Nephritic Syndrome and Hypertension

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anbuitachi

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why does hypertension occur in nephritic syndrome? it is listed as a key characteristic.. First aid says it's due to sodium retention.. but it doesn't say why sodium retention occurs in nephritic syndrome.. Does anyone know why this occurs? [And does it also occur in nephrotic syndrome?]
 
why does hypertension occur in nephritic syndrome? it is listed as a key characteristic.. First aid says it's due to sodium retention.. but it doesn't say why sodium retention occurs in nephritic syndrome.. Does anyone know why this occurs? [And does it also occur in nephrotic syndrome?]

I believe the mechanism's not fully understood.. from what I know about what's theorized... .when you have Nephritic or Nephrotic syndrome, you are losing protein (mainly albumin)...and by losing protein, you plasma loses it's main source of oncotic pressure keeping fluid in the intravascular space - hence lower blood pressure. Your kidney then responds to this lower blood pressure by secreting renin -> angiotensin -> aldosterone -> increased sodium retention. hence the periorbital edema and hypertension you see in Nephritic syndrome... on the other hand in Nephrotic syndrome, you lose so much protein that even though you are retaining salt... it doesn't compensate and you won't be getting hypertension. Just from what I've gathered.... is this correct, I don't know if anyone knows.. it's just a theory that makes sense somewhat.

All we need to know is really that you get hypertension in Nephritic, while not in Nephrotic (here you get edema, mainly in your lower extremeties).
 
Hey i have another theory... nephritic syndrome is mainly characterized by mesangial proliferation that damages and constricts the glomerular capillary network, it thus reduces blood flow to to the juxtaglomerular apparatus and this activates the renin-angiotensin-aldosterone cascade, resulting in increased salt and water retention and hypertension...
 
I believe the mechanism's not fully understood.. from what I know about what's theorized... .when you have Nephritic or Nephrotic syndrome, you are losing protein (mainly albumin)...
There can be some protein loss with nephritic syndrome, but it is not a great deal. IIRC it is defined as protein loss less than some given value.
and by losing protein, you plasma loses it's main source of oncotic pressure keeping fluid in the intravascular space - hence lower blood pressure.
Oncotic pressure pulls. Just wanted to clarify this. I think you're end result is accurate but it was a little confusing to read. in nephrOTic syndrome you lose protein, and your liver compensates by releasing triglycerides.
Your kidney then responds to this lower blood pressure by secreting renin -> angiotensin -> aldosterone -> increased sodium retention. hence the periorbital edema and hypertension you see in Nephritic syndrome... on the other hand in Nephrotic syndrome, you lose so much protein that even though you are retaining salt... it doesn't compensate and you won't be getting hypertension. Just from what I've gathered.... is this correct, I don't know if anyone knows.. it's just a theory that makes sense somewhat.

All we need to know is really that you get hypertension in Nephritic, while not in Nephrotic (here you get edema, mainly in your lower extremeties).

? I believe nephrotic syndrome you still get generalized edema, aka anasarca.

http://emedicine.medscape.com/article/244631-clinical#2
^This is correct. I believe the non-dependent edema is more of a feature of nephrotic than nephritic.

Azotemia is also a feature of nephritic syndrome. Remember that you are damaging the glomeruluses (glomeruli?) and filling the tubes full of dessicated RBCs (eventually). Filtration is down and the renin/angiotensin system is more than likely having a holy tantrum because of it. Therefore you get hypertension.

With nephrotic, the BP is actually low due to oncotic derangement (rather than perceived as low) so the renin/angiotensin activation is appropriate which is why a BP disturbance in either direction isn't a classic feature.
 
why does hypertension occur in nephritic syndrome? it is listed as a key characteristic.. First aid says it's due to sodium retention.. but it doesn't say why sodium retention occurs in nephritic syndrome.. Does anyone know why this occurs? [And does it also occur in nephrotic syndrome?]

Hypertension occurs in nephritic syndrome due to increased inflammation at the glomerulus. This leads to hemodynamic changes that cause the over all GFR to decrease, and thus oliguria. It is the overall decreased ability to make urine, due to inflammatory damage, that causes hypertension. Also casts from inflammatory debris can cause blockage in the tubules leading to pathological overactivation of RAAS, by tricking the JG apparatus into thinking you're volume depleted.

Compare that to Nephrotic Syndrome, where albumin is lost due to effacement of foot proteins without inflammation. Only albumin is lost, leading to a decreased osmotic pressure in the vessels, causing edema. This decreased effective arterial volume activates RAAS also, however, in this case it is compensating for the decrease in systemic blood pressure from the edema, so the activation of RAAS just normalizes the previously low blood pressurel - thus no hypertension.

Sorry I am four years late 🙁
 
Hypertension occurs in nephritic syndrome due to increased inflammation at the glomerulus. This leads to hemodynamic changes that cause the over all GFR to decrease, and thus oliguria. It is the overall decreased ability to make urine, due to inflammatory damage, that causes hypertension. Also casts from inflammatory debris can cause blockage in the tubules leading to pathological overactivation of RAAS, by tricking the JG apparatus into thinking you're volume depleted.

Compare that to Nephrotic Syndrome, where albumin is lost due to effacement of foot proteins without inflammation. Only albumin is lost, leading to a decreased osmotic pressure in the vessels, causing edema. This decreased effective arterial volume activates RAAS also, however, in this case it is compensating for the decrease in systemic blood pressure from the edema, so the activation of RAAS just normalizes the previously low blood pressurel - thus no hypertension.

Sorry I am four years late 🙁

Still helped me, thanks!
 
Hypertension occurs in nephritic syndrome due to increased inflammation at the glomerulus. This leads to hemodynamic changes that cause the over all GFR to decrease, and thus oliguria. It is the overall decreased ability to make urine, due to inflammatory damage, that causes hypertension. Also casts from inflammatory debris can cause blockage in the tubules leading to pathological overactivation of RAAS, by tricking the JG apparatus into thinking you're volume depleted.

Compare that to Nephrotic Syndrome, where albumin is lost due to effacement of foot proteins without inflammation. Only albumin is lost, leading to a decreased osmotic pressure in the vessels, causing edema. This decreased effective arterial volume activates RAAS also, however, in this case it is compensating for the decrease in systemic blood pressure from the edema, so the activation of RAAS just normalizes the previously low blood pressurel - thus no hypertension.

Sorry I am four years late 🙁

Helped me too!
 
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