a patient with chronic hypertension secondary to renal artery stenosis

[Oak]

Which of the following would be expected to be decreased in a patient with chronic hypertension secondary to renal artery stenosis?

A. Atrial natriuretic peptide levels
B. Blood urea nitrogen (BUN) levels
C. Glomerular filtration rate in response to captopril
D. Net acid excretion
E. Potassium secretion

[Alpine]

im not sure is it C ??? as people say if u r not sure go for C when there is multiple question

[Oak]

Yup your hunch is absolutely correct, the correct answer is C.

Renal artery stenosis can decrease the renal perfusion pressure sufficiently to increase renin secretion significantly, which increases angiotensin II (AII), which, in turn, increases aldosterone. Chronic hypertension due to renal artery stenosis is the result of elevated levels of AII and aldosterone. Aldosterone increases retention of sodium from the collecting duct, and water follows; AII increases reabsorption of sodium from the proximal tubule, and water follows. AII is also a vasoconstrictor, increasing peripheral vascular resistance.

Vasoconstriction of the renal vasculature decreases renal plasma flow, which would be expected to decrease glomerular filtration rate proportionately. AII, however, preferentially vasoconstricts the efferent arteriole in the nephron, maintaining a reasonable glomerular filtration rate even with the reduced renal plasma flow. Captopril (an angiotensin-converting enzyme inhibitor) inhibits the conversion of angiotensin I to AII. The captopril-mediated decrease of AII will actually decrease glomerular filtration in the kidney with renal artery stenosis, because decreasing efferent constriction causes the glomerular capillary pressure to fall.

Atrial natriuretic peptide (choice A) levels would be expected to increase with increased water and sodium retention due to renal artery stenosis.

BUN (choice B) would be expected to increase or stay the same with renal artery stenosis, depending on the extent of AII-mediated efferent arteriole vasoconstriction.

Metabolic alkalosis, due to the increased net acid secretion (compare with choice D) from hyperaldosteronism, is typical in renal artery stenosis.

Potassium secretion would increase, rather than decrease (choice E), due to the effects of excessive aldosterone secondary to renal artery stenosis.

[Hero]

Originally Posted by Oak

AII, however, preferentially vasoconstricts the efferent arteriole in the nephron, maintaining a reasonable glomerular filtration rate even with the reduced renal plasma flow. Captopril (an angiotensin-converting enzyme inhibitor) inhibits the conversion of angiotensin I to AII. The captopril-mediated decrease of AII will actually decrease glomerular filtration in the kidney with renal artery stenosis, because decreasing efferent constriction causes the glomerular capillary pressure to fall.

I was curious to know why ACE-I are contraidicated in renal artery stenosis, this explanation solved my question. Tnx

[de.malady]

Originally Posted by Hero

I was curious to know why ACE-I are contraidicated in renal artery stenosis, this explanation solved my question. Tnx

In case of -Renal Artery Stenosis-, ACEI may aggravate already deteriorated ranal function; which can be suspected in the form of severe Hypotension..

[ps: or may b -Oak- has a better explanation for this..]

[Hero]

Originally Posted by Graduate 06

In case of -Renal Artery Stenosis-, ACEI may aggravate already deteriorated ranal function.

This is true, but what is the mechanism? I have already highlighted the exact mechanism. Actually in renal artery stenosis, efferent arteriole constriction by angiotensin II maintains the glomerular filtration and ACE-I inbihits the conversion of AI to AII and thus glomerular filtration is reduced --renal failure occurs. That's why ACE-I is usually not used in renal artery stenosis.
But ACE-I is drug of choice in diabetic nephropathy. Why?

[kenneth masamaro]

Originally Posted by Hero

This is true, but what is the mechanism? I have already highlighted the exact mechanism. Actually in renal artery stenosis, efferent arteriole constriction by angiotensin II maintains the glomerular filtration and ACE-I inbihits the conversion of AI to AII and thus glomerular filtration is reduced --renal failure occurs. That's why ACE-I is usually not used in renal artery stenosis.
But ACE-I is drug of choice in diabetic nephropathy. Why?

To answer your question,Diabetic nephropathy is characterized by among other things, tubulointerstitial fibrosis.Its pathogenesis is mediated by a number of chemokines with MCP-1(monocyte chemoattractant protein)showing the highest association.It is known that AT-II(angiotensin II) induces the MCP-1 gene.It follows that inhibitors of AT-II would abrogate MCP-1 expression and therefore improve diabetic nephropathy.