Chronic glomerulonephritis and high BP

[MicA]

---

Members do not see this ad.

Sorry I am really struggling to get my head around this.

Surely glomerulonephritis causes increased proteins in urine -> less proteins in plasma -> increased GFR -> increased urine output -> decreased BP -> decreased GFR.

This can then be compensated for by RAAS which would vasodilate afferent arteriole and vasoconstrict efferent arteriole which increases GFR again.

But how do you end up with a BP of 180/90

 

[Rollo]

It's the angiontensin II that constricts arterioles all over the body thus increasing systemic arterial blood pressure.

This is how ACE inhibitors work in lowering BP...they inhibit Angiotensin Converting Enzyme which blocks the production of angiotensin II thus lowering BP.

 

[VenusinFurs]

After some searching:
-Daily proteinuria is actually relatively minimal compared to stock of proteins in blood. We have a gradual loss of protein to urine over time.
-progressive loss of nephrons (fibrosis) leads to a reduction in overall GFR for the whole kidney, leading to azotemia and uremia and all that good stuff.
-RAAS is activated to attempt to increase GFR in the remaining nephrons, leading to systemic vasoconstriction and hypertension.

http://emedicine.medscape.com/article/239392-overview