further worsening edema in the lungs, etc.
I do understand how protein administration is important to maintain intravascular osmotic pressure to keep plasma within the vessels and not in the tissues.
according to baird, hicks, and swearingen's book called "manual of critical care nursing" for acute renal failure anyways protein restriction must maintain daily requirements but be minimal to prevent worsening of azotemia r/t the kidney's inability to excrete nitrogenous byproducts of protein catabolism like urea and BUN. Sounds like a good reason to me.
According to my medsurg book (ignatavicius and workman) ACEI prevent proteinuria but it does not elaborate on a microcellular level
Also from my medsurg book:
If GFR is normal, dietary intake of proteins is needed. If GFR is decreased, restriction of protein is warranted because of the same mechanism described above for ARF. With decreased GFR = decreased ability to excrete nitrogenous bases = azotemia = all those complications like encephalopathy, etc.
Does that make sense? It is confusing; however, because in nephrotic syndrome I'd expect there to be protein wasting so less accumulation of catabolic end products. If anyone can further clarify this concept, I'd be much appreciative.
This is just another example of how nursing is never black and white. the answer to your questions depends on how severe the edema is, if it's affecting the patient's ABCs, and if the azotemia is of greater importance. Perhaps intravascular volume can be maintained with dextran or another colloidal infusion, if protein restriction is the case?
Last edit by fiveofpeep on Oct 28, '08
: Reason: curiosity
Mar 31, '09
by Mr. Brunner
Yes, Captopril is an ace inhibitor, which prevents conversion of (RAAS) RENIN- Angiotensin -Aldosterone- System from pushing through. In the Pathophysiology of Nephrotic Syndrome, due to the leakage of proteins through the glomerulus, this RAAS is activated because of hypovolemia which promotes production of Aldosterone (salt) a substance which retains water in our bodies thereby aggravating edema. When you prevent the production of Aldosterone by using ACE inhibitors you are in theory lessening edema. But of course this done under a doctor's supervision.
Patients with Nephrotic Syndrome are under adequate protein diet with sources from high biologic content like egg whites because the goal of the treatment is to replace lost proteins unless the patient is already on an end stage renal failure, in which case you decrease protein intake. A by product of protein catabolism is ammonia which is the body must get rid off. A damaged kidney can't excrete this substance very well that's why you have to lessen protein intake if the damage is too profound.
Last edit by Mr. Brunner on Mar 31, '09