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Lecture 6

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Department
Nursing
Course
NURS 203
Professor
All Professors
Semester
Winter

Description
Lecture 6 Combo of Nephritic and Nephrotic Syndrome IgA Glomerulonephritis (burger’s dz) IgA glomerulonephritis is a VARIANT of Henoch Schonlein purpura b/c it is an immune complex dz, anti IgA Abs (so is Henoch Schonlein – palpable purpura in buttocks of legs, polyarthritis, GI bleed, hematuria (RBC casts)) On immunofluorence, everything shows up in the mesangium. Example: in kids, presents with episodes of gross hematuria, goes away, comes back a few years later; in adults, presents with episodic bout of microscopic hematuria. So, have a lil hematuria, goes away, and comes again. Lil proteinuria, no HTN. When it starts getting worse (10 years later), that’s when it will be bad (so its not b9). It is the MC of all glomerulonephritis and is type III HPY. BUN/Cr – Prerenal Azotemia Can separate prerenal azotemia vs. renal failure BUN = blood urea nitrogen and Cr = end product of creatine metabolism. Urea can be filtered and reabsorbed in the prox tubule (so its not a perfect clearance substance); Cr is only filtered in the kidney and is reabsorbed or secreted. (lnulin clearance is better). If you take the normal BUN level (10), and normal Cr level (1mg/dL), will have the normal ratio of 10:1. When you have prerenal azotemia, there is an increase in BUN (this is what azotemia means). Pre = before, therefore there is something wrong ‘before’ the kidney – in other words, there is nothing wrong with the kidney, but the CO is decreased (from any cause - ie CHF, MI, hypovolemia, cardiomyopathy, etc). Anything that decreases CO will lead to prerenal azotemia b/c the GFR will decrease. If you have less renal blood flow, you will filter less and the GFR will decrease. So, when it decreases, it gives the prox tubule more time to reabsorb little bit more urea than normal. So, there is increase prox tubule reabsorption of urea. What about Cr? We know that it is not reabsorbed, but you do have to get rid of it through the kidneys. So, even though it is not reabsorbed, the GFR is decreased, there is a back up of Cr and will not be able to clear it as fast. Therefore, there will be an increase in serum Cr. There is little more of an increase is urea b/c it is being reabsorbed than with Cr. So, there is a disproportionate increase of BUN/Cr. All you have to remember is 15:1. So, greater than a 15:1 BUN/Cr = prerenal azotemia. Example: the pt has CHF, BUN is 80 and Cr is 2. So, both are elevated, but the BUN/Cr ratio is 40:1, indicating that it is prerenal azotemia, and the pt does NOT have ATN. Lets say pt truly has renal failure – oliguria, renal tubular casts, acute renal failure. This will affect the BUN/Cr EQUALLY b/c something is wrong with the kidney, therefore the same effect on the BUN is the same on Cr. For both, urea has to be filtered out of the kidney and it has failed – both increased proportionate to each other b/c both have the same problem and kidney is screwed up; cannot get rid of urea, can’t get rid of creatinine, so they increase in proportion to each other b/c the urea is not being reabsorbed anymore b/c the kidney is in shock. Example: BUN = 80, Cr = 8, therefore the B
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