Renal disease

Question 1

What can glomerular disease lead to in terms of plasma proteins in theory?

Answer 1

1. More filtration of plasma proteins
2. Tubular catabolism of albumin or albuminuria
3. Hypoalbuminemia
4. Reduced oncotic pressure
5. Water moves from intravascular to interstitial spaces
6. Edema

Question 2

What can happen with Na filtration and excretion in a good kidney vs. a nephrotic kidney?

Answer 2

More filtration in a good kidney than the nephrotic one

Question 3

What happen with the colloid osmotic pressure gradient when plasma albumin drops too low (ie below 2)? What are the normal levels of plasma and interstitial CP?

Answer 3

The transcap COP will drop as well, and fluid will move into interstitium; 24 and 12, promoting reabsorption depending on the hydrostatic pressure

Question 4

What argues against hypoalbuminemia/hypovolemia in nephrotic syndrome edema?

Answer 4

1. Most patients with normal/increased plasma volume
2. Variable natriuresis after volume expansion
3. We only see Na retention in diseased kidney
4. Edema can resolve without albumin improvement
5. No edmea in congenital analbuminemia

Question 5

Given the arguments against hypoalbuminemia/hypovolemia in nephrotic syndrome edema, what is another hypothesis of glomerular disease and edema? In which case of glomerular disease would you NOT GIVE DIURETICS? What do diuretics draw from? Which case has increased renin?

Answer 5

1. Primary renal sodium retention
2. Plasma volume expansion
3. Increased capillary hydrostatic pressure
4. Water moves from intravascular to interstitial spaces;
   To those with reduced oncotic pressure!!
   Blood vessels!!
   Increased capillary hydrostatic pressure = less renin, while reduced oncotic pressure leads to MORE RENIN

Question 6

With increased glomerular permeability, what is the key consequence? What can branch off that? What can further branch of THAT?

Answer 6

Loss of plasma proteins, leading to loss of Ig, losing hormones, vitamins, and metals, and thromboembolism;
leads to albuminuria (hyperlipidemia because of more hepatic lipoprotein synthesis, malnutrition, hypoalbuminemia, and ultimately edema)

Question 7

Given change in equality of osmo between ICF and ECF, what shifts? What is the hormone that determines overall body fluid osmolarity? Equation for plasma osmolarity…

Answer 7

Water/fluids; ADH/AVP, influencing principal cells;

Posm = 2Na + glucose/18 + BUN/2.8

Question 8

What does increased osmolality stimulate? What does this stimulate?

Answer 8

Hypothalamic osmoreceptors, stimulating thirst and ADH

Question 9

Trace out the path of ADH…

Answer 9

Bind V2 receptors, leads to AC activity, cAMP, PKA, and then exocytosis/fusion of receptors with apical membrane;

Question 10

What osmotic factor influences ADH release? What non-osmotic factors influence ADH release? (Think of a person from the hood)

Answer 10

Plasma osmolality;

Volume/BP, nausea, pain, physical stress, narcotics, booze, A II, prostaglandins, ANP

Question 11

Clinical criteria for SIADH…

Answer 11

1. POsm < 275
2. Inappropriately concentrated urine
3. Euvolemia
4. Urine Na >40
5. No diuretic use or renal/adrenal/thyroid disease

Question 12

What are types of SIAD?

Answer 12

Malignancy, adaptation (person lives at lower set point), possible tumor keeping levels elevated, or gain of function in V2 receptor that keeps ADH/AVP levels low

Question 13

What are vasopressin levels like in SIADH? What can happen with excess of ADH?

Answer 13

Exaggerated activity; eventually have vasopressin escape, or decrease in apical water channel AQ-2 mRNA

Question 14

What does A II preferentially work on? With vascular disease or CHF, what could ACE inhibitors do?

Answer 14

Works on vasoconstricting the efferent arteriole, decreasing RPF but increasing the GFR; could lead to risk of decrease in GFR

Question 15

What does renin secretion by macula densa stimulate?

Answer 15

baroreceptor reflex in afferent arteriole, SNS, catecholamines, Cl delivery in MD

Question 16

How do NSAIDs affect renal function? What is the function of NSAIDs?

Answer 16

Primarily by affecting afferent arteriole vasodilation, in that you’re constricting aa more and decreasing GFR; could have acute interstitial nephritis;
Inhibit cyclooxygenase enzymes that would produce vasodilator prostaglandins (PGE2 and PGI2), affecting people with CHF, cirrhosis, diuretics, older (acute kidney injuries)

Question 17

What is dys-autoregulation?

Answer 17

NSAIDs (vasoconstriction of aa) + intravascular volume depletion (diuretics, history of CHF, gastroenteritis leading to vomiting) + ACE inhibitors (vasodilation of ea)