Nephrotic Syndrome Question

Nursing Students General Students

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Specializes in Eventually RN, BSN, CNRA.

From my understanding, this is how Nephrotic Syndrome works, and I think I have a grasp on it until the end. I have a worksheet I'm following which is basically a bunch of arrows directing me through the process, and I'm trying to make sense of it. The bold is what the worksheet says, under is it my opinion of what it's trying to tell me. Please correct me if I'm wrong along the way, my question will follow because I get lost towards the end.

1.)INCREASE POROSITY OF GLOMERULAR MEMBRANE

Meaning an excess of things the kidneys and bladder need to eliminate, which leads to...

2.) Proteinuria and Hypoalbuminemia

Proteinuria is when protein leaks into the urine and Hypoalbuminemia is obviously low levels of albumin. Albumin is essential for maintaining osmotic pressure needed for proper distribution of body fluids. Therefore leading to..

3.) Decreased Osmotic Pressure and Increased Albumin Production and Lipo-Protein production

The decreased Osmotic pressure is because of the low albumin, which causes low serum protein (which will obviously be low because of the protein leaking from the blood to the urine) and low plasma pressure. The increased Albumin and Lipo-Protein production is the bodies defense to the already low albumin and protein. All of this leads to...

4.)Hyperlipidemia

This is caused because the body is over-producing to compensate for the loss, which leads to the fluid shifts and the massive edema.

5.)Hypovolemia

Here is where I begin to become confused. Hypovolemia is a state of decreased blood volume, which includes the kidneys, although I'm not sure why this happens. Because of the hypovolemia, you have lower renal blood flow which leads to..

6.) Increased Renin Production

Renin stimulates the production of Angiotensin which causes the blood vessels to constrict and stimulates the release of aldosterone. Which leads to.. *this is where I become greatly confused...

7.) Increased ADH (Anti-Diuretic Hormone)

I know what ADH does, which is basically stop urine output, I just don't understand how the chart goes from the vasoconstriction and aldosterone (I'm not even sure what aldosterone does) release to the increase of ADH.

Does anyone have any imput on this? Thanks a TON in advance.

For starters, in question number 1, increased porosity of the glomerular membrane means that it has become more permeable d/t damage. This means that more proteins and RBC's can escape.

You have the right idea about the osmotic pressure of the blood being decreased, leading to escape of fluids into the interstitial space (edema).

A combination of fluid shifts, and loss through urine creates hypovolemia, meaning decreased vascular volume.

When the kidney's sense the decrease in fluid volume, they activate the renin-angiotension mechanism to try to retain fluid as a means of preservation.

I reccomend that you spend time some time getting to know the renin-angiotension mechanism, because this will explain your questions. It is a system that will continue to come up throughout school as a lot of medications work to inhibit the RAAS, and all of your cardiac conditions will be linked to the kidneys and RAAS.

Hope this helps.

Specializes in SNU/SNF/MedSurg, SPCU Ortho/Neuro/Spine.

5.)hypovolemia

here is where i begin to become confused. hypovolemia is a state of decreased blood volume, which includes the kidneys, although i'm not sure why this happens. because of the hypovolemia, you have lower renal blood flow which leads to.. hypovolemia because of osmosis the fluid is going to (google 3rd spacing) now the fluids left the veins and went to the body so the osmolarity of the vascular fluid increases (you will see a lot more particles and what not) then with low renal flow, and more stuff to get rid of your kidneys get over worked and beg for water. because of all of that you can now have complications since your are trying to get rid of a whole lot of things without enough medium (water) so things that are excreted through the kidneys starts to back up and acumulate (the urine becomes concentrated) ...

6.) increased renin production

renin stimulates the production of angiotensin which causes the blood vessels to constrict and stimulates the release of aldosterone. which leads to.. *this is where i become greatly confused...all right, this is not hard, so then renin starts producing angiotensin (vasoconstructor) that will help get the blood flow to the kidneys, now if that is not enough then a little enzime called ace will kick in and convert angiotensin l into angiotensin ll, which is a more potent vaso constrictor, that will now try to get the job done. now angiotensin causes the release of aldosterone which will make the kidney tubules absorb more sodium and water this increases the volume of fluid in the body, which also increases blood pressure

7.) increased adh (anti-diuretic hormone)

i know what adh does, which is basically stop urine output, i just don't understand how the chart goes from the vasoconstriction and aldosterone (i'm not even sure what aldosterone does) release to the increase of adh.

does anyone have any imput on this? thanks a ton in advance.

hope it helped!!! i tried to build a little story for you :D

Specializes in Eventually RN, BSN, CNRA.

Both of you helped a ton. I cannot begin to thank you enough.

My take on RAAS -

When blood volume or blood pressure is low, the body releases Renin, which by itself does little to nothing to effect your B/P, but it does convert inactive forms of angiotensin to angiotensin I. Angiotensin I is able to atler B/P slightly, although not much, but much more effective when angiotensin converting enzymes (ACE) produced in the lungs convert it to angiotensin II. Angiotensin II is a more powerful hormone that can increase blood pressure, but it also releases aldosterone via the adrenal cortex. Aldosterone causes the kidneys to retain both water and sodium, which leads to edema and the increased blood pressure.

This leads me to a new question. When aldosterone is released and water retention begins, is that because of the ADH? Does aldosterone release, or induce the release of ADH. If the answers yes then all my questions are done and I think I have a grasp on this. If aldosterone and ADH have nothing in common, then I still have no idea where the ADH comes from.

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