Kidney, GFR and RAAS

[nursinghealth]

Hello!

I have a question about kidney function.

I understand that a reduction in BP causes Juxtaglomerular cells in the kidney to secrete Renin in order to conserve fluid and increase BP. I also understand that the GFR measures the amount of filtrate produced by the urine per minute. High BP = increased GFR. Low BP = reduced GFR.

According to my textbook's explanation of the pathophysiology of glomerulonephritis, an increase in the flow of filtrate stimulates the RAAS. HOW IS THIS POSSIBLE? (*shakes head*) If there is excess filtrate, does that not mean the pressure is also high? I assumed the RAAS would be triggered if filtrate production was low.

What am I missing here?

Thanks for your help!

[nurseprnRN, BSN, RN]

Hello!

I have a question about kidney function.

I understand that a reduction in BP causes Juxtaglomerular cells in the kidney to secrete Renin in order to conserve fluid and increase BP. I also understand that the GFR measures the amount of filtrate produced by the urine per minute. High BP = increased GFR. Low BP = reduced GFR.

According to my textbook's explanation of the pathophysiology of glomerulonephritis, an increase in the flow of filtrate stimulates the RAAS. HOW IS THIS POSSIBLE? (*shakes head*) If there is excess filtrate, does that not mean the pressure is also high? I assumed the RAAS would be triggered if filtrate production was low.

What am I missing here?

Thanks for your help!

See bolded section below... Increased aldosterone decreases the end-production of urine by increasing Na+/water retention. Perhaps they meant to say something like really high filtrate production (perhaps from some other cause than elevated BP) can prompt the RAAS signal to reabsorb more.

From the redoubtable Wikipedia (which is often a good place to start)

The renin–angiotensin system (RAS) or the renin–angiotensin–aldosterone system (RAAS) is a hormone system that regulates blood pressure and fluid balance.

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the prorenin already present in the blood into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I.^[2]Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin-converting enzyme found in the lungs. Angiotensin II is a potent vaso-active peptide that causes blood vessels to constrict, resulting in increased blood pressure.^[3] Angiotensin II also stimulates the secretion of the hormone aldosterone^[3] from the adrenal cortex. Aldosterone causes the tubules of the kidneys to increase the reabsorption ofsodium and water into the blood, while at the same time causing the excretion of potassium (to maintain electrochemical balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.

If the renin–angiotensin–aldosterone system is abnormally active, blood pressure will be too high. There are many drugs that interrupt different steps in this system to lower blood pressure. These drugs are one of the main ways to control high blood pressure (hypertension), heart failure, kidney failure, and harmful effects of diabetes.^[4][5]