Why captopril with Nephrotic Syndrome???

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    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!
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    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
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    what is going on (the pathophysiology) when the kidney fails? what hormones that affect blood pressure produced by the kidney are manufactured in smaller amounts when diseases like nephrotic syndrome happen? how does an ace (angiotensin converting enzyme) inhibitor correct that problem? look up the answer to this question: what happens when massive amounts of protein are lost through the kidneys with nephrotic syndrome? now, look up the definition of the medical term anasarca and contrast it with edema.
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    Suesquatch - yes you can have hypotension without hypovolemia, but the patho here with nephrotic syndrome is that hypoalbuminema causes hypovolemia. I could see an ACE-inhibitor helping with the anasarca and possible effusions, but wouldnt it at the same time collapse an already hypovolemic intravascular space??

    Daytonite - Sorry, but you just lost me. Trying to figure out where youre trying to steer me. Anasarca is basically generalized edema, from what I understand. I'm absolutely lost with this. I cant figure out two questions. One I have already asked about the captopril. The other is that my book says "low protein diet" for Nephrotic Syndrome. I saw one of your other posts saying to increase protein for Nephrotic syndrome. Hoping you can explain it to where I can understand it. Thanks.
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    This may be helpful:

    Use of an angiotensin-converting enzyme (ACE) inhibitor, such as enalapril VASOTEC, quinapril ACCUPRIL, or lisinopril PRINIVIL, ZESTRIL
    , or an angiotensin II receptor blocker (ARB), such as candesartan ATACAND, losartan COZAAR, or valsartan
    DIOVAN, alone or in combination is the mainstay of both prevention and treatment. When a person with a disease such as systemic lupus erythematosus or diabetes mellitus has mild or moderate proteinuria, an ACE inhibitor or ARB is used as soon as possible because it may prevent proteinuria from increasing and kidney function from worsening.

    When a person who already has nephrotic syndrome is treated with an ACE inhibitor or ARB, symptoms may improve, the amount of protein excreted in the urine usually decreases, and lipid concentrations in the blood are likely to decline. However, these drugs can increase the potassium levels in the blood in people who have moderate to severe kidney failure, which can cause potentially dangerous heart rhythm abnormalities.
    http://www.merck.com/mmhe/sec11/ch144/ch144c.html
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    Okay - I do get that fact that captopril is beneficial in the treatment of nephrotic syndrome, I was just hoping someone could explain it on a cellular level. How or why does it decrease proteinuria/increase kidney function. Is it just one of those unknowns?

    And Daytonite, I'll ask again if you didnt see my question above, why would my notes have Low Protein diet for Nephrotic Syndrome?? I saw one of your old posts saying that you had a patient with nephrotic syndrome and were giving them 3 steaks a day. Is it that you give them low protein in acute stages, and then once the infarct has diminished you up the protein?? Thanks again for all replies.
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    In nephrotic syndrome the patient loses huge amounts of protein through the kidneys--big time. This is why they blow up like balloons. That is called anasarca--generalized body edema. Patients with nephrotic syndrome are often placed on high protein diets to replace the protein they are losing through their kidneys.

    These patients are often on the way to chronic renal failure. It is just a matter of time. The kidneys control the blood pressure through the release of the hormones renin, angiotensin and aldosterone whose job is to maintain blood volume and blood pressure. They are powerful vasoconstrictors. If sodium is being lost along with the large amounts of proteins through the urine [urine is water and sodium follows water], the kidney releases more renin, angiotensin and aldosterone to ramp up the blood volume which is also going to raise the blood pressure. This is not a wanted effect. ACE inhibitors will counteract the vasoconstrictive effect of those hormones causing vasodilation and, thus, lowering of the blood pressure.

    Does that help?
    SuesquatchRN likes this.
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    Quote from bayoufrogg
    And Daytonite, I'll ask again if you didnt see my question above, why would my notes have Low Protein diet for Nephrotic Syndrome?? I saw one of your old posts saying that you had a patient with nephrotic syndrome and were giving them 3 steaks a day. Is it that you give them low protein in acute stages, and then once the infarct has diminished you up the protein?? Thanks again for all replies.
    I think you should clarify this with your instructor. NS patients dump huge amounts of protein in their urine. Unless the protein is being replaced by some other means, i.e., albumin infusions, their fluids go into their intracellular spaces and they get very edematous.

    http://en.wikipedia.org/wiki/Nephrotic_syndrome
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    She mentioned that the protein that is spilling through the plasma membrane of the kidney is not going with ease. In her lecture, protein is allowed to go through, but with even more damage to the membrane. For this reason, she said low protein diet.

    Would albumin infusion along with low protein diet be the best overall possible patient tx to cover all bases??
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    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


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