Nephrology

Question 1

What is the function of ADH and what conditions stimulate its release?

Answer 1

ADH is the main regulator of urine concentration and subsequently is used to regulate osmolality in the body. Osmoreceptors in the hypothalamus sense increase in osmolality, stimulate ADH release from the posterior pituitary.

Decrease in blood volume or blood pressure can also trigger ADH release to help increase BP; drugs can induce ADH release (morphine, cyclophosphamide) or inhibit it (alcohol, clonidine)

Question 2

What is the effect of vasoconstriction of the efferent arteriole on renal blood flow and GFR?

Answer 2

Increase in efferent arteriole resistance (i.e. vasoconstriction) causes initially an increase in GFR but reduced renal blood flow. Past a certain point (approx double normal resistance), GFR also starts to decline with continued increase in resistance

Question 3

Where in the nephron does Mg absorption occur?

Answer 3

In the thick ascending loop of Henle

Question 4

What is the action of PTH on the kidneys?

Answer 4

Increases calcium reabsorption in the thick ascending loop of Henle and distal tubule and increases Vitamin D activation to increase calcium absorption by the gut

Question 5

What decreases sodium secretion by the kidneys?

Answer 5

Atrial natriuretic peptide (stimulated by atrial stretch), decreased aldosterone levels, decreased angiotensin II levels, decreased SNS levels

Question 6

What is the role of the macula densa in regulating the GFR?

Answer 6

Specialized cells in the juxtaglomerular apparatus, initial portion of the distal tubule. They sense decreased delivery of sodium chloride due to low BP and subsequently cause afferent arteriole vasodilation and renin release (stimulates angiotensin II conversion)

Question 7

How are nitric oxide and bradykinin involved in controlling the GFR?

Answer 7

NO is present in higher levels in the afferent arteriole, acts to protect a.a. from effects of angiotensin II in order to maintain GFR. Also acts as an autocoid (EDNO) to maintain basal levels of vasodilation in the kidneys. Drugs or damage to kidneys that leads to decreased NO levels leads to vasoconstriction and decreased GFR

Bradykinin does not appear to be of major importance in regulating GFR under normal circumstances. May help to dampen vasoconstriction of a.a. by SNS or angiotensin II . Bradykinin stimulates NO production

Question 8

What is the mechanism for increased urine production in CKD?

Answer 8

Pressure natriuresis/diuresis occurs due to increased load on surviving nephrons. There is also impaired genesis of the medullary gradient (medullary washout) secondary to disruption of the medullary architecture/counter-current multiplier and impaired response to ADH

Question 9

Which glomerular disease least likely to respond to immunosuppressive steroids (amyloidosis, segmental glomerulosclerosis, membranous glomerulonephritis, minimal change glomerulopathy)?

Answer 9

Amyloidosis

Question 10

What percentage of sodium is reabsorbed in the proximal tubule?

Answer 10

~65%

Question 11

What are some conditions that increase GFR?

Answer 11

Increased systemic BP (however, mild to moderate changes in BP are buffered by autoregulation in the kidneys), decreased afferent arteriole resistance, increased efferent arteriole resistance, increase in arterial colloid osmotic pressure or filtration fraction, angiotensin II (increases GFR at expense of decreased renal blood flow), EDNO, high-protein diet, hyperglycemia, fever, glucocorticoids

Question 12

What is the therapy for calcium oxalate bladder stones?

Answer 12

Dissolution is not possible, surgical removal is necessary. Prevention strategies include increasing water intake to form dilute urine, increasing urine pH, hydrochlorathiazide (enhances renal reabsorption of Ca), potassium citrate (augments renal excretion of citrate which binds with Ca)

Question 13

A cat with ckd has upcr of 0.5 on 3 different tests, what is the next step?

Answer 13

Depends on IRIS stage. UPCR > 2.0 is cutoff for managing proteinuria if IRIS stage I, UPCR > 0.4 in a cat is consistent with clinically significant proteinuria in IRIS stages II-IV. Since it has been checked 3 times already, it likely warrants treatment (assuming IRIS stage II-IV). Check BP if not assessed yet and start ACE-i (enalapril or benazepril)

Question 14

Dog has UPCR of 6.2 in 3 pooled urine over 24h. What is constituting the bulk of the proteins in the urine?

Answer 14

Albumin

Question 15

Why do normal patients not have glucosuria?

Answer 15

It’s resorbed with Na in the proximal tubule

Question 16

What causes a false positive urine dipstick protein?

Answer 16

PH > 8 (alkaline urine)

Question 17

Where do aminoglycosides act on the kidney to cause toxicity?

Answer 17

Proximal tubules (proximal convoluted tubule - PCT)

Question 18

What causes <1% fractional excretion of Na?

Answer 18

Effective volume depletion (hypovolemia)

Question 19

What does increased Symmetric dimethylarginine (SDMA) correlate with?

Answer 19

Decreased GFR. SDMA indicates a process of protein degradation including arginine being methylated and forming numerous molecules including ADMA and SDMA. >90% of SDMA is excreted through the kidneys.

Question 20

In a feline patient with small kidneys and ureterolith, unresponsive to 24 hr of medical therapy – what is the next therapeutic option?

Answer 20

Place a Subcutaneous Ureteral Bypass system (SUB)

Question 21

Why is calcitriol a treatment for CKD? What is its function?

Answer 21

It’s a vitamin D analog and regulates calcium homeostasis in the body. PTH transcription/synthesis/secretion. Do not use in patients with hypercalcemia or hyperphosphatemia.

Question 22

What enzyme catalyzes the conversion of vitamin D in the kidneys?

Answer 22

1-hydroxylase (catalyzed by PTH)

Question 23

An increase in what factor would decrease GFR?

Answer 23

Increased glomerular oncotic pressure (or capillary colloid osmotic pressure)

Question 24

Dog with a USG of 1.005 and fails to respond to water deprivation test or vasopressin, what is the diagnosis?

Answer 24

Nephrogenic DI.

Question 25

Mechanism for PUPD in CKD?

Answer 25

Solute diuresis

Question 26

What does the juxtaglomerular complex do?

Answer 26

Secrete renin

Question 27

Nephrogenic DI causes depletion of which electrolyte?

Answer 27

Sodium

Question 28

How to prevent CaOx stones?

Answer 28

Want to reduce urinary quantity of calcium and bind oxalate with diet. Can give K citrate for acidic urine.

Question 29

USG of 1.003, what is your next step (AXR, vasopressin trial, water deprivation test, or urine culture)?

Answer 29

UMIC.

Question 30

Hormones that decrease GFR?

Answer 30

Epi, norepi, and endothelin

Question 31

What would cause a FeNa >1%?

Answer 31

AKI

Question 32

Osmosis due to protein is related to which of the following properties (charge, number, mass, or shape)?

Answer 32

Number

Question 33

Localization of osmoreceptors for ADH?

Answer 33

Anterior hypothalamus

Question 34

Patient with anion gap of 13, HCO3 42, and low Cl, what is going on?

Answer 34

Metabolic alkalosis, most likely from upper GI sequestration of Cl.

Question 35

Most likely finding with pre-renal azotemia (elevated BUN, FeNa <1%, and plasma or urine osmolarities)?

Answer 35

FeNa <1% due to hypovolemia.

Question 36

On which part of the kidney does Mannitol act on?

Answer 36

Osmotic diuretic acts on the PCT.

Question 37

What are the histopathologic findings of lyme associated renal failure?

Answer 37

Membranoproliferative GN- immune complex deposition on subendothelial side of GB, thickened capillary loops, and mesangial hypercellularity.