Renal Diseases - RM

Question 1

What 3 things characterize nephrotic syndrome?

Answer 1

proteinuria, hypoalbuminemia, edema

Question 2

What is anasarca?

Answer 2

generalized systemic edema

Question 3

What is minimal change disease?

Answer 3

nephrotic syndrome where there is diffuse loss of podocyte foot processes, causing loss of electrical charge so proteins and fluids can leak

Question 4

What is the underfill hypothesis for edema?

Answer 4

glomerular disease–>increased filtration of plasma proteins–>tubular catabolism of albumin and excretion of albumin–>hypoalbuminemia–>reduced oncotic pressure–>edema

Question 5

What is the overfill hypothesis for edema?

Answer 5

glomerular disease–>primary renal Na retention–>plasma volume expansion–>increased capillary hydrostatic pressure–>edema

Question 6

What is puromycin aminonucleoside used for (PAN)?

Answer 6

can selectively infuse it into one kidney to make it nephrotic for experimental model

Question 7

What occurs in a PAN- model of nephrotic syndrome where one kidney is affected and one is fine? What does this suggest?

Answer 7

• get proteinuria even without hypoalbuminemia
• Na excretion is normal or even high in good kidney, but significantly reduced in PAN-perfused kidney
• suggests that there is an intrarenal factor promoting Na retention by nephrotic kidney

Question 8

How is the ANP response to water immersion different in healthy patients and those with nephrotic syndrome (NS)?

Answer 8

in NS pts, the effect is blunted
-can measure a lot of ANP in response to stretch from increased central vascular volume due to water diffusing into body, but the effect in the kidney is reduced and there is not as much diuresis

Question 9

What is the normal transcapillary gradient of oncotic pressure?

Answer 9

12 mmHg

Question 10

Why doesn’t the normal transcapillary oncotic pressure gradient change with hypoalbuminemia until plasma albumin level falls below 2?

Answer 10

there is a compensatory fall in interstitial oncotic pressure along with the fall in plasma oncotic pressure in hypoalbuminemia, but the mechanism fails when levels of albumin fall below 2
-at that point, fluid will shift into interstitial space

Question 11

What are the arguments against hypoalbuminemia causing edema in nephrotic sydnrome patients?

Answer 11

• most patients have normal or increased plasma volume
• Na retention in PAN-perfused kidney has edema without changes in albumin
• edema may resolve without changes in albumin levels
• no edema in congential analbuminemia patients
• variable natriuresis in pts with volume expansion (should have increased to increase water outflow too)

Question 12

In which case (underfill or overfill) is the renin-angiotensin-aldosterone system activated? suppressed?

Answer 12

• in underfill, RAAS activated, high renin

- in overfill, RAAS suppressed, low renin

Question 13

In which case is it appropriate to use diuretics? what can you measure first to be sure?

Answer 13

• use in overfill cases

- measure renin to make sure levels are low

Question 14

How can increased glomerular permeability cause hyperlipidemia?

Answer 14

reduced albumin–>compensatory hepatic synthesis–> hepatic lipoprotein synthesis as well as reduced lipoprotein lipase activity–>hyperlipidemia

Question 15

What is the signaling path for ADH?

Answer 15

ADH–> V2 receptors –> adenyl cyclase –> increased cAMP –> PKA –> insertion of aquaporin channels into apical membrane and synthesis of more aquaporins

Question 16

What are nonosmotic factors that influence ADH release?

Answer 16

volume, blood pressure, nausea, pain, stress, hypoglycemia, narcotics, angiotensin II, ethanol, caffeine, prostaglandins, ANP

Question 17

What type of patients are frequently hyponatremic?

Answer 17

people recoverying from surgery

Question 18

What is SIADH?

Answer 18

inappropriate secretion of ADH

-hypoosmolar plasma with inappropriately concentrated urine (that should be dilute)

Question 19

What is vasopressin escape?

Answer 19

eventually develop a new steady state of ADH activity–>have a decrease in aquaporin mRNA since it is not longer tied to ADH quantity

Question 20

What is the positive feedback that occurs in CHF?

Answer 20

CHF is hypervolemic state but with decreased effective circulating volume, so that is sensed by kidneys as hypoosmotic due to decreased afferent arteriole flow, causes renin release to increase water retention in edematous patient even more

Question 21

What segment of the nephron does angiotensin II preferentially cause vasoconstriction of?

Answer 21

efferent arterioles

Question 22

How do ACE inhibitors affect GFR in normal patients and those with underlying vascular disease or CHF?

Answer 22

• in normal patients, increases renal blood flow and GFR

- in pts with vascular disease or CHF, decreases GFR due to reduction in efferent arteriole constriction

Question 23

What 4 things stimulate renin secretion by macula densa?

Answer 23

baroreceptors/myogenic reflexes in afferent arteriole
SNS
catecholamines
decreased Cl in macula densa

Question 24

What 3 things inhibit renin secretion by macula densa?

Answer 24

ADH
ANP
BNP

Question 25

What do prostaglandins cause dilation of?

Answer 25

afferent arterioles

Question 26

What is the effect of NSAIDS?

Answer 26

inhibit cyclooxygenase enzymes that produce vasodilation (PGE2 and PGI2)

Question 27

What is the effect of NSAIDS in the kidneys of normal patients?

Answer 27

in normal patients, renal prostaglandin production is low so NSAIDS have little effect

Question 28

What is the effect of NSAIDS in the kidneys of a patient with acute kidney injury/compromise of renal perfusion (volume depletion, CHF, cirrhosis, diuretics, advanced age)

Answer 28

many vasodilatory prostaglandins are secreted in these kidneys to keep blood flow to kidney
-if you give dose of NSAID it can put patient into renal failure by blocking the prostaglandin-mediated vasodilation

Question 29

What causes dysautoregulation?

Answer 29

NSAID + ACE inhibitor + intravascular volume depletion

drug induced acute renal failure