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Review Flashcards

1
Q

Which of these would be consistent with a finding of diabetes insipidus?
a. Hyponatremia with hyperosmotic urine
b. Hypernatremia, hyperkalemia and hyperosmotic urine
c. Hypoinsulinemia with glucosuria and proteinuria.
d. Hypernatremia, hyperchloremia and hypoosmotic urine.
e. Hypoalbuminemia, euglycemia hypoosmotic urine.

A

d. Hypernatremia, hyperchloremia and hypoosmotic urine.

disruption of AVP system —> excessive water loss —> hypernatremia and dilute urine

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2
Q

which of the following would occur from a mutation in the nephrin gene?
a. increased ECV
b. heavy proteinuria
c. hypolipidemia
d. hypernatremia
e. hypoalbuminuria

A

b. heavy proteinuria

nephrin: structural protein of glomerular filtration barrier, loss of integrity leads to hyperfiltration

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3
Q

Blood/urine analysis shows that a patient is hyponatremic with elevated total urine Na+ - a loss of function mutation in which of the following could cause this?
a. mineralocorticoid receptor
b. TGF mechanism
c. ROMK2
d. AT2-R
e. V2-R

A

a. mineralocorticoid receptor - mutation would prevent aldosterone binding, inhibiting its ability to induce Na+ reabsorption

b. TGF mechanism - monitors GFR by sensing NaCl in urine
c. ROMK2 - K+ pump (for secretion)
d. AT2-R - angiotensin receptor with opposite effects of main AT1-R
e. V2-R - loss of function defines nephrogenic diabetes insipidus (AVP binds here)

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4
Q

effective circulating volume is most dependent upon which of the following?
a. GFR
b. Intravascular volume.
c. Plasma sodium.
d. Cardiac output.

A

d. Cardiac output.

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5
Q

patient is a 48yo M presenting with chronically elevated blood pressure for the past year. He is currently taking the max prescribed dose of two diuretics and leaves a healthy lifestyle. Aside from a blood pressure of 150/85mmHg, PE is unremarkable. Which of the following is most likely pathogenesis of his resistant hypertension?
a. Catecholamine producing tumor (pheochromocytoma)
b. Tachycardia secondary to hyperthyroidism.
c. Volume overload secondary to acute kidney failure.
d. Renal artery stenosis.
e. Arginine, vasopressin resistance.

A

d. Renal artery stenosis —> effectively lowers renal perfusion, which is sensed by baroreceptors and causes RAAS activation

key is high BP is only presenting symptom (all others would have other symptoms)

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6
Q

Which two causes of metabolic alkalosis are not fluid responsive?

A
  1. Hyperaldosteronism
  2. Hypokalemia

all other common causes (diuretics, vomiting, contraction alkalosis) will get better with IV fluids

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7
Q

which of these would most appropriate for treatment of essential hypertension?
a. Furosemide.
b. Spironolactone.
c. Eplerenone
d. Thiazide diuretic
e. acetazolamide

A

d. Thiazide diuretic

furosemide is for more severe conditions like edema from CHF; spironolactone and eplerenone are aldosterone antagonists (strong drugs - save these for high aldosterone)

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8
Q

A patient with hypertension is resistant to a thiazide diuretic, calcium channel blocker, and angiotensin receptor blocker in combination. Blood labs show the following: Na+ 145, K+ 3, Cl- 95, Cr 1.4, BUN 20 - these results are most suspicious for which of the following?
a. constitutive activation of V2R
b. Loss of function of SGLT.
c. Hyperaldosteronism.
d. AT1 insensitivity
e. SIAD

A

c. Hyperaldosteronism

HTN resistant to 3 meds + hypokalemia + borderline hypernatremia = likely hyperaldosteronism —> Na+ retention, K+ secretion

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9
Q

What is the most common cause of increased blood urea nitrogen (BUN) in the absence of kidney failure?

A

dehydration - BUN reabsorption is coupled to sodium

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10
Q

what does a urine specific gravity of 1.0 indicate?

A

urine specific gravity of 1.0 = urine is pure H2O (impossible)

upper limit in humans is 1.035

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11
Q

Which three transporters in the kidneys are responsible for the 100% resorption of glucose from the kidneys?

A
  1. SGLT
  2. GLUT
  3. Na+/K+ ATPase (follows glucose)
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12
Q

What is the main transporter of sodium in the thick ascending limb (TAL) of the kidney?

A

NKCC: mediates transport of Na+, K+, and Cl-

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13
Q

A patient is prescribed furosemide for their hypertension. On follow-up, BP is lowered but pulse has risen and weight has dropped. Which of the following aberrant blood labs is most likely?
a. Hyperaldosteronemia, metabolic acidosis, hyperkalemia
b. Depressed PTH, hypercalcemia, hypophosphatemia
c. hypocalcemia, hyponatremia, hypokalemia

A

c. hypocalcemia, hyponatremia, hypokalemia

furosemide (loop diuretic) blocks NKCC - hypocalcemia because calcium reabsorption is coupled to Na+/K+ in TAL

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14
Q

A patient has a genetic mutation which prevents the targeting of AQP2 into the apical membrane of principal cells. Which of the following describes this disorder?
a. Pseudohyperaldosteronism
b. Nephrogenic diabetes insipidus
c. Nephrotic syndrome.
d. SIAD
e. Polycystic kidney disease.

A

b. Nephrogenic diabetes insipidus —> AVP resistance and hypernatremia due to H2O wasting

recall AVP binds V1 and V2 receptors

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15
Q

Describe the non-osmotic release of ADH

A

major physiologic trigger for ADH secretion (from posterior pituitary) is plasma osmolarity, sensed by the hypothalamus —> increased water reabsorption

However, with very low effective circulating volume (ECV), ADH secretion is triggered to increase blood volume (“non-osmotic release”)

this could be triggered by vomiting, diarrhea, hemorrhage, etc

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16
Q

what are the classic causes of renal papillary necrosis? (there’s a pneumonic ofc !)

A

SAAD papa:
Sickle cell
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus

[papa for papillary]

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17
Q

what are the common pathogens that cause UTI? (mnemonic !)

A

KEEPS:
Klebsiella
E. coli (most common)
Enterococcus
Proteus mirabilis (—> struvite stones)
Staphylococcus saprophyticus

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18
Q

which paraneoplastic syndromes can be caused by renal cell carcinoma? (mnemonic !)

A

PEAR:
PTHrP (PTH related protein)
EPO
ACTH
Renin

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19
Q

Pt is a 43yo F presenting with flank pain. Creatinine clearance is 50 mL/min, urine protein is normal, fasting blood glucose = 85, mg/dL, serum osmolarity = 285mOsm/kg. Which of the following lab values would most likely be detected in this patient?
a. Elevated plasma creatinine, hypernatremia, reduced BUN.
b. Elevated plasma creatinine, low urine creatinine, elevated BUN.
c. Reduced plasma creatinine, elevated urine creatinine, and normal serum albumin
d. Normal plasma creatinine, hyponatremia, and hypoalbuminemia.

A

b. Elevated plasma creatinine, low urine creatinine, elevated BUN.

Inverse relationship between GFR (creatinine clearance) and both plasma creatinine and BUN

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20
Q

which of the following intrarenal mechanisms is likely to be involved in the formation of diabetic nephropathy?
a. Increased nephrin expression.
b. Expression of pro fibrotic growth factors.
c. Reduced SGLT function.
d. Auto immune destruction of glomeruli.

A

b. Expression of pro-fibrotic growth factors.

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21
Q

blood labs for my post surgical. Patient show: sodium = 134 meq/L, fasting glucose = 60 mg/dL, and BUN = 8 mg/dL. Which of the following reflects this patient’s total plasma osmolality relative to normal?
a. Within normal limits.
b. Lower than normal.
c. Higher than normal.

A

b. Lower than normal.

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22
Q

A 16yo girl sustains a blow to the head. Following, she reports extreme thirst and frequent urination. Blood labs show plasma osmolality = 325mOsm/kg and urine osmolarity = 200 mOsm/kg. What is the most likely cause?
a. Anterior pituitary function.
b. Hyperaldosteronism.
c. Diabetes mellitus.
d. AVP deficit.

A

d. AVP deficit.

Thirst + frequent urination + hyperosmolarity with hypo osmolality urine = diabetes insipidus

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23
Q

A three-year-old girl is brought to the pediatrician due to polyuria, polydipsia, weakness, and fatigue. She is hypotensive and borderline tachycardic. Blood labs show HCO3- = 32meq/L, pH = 7.50, PRA and PAC elevated. K+ = 3.5meq/L, glucose = 95mg/dL. A loss of function mutation in which of the following is most likely?
a. SGLT2
b. AT2
c. Mineralcorticoid receptor
d. ROMK2
e. V2R

A

e. V2R

Polydipsia + polyuria + elevated PRA (plasma renin activity) & PAC (plasma aldosterone concentration) in response to hypotension = loss of vasopressin activity

Euglycemia rules out LOF in SGLT2

AT2 function is opposite of AT1 (main receptor) and significance is unclear

MR/ROMK defect would lead to hyperkalemia

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24
Q

Pt is 57yo M with resistant hypertension. He reports feeling well and has normal renal function. BP = 165/80mmHg. K+ = 3 meq/L, Cl- = 100 meq/L, Ca2+ = 10 mg/dL, BUN = 15 mg/dL. further testing would most likely show:
a. Elevated plasma metanephrines.
b. Plasma Na+ = 160 meq/L
c. Elevated plasma catecholamines.
d. Elevated plasma aldosterone: PRA ratio
e. Metabolic acidosis.

A

d. Elevated plasma aldosterone: PRA (plasma renin activity) ratio

resistant hypertension with hypokalemia = hyperaldosteronism

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25
Q

medullary rays contain which of the following?
a. renal corpuscles.
b. Collecting ducts
c. Distal convoluted tubule’s.
d. Proximal convoluted tubule’s.
e. Papillary ducts

A

e. Collecting ducts !!

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26
Q

A patient with small cell lung carcinoma presents with Na+ = 122 meq/L, plasma osmolality 250 mOsm/kg H2O, urine specific gravity 1.038. What do these most likely indicate?
a. Dehydration.
b. AVP excess
c. Decreased GFR
d. Hyperadrenal syndrome.

A

b. AVP excess

Hypo-osmolality with concentrated urine = SIADH

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27
Q

which of the following dermatomes would most likely be associated with loin pain from a stone in the upper portion of the ureter?
a. T10-T12
b. L1-L2
c. S2-S4

A

a. T10-T12

afferent visceral pain information follows sympathetics from the lesser (T10-T11), least (T12), and lumbar (L1-L2) splanchnic nerves - a stone in the proximal portions of the ureter is more likely to be felt in the loin/flank

As stone to send the pain refers to the groin

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28
Q

occlusion of the umbilical artery in the pelvis may result in reduced perfusion of the:
a. Ureters.
b. Urinary bladder.
c. Kidneys.
d. Urethra.

A

b. Urinary bladder.

prior to reaching the anterior abdominal wall where it becomes fibrotic postnatally, the umbilical artery gives off some superior vesicle branches to the bladder

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29
Q

A patient with multiple myeloma has an elevation in the total protein levels in the CRM. Which of the following changes would you expect?
a. No change in GFR, increased filtration fraction.
b. Increase GFR, decreased filtration fraction.
c. Decreased GFR, increased filtration fraction.
d. Decreased GFR, no change in filtration fraction.
e. Decreased GFR, decreased filtration fraction.

A

e. Decreased GFR, decreased filtration fraction.

decreased GFR due to increased plasma osmolarity with no change in RPF – this would decrease filtration fraction

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30
Q

what is the effect of NSAIDs on GFR and RPF and filtration fraction?

A

Prostaglandins dilate the afferent arteriole —> therefore NSAIDs cause constriction of the afferent arterial

—> reduced GFR and RPF = no change in filtration fraction

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31
Q

Pt is 33yo M with well-controlled hyperglycemia. BP is 140/80, Na+ = 140, K+ = 6.2, Cl- = 101, Ca2+ = 9, fasting glucose = 125. How would a normal physiologic response to his present homeostasis change the following?
a. PRA
b. aldosterone
c. urine K+

A

a. PRA (plasma renin activity): low
b. aldosterone: high
c. urine K+: high

normotensive patient so PRA should be low, hyperK+ will drive aldosterone secretion and increased filtered load of K+

32
Q

into what do the following develop?
a. metanephros
b. mesonephros
c. mesonephric duct
d. urogenital sinus

A

a. metanephros —> permanent kidney
b. mesonephros —> regresses
c. mesonephric duct —> caudal end forms ureteric bud —> collecting system, ureters, bladder trigone
d. urogenital sinus —> anterior portion of cloaca, urinary bladder and urethra

33
Q

Pt is 17yo in ED for traumatic hemorrhage. BP 90/40, HR 135. Na+ = 140, K+ = 3.5, Cl = 100, HCO3 = 13, pH = 7.35, PaO2 = 90, PaCO2 = 24. Which of the following best describes this acid-base disorder?
a. metabolic acidosis
b. primary metabolic acidosis with respiratory alkalosis
c. primary metabolic acidosis with respiratory acidosis
d. primary respiratory alkalosis with metabolic acidosis

A

b. primary metabolic acidosis with respiratory alkalosis

acidemia with low bicarb = metabolic acidosis

predicted CO2 = 27.5 +/- 2 and measured CO2 is below this, therefore there is respiratory alkalosis

34
Q

Pt is 67yo in ED presenting with ataxia, dizziness, vomiting, and agitation. Blood ethanol and drug screen are negative. RR is 40/min, pH = 7.10, PaCO2 = 20, PaO2 = 95. BUN = 20, Cr = 1, glucose = 80, lactate = 0.75. Which is most likely?
a. renal tubular acidosis
b. protracted diarrhea
c. diabetic ketoacidosis
d. methanol ingestion
e. surreptitious diuretic use

A

d. methanol ingestion

metabolic acidosis with elevated AG (32) - either toxic ingestion or endogenous acid, and patient is neg. for lactic and keto acidosis —> must be methanol ingestion (serum osmolarity would be increased if it was measured)

[diuretic overdose = alkalosis]

35
Q

Pt is 49yo M with progressive nausea, fatigue, malaise. No fever. Decrease in urination. BP 178/88, mild pitting ankle edema. Cr = 4.4, elevated from 3 months prior. Urinalysis positive for protein and heme and RBC casts. Biopsy shows ribbon-like antibody staining. This disorder is most likely caused by:
a. anti-phospholipase A2 receptor antibodies
b. anti-glomerular basement membrane antibodies
c. immune complex deposition in subepithelial space
d. IgA deposition in mesangium
e. small vessel vasculitis

A

b. anti-glomerular basement membrane antibodies

pt has rapidly progressive glomerulonephritis (RPGN), caused by either immune complex deposits (granular, Type II), small vessel vasculitis (pauci immune, Type III), or anti-GBM antibodies (ribbon like - linear, Type I)

36
Q

Pt is 34yo M presenting with edema. BP is 150/95, Cr is 2.4 (normal 0.6-1.5), albumin 2.9 (normal 3.5-5.5). Urine protein is 3+. Light microscopy shows segmental collapse and sclerosis of the glomerulus. What is the diagnosis?

A

decline in GFR (elevated plasma Cr) + proteinuria + hypoalbuminemia = nephrotic syndrome

light microscopy is consistent with focal segmental glomerulosclerosis (FSGS)

37
Q

which of the following is consistent with focal segmental glomerulosclerosis (FSGS)?
a. immune complex deposition in the mesangium and subepithelium
b. anti-glomerular basement membrane antibody deposition
c. mesangial and endothelial cell proliferation secondary to inflammation
d. podocyte injury resulting in cytoskeletal rearrangement and epithelial cell loss

A

d. podocyte injury resulting in cytoskeletal rearrangement and epithelial cell loss

FSGS is nephrotic syndrome caused by podocyte injury

38
Q

child with puffy face + proteinuria + normal creatinine = (most likely)

A

child with nephrotic syndrome (puffy face, proteinuria) is most likely minimal change disease

39
Q

Pt is 8yo presenting with facial and lower extremity edema of 1 week duration. Parents note increased fatigue for past 3 weeks. BP is 90/55. Periorbital edema noted. Cardiac/pulm exams normal. Proteinuria is noted and serum albumin is low. Which of the following will likely be increased in serum?
a. fibrinogen
b. triglycerides
c. immunoglobins

A

b. triglycerides

patients with nephrotic syndrome and hypoalbuminemia will have increased apolipoproteins leading to increased cholesterol and triglycerides

40
Q

Pt is 30yo F with PMH of HTN and HCV, 32 weeks pregnant. Prenatal evaluation notes progressive increase in BUN and creatinine. Urinalysis +1 for protein and RBC with RBC casts. Renal biopsy shows mesangial cell proliferation and thickening of glomerular basement membrane. Silver stain demonstrates “tram track” appearance of basement membranes. Immunofluorescence of glomeruli would demonstrate:
a. pauci immune staining
b. IgA staining in mesangium
c. granular IgG and C3 staining in capillary loops
d. intense staining with C3 only
e. ribbon-like IgG staining along basement membrane

A

c. granular IgG and C3 staining in capillary loops

most common membranous proliferative glomerulonephritis (MPGN) is Type 1 - immune complex mediated (IgG and C3)

Type 2 MPGN only stains for C3

41
Q

Pt is 64yo M presenting with prostatic hypertrophy and bilateral hydronephrosis. Which of the following changes is most likely?
a. increased GFR, increased FF
b. decreased GFR, increased FF
c. decreased GFR, no change in FF
d. decreased GFR, decreased FF

A

d. decreased GFR, decreased FF

hydronephrosis = dilation of renal calyces (urine is not flowing)

obstruction of urine flow decreases GFR without changing renal blood flow —> decreased filtration fraction

42
Q

how will each of the following urine chemistries be affected by a blood glucose of 520mg/dL (compared to baseline)?
a. pH
b. HCO3-
c. H2PO4-
d. NH4+

A

a. pH: LOW
b. HCO3-: LOW
c. H2PO4-: HIGH
d. NH4+: HIGH

kidneys respond to high acid load (ketoacidosis) by maximally acidifying urine, reabsorbing all bicarb, and increasing urine buffers (phosphate, ammonium)

43
Q

Pt is 54yo M presenting with peri-orbital edema and proteinuria. No blood, ketones, or glucose are noted. Serum albumin is 2. Light microscopy shows thickened basement membrane. Most likely diagnosis is:
a. minimal change disease
b. focal segmental glomerulosclerosis
c. membranous nephropathy
d. membranoproliferative glomerulonephritis

A

c. membranous nephropathy

adult with nephrotic syndrome (proteinuria + decreased albumin + puffy face) is either FSGS or membranous nephropathy - thickened basement membrane on LM indicates membranous nephropathy

44
Q

10yo M presents to ED with periorbital edema, HTN, cola-colored urine. Pt had recent episode of upper respiratory infection (URI) 10 days prior. Light microscopy is likely to show:
a. duplication of glomerular basement membrane (“tram tracks”)
b. normal appearing glomeruli
c. crescents in Bowman’s space
d. edematous, hypercellular glomeruli
e. significant interstitial inflammatory cell infiltrate

A

post-streptococcal glomerulonephritis —> d. edematous, hypercellular glomeruli

a. duplication of glomerular basement membrane (“tram tracks”) - membranoproliferative glomerulonephritis
b. normal appearing glomeruli - minimal change disease
c. crescents in Bowman’s space - rapidly glomerulonephritis
e. significant interstitial inflammatory cell infiltrate - acute interstitial nephritis

45
Q

Which of the following would you expect to see in a patient with a crush injury presenting with myoglobin in the urine?
a. BUN:Cr ratio > 20:1
b. increased blood eosinophils
c. urine sodium < 10 mEq/M
d. muddy brown casts
e. nephrotic-range proteinuria
f. red blood cell casts

A

d. muddy brown casts

crush injury, cells spill contents —> high myoglobin, toxic to renal tubules (intra-renal acute tubular necrosis/ATN) —> muddy brown casts

46
Q

which of the following support a pre-renal cause of oliguria?
a. urine sodium = 10 mEq/L
b. muddy brown casts in urine
c. BUN:Cr ratio of 15
d. serum sodium = 122 mEq/L

A

a. urine sodium = 10 mEq/L

pre-renal oliguria due to renal hypoperfusion

47
Q

how would the following parameters be affected by dextrose infusion?
a. ECF volume
b. ICF volume
c. osmolarity

A

a. ECF volume - increase
b. ICF volume - increase
c. osmolarity - decrease

dextrose gets metabolized, leaving free water behind - increases ECF, but also makes a gradient for osmotic influx into cells, increasing ICF too

free water decreases osmolarity in both compartments

48
Q

Pt is 67yo with recent diagnosis of small cell lung cancer presenting with unsteadiness. Na+ = 115, K+ = 4, Cl- = 88, HCO3 = 20, BUN = 9, Cr = 1, serum osmolarity = 261. What is going on acutely with this patient?

A

hypotonic hyponatremia !

this will cause cells to swell, including in brain (cerebral edema) - look out for neurological symptoms including nausea, headache, confusion, seizure, coma

49
Q

insulin + dextrose and albuterol are used for emergency treatment of hyper___

A

insulin + dextrose and albuterol are used for emergency treatment of hyperKALEMIA

insulin and catecholamines increase Na/K ATPase pump activity, inducing increased updates of K+ into cells

50
Q

what is the function of the protein that is mutated in renal clear cell carcinoma?

A

renal clear cell carcinoma caused by loss of expression of VHL protein, which is responsible for ubiquitination of HIF1alpha

loss of VHL causes increase in VEGF and PDGF

51
Q

hydronephrosis correlates with:
a. decreased oncotic pressure in Bowman’s space
b. decreased renal plasma flow
c. increased oncotic pressure in Bowman’s space
d. increased hydrostatic pressure in Bowman’s space
e. increased renal plasma flow

A

d. increased hydrostatic pressure in Bowman’s space

fluid backup prevents filtration —> decreased GFR and FF (filtration fraction)

52
Q

what occurs in obstructive nephropathy?

A

obstructive nephropathy opposes GFR, causing tubule injury —> loss of cell polarity and reabsorption function (similar to acute tubular necrosis, ATN)

in recovery phase, resorptive function is not yet recovered, so despite low volume status, urine cannot be concentrated or reabsorb sodium, and there is K+ wasting

53
Q

A 63yo victim of MVA is 8 hours post-op when decreased urine output is reported. There was a prolonged period of hypotension in the operating room. BP is 100/75, HR 90/min. No hemorrhaging. Which of the following is most likely to be noted?
a. increased urine Na+ (>40)
b. low urine osmolarity (<300)
c. high BUN:Cr ratio (>20)
d. low serum Na+ (122)

A

c. high BUN:Cr ratio (>20)

patient had period of hypotension —> renal hypoperfusion —> pre-renal oliguria —> HIGH BUN:Cr ratio (>20)

in pre-renal oliguria, kidneys are still functioning - so there should be increased Na+ reabsorption and effective concentration of the urine (responding to hypo-perfusion)

54
Q

32yo F with no significant PMH presents with HTN and muscle weakness. Blood samples show Na+ = 147, K+ = 2.3, Cl- = 110, HCO3 = 30. ABG confirms metabolic alkalosis. Serum aldosterone is undetectable. Which of the following is the most likely cause?
a. Bartter Syndrome
b. Gitelman Syndrome
c. surreptitious thiazide use
d. liquorice ingestion
e. surreptitious spironolactone use

A

d. liquorice ingestion - blocks 11-beta hydroxy-steroid dehydrogenase, which converts cortisol to cortisone in principle cells, allowing excess cortisol to act on mineralocorticoid receptor —> SAME (syndrome of apparent mineralocorticoid excess)

patient is HTN, likely holding onto Na+ (a/b associated with Na+ wasting, c/e are drugs that block Na+ reabsorption)

55
Q

a defect in which of the following is most likely to cause hypocalcuria and hypomagnesium?
a. NKCC in TAL
b. NCC co-transporter in DCT
c. Na+/HCO3 co-transporter in PCT
d. Cl-/HCO3 exchanger in DCT
e. H+ ATPase in DCT

A

b. NCC co-transporter in DCT

NCC defect = Gitelman Syndrome —> low urine Ca2+ and low serum Mg2+ (moving in opposite directions)

56
Q

how do aminoglycosides exert nephrotoxicity?

A

aminoglycosides exert tubular cell toxicity preferentially in the proximal tubular cells - freely filtered by glomeruli and quickly taken up by PCT cells, incorporated into lysosomes and alter metabolism pathways

57
Q

Pt is 44yo F with PMH of primary hyperparathyroidism presenting with gradual onset of polydipsia and polyuria. Lab values notable for Ca2+ of 14.3. Serum Na+ = 147, urine osmolarity = 75. Which is the best explanation?
a. SIADH
b. central diabetes insipidus
c. undiagnosed diabetes mellitus
d. primary polydipsia
e. nephrogenic diabetes insipidus

A

e. nephrogenic diabetes insipidus

elevated plasma osmolarity + maximally dilute urine = lack of vasopressin production or response

hyperparathyroidism most likely causing hypercalcemia-induced nephrogenic diabetes insipidus - remember that calcium blocks aquaporin channels

58
Q

which two antithrombotic proteins are lost in massive protein urea from nephrotic syndrome?

A
  1. ATIII (antithrombin 3)
  2. protein C

—> increased thrombosis risk

59
Q

antibodies against PLA2-R (phospholipase A2 receptor) are associated with which glomerular pathology?

A

membraneous nephropathy —> podocyte injury, silver stain “spikes”, subepithelial immune deposits, diffuse capillary wall thickening on LM (light microscopy)

most cases are primary presentations (not secondary to something else)

60
Q

What is the most common genetic cause of Alport syndrome?

A

X-linked loss of alpha 5 collagen chain

—> lens disorder and deafness, fibrillated/split glomerular basement membrane (all because of missing collagen)

61
Q

URI (upper respiratory infection) + gross hematuria in a 20 year old patient, you’re thinking…

A

IgA nephropathy!

antibodies form against IgA and are deposited in mesangium

hematuria is only symptom

62
Q

if immunofluorescence staining for membranoproliferative glomerulonephritis detects only C3, what type is it?

A

IgG + C3 = Type I (more common, associated with Hep B/C or SLE)

C3 only = Type II

63
Q

when you see crescents on light microscopy of glomeruli, what do the following immunofluorescence patterns mean?
a. granular deposits
b. linear deposits
c. nothing

A

crescents (glomerular basement membrane rupture) = rapidly progressive glomerulonephritis (RPGN)

a. granular deposits - immune complex deposition (Type II)
b. linear deposits (“ribbon”) - anti glomerular basement membrane (Type I)
c. nothing (pauci-immune) - small vessel vasculitis (Type III)

64
Q

acute decline in GFR (rise in Cr, fall in urine output) + inflammatory infiltrate and eosinophilia + WBC casts + flank pain + skin rash/itching =

A

acute (tubule) interstitial nephritis (AIN) - most often caused by allergic reaction to drugs

65
Q

how do the following present in pre-renal azotemia vs acute tubular necrosis (ATN)?
a. BUN:Creatinine ratio
b. urine Na+ concentration
c. fractional excretion of Na+
d. urine osmolarity

A

pre-renal azotemia:
a. BUN:Creatinine: >20
b. urine [Na+]: <20
c. fractional excretion of Na+: <1%
d. urine osmolarity: >500

ATN:
a. BUN:Creatinine: 10-15
b. urine [Na+]: >40
c. fractional excretion of Na+: >1%
d. urine osmolarity: 300-350

66
Q

what happens to FGF-23 levels as renal function declines?

A

FGF-23: fibroblast growth factor 23, decreases phosphate reabsorption

as GFR decreases (renal function declining) phosphate and FGF-23 levels rise

rising FGF-23 causes decrease in calcitriol production —> hypocalcemia, which increases PTH production

67
Q

how do crystals of the following types of kidney stones appear?
a. uric acid
b. struvite
c. cystine
d. calcium oxalate
e. calcium phosphate

A

a. uric acid: overproduction occurs with rapid cell turnover/lysis (ex, multiple myeloma), requires acidic pH, formation of crystals in distal tubules/collecting ducts —> rhomboid (almond) shaped crystals (radiolucent)

b. struvite: urease+ bacteria UTI, requires alkaline pH —> coffin shaped crystals

c. cystine: requires PMH of cystinuria, associated with mutation in proteins responsible for cystine (amino acid) transport —> hexagonal crystals

d. calcium oxalate: associated with Type I RTA, acidic urine —> envelope/dumbbell shaped crystals (square with X across it)

e. calcium phosphate: requires alkaline urine —> amorphous, wedge-shaped rosettes shaped crystals (daisy, starburst)

68
Q

urothelium in the renal calyces and ureters is from ______, while urothelium in the urinary bladder and urethra is from ______

A

urothelium in the renal calyces and ureters is from URETERIC BUD,

while urothelium in the urinary bladder and urethra is from UROGENITAL SINUS

69
Q

causes of Type I (distal) RTA?

A

ABCD’s:
Autoimmune (SLE)
Basolateral exchanger (HCO3/Cl)
Chemotherapy, Calcium
Drug (amphotericin)

70
Q

Pt is 35yo F recently diagnosed with SLE. Urine dipstick is negative for protein, blood, and glucose. Serum Na+ = 143, K+ = 2, Cl = 120, HCO3 = 13, pH = 7.2, pCO2 = 31, pO2 = 102. Urine Na+ = 70, K+ = 25, Cl- = 65, pH = 6. Her acid base disorder would be most consistent with:
a. Toxic ingestion.
b. Increased proximal bicarbonate secretion
c. Impaired distal hydrogen excretion.
d. Increased ammoniagenesis
e. Increased endogenous acid production.

A

c. Impaired distal hydrogen excretion.

Patient has Type I (distal) RTA - inability to secrete H+, associated with autoimmune disorders like SLE, ALKALINE URINE (pH >5)

71
Q

which of the following would be consistent with a Type 1 RTA?
a. positive urine anion gap
b. bicarbonaturia
c. urine potassium wasting.
d. Uric acid crystals in the urine

A

Type I (distal) RTA - inability to secrete H+, associated with autoimmune disorders like SLE, ALKALINE URINE (pH >5)

—> a. positive urine anion gap and c. urine potassium wasting

72
Q

Pt is 44yo M presenting with a 3 month history of fatigue. In the past two weeks, he has noted puffiness in his hands and feet. BP = 150/90. Periorbital edema and bilateral pedal edema is noted. Urinalysis +4 for protein, no blood/ketones/glucose. Renal biopsy is stained with silver. Additional pathologic findings associated with this disorder include:
a. Duplication of the glomerular basement membrane.
b. IgA deposition in the mesangium
c. Thickening of the glomerular capillary wall.
d. Absence of collagen staining in the GBM.

A

patient has membranous nephropathy - silver staining shows c. Thickening of the glomerular capillary wall.

73
Q

Pt is 44yo M presenting with a 3 month history of fatigue. In the past two weeks, he has noted puffiness in his hands and feet. BP = 150/90. Periorbital edema and bilateral pedal edema is noted. Urinalysis +4 for protein, no blood/ketones/glucose. Renal biopsy is stained with silver. Serological testing would show:
a. low C3, normal C4
b. anti-neutrophilic cytoplasmic antibodies
c. anti-phospholipase A2 receptor antibodies
d. anti-glomerular basement membrane antibodies

A

c. anti-phospholipase A2 receptor antibodies

patient has membranous nephropathy - thickening of the glomerular capillary wall

74
Q

to differentiate Liddle syndrome from SAME (syndrome of apparent mineralcorticoid excess), you should assess:
a. urine aldosterone.
b. serum sodium concentration.
c. Urine pH and anion gap.
d. Aldosterone to renin ratio
e. urine cortisol and cortisone.

A

e. urine cortisol and cortisone.

SAME is due to deficiency of 11β-hydroxysteroid dehydrogenase, which results in a defect of the peripheral metabolism of cortisol to cortisone.

75
Q

you are evaluating a patient for oliguria. The patient is on day five of antibiotic therapy with an aminoglycoside. The patient is hemodynamically stable, but reports increased suprapubic discomfort. What is the best next step?

A

always rule out urinary obstruction - common cause of oliguria and easy to fix

76
Q

what is the hereditary pattern of Liddle Syndrome?

A

Liddle Syndrome: autosomal dominant GOF of ENaC (Na+ channel) in collecting tubule of nephron —> high BP, high pH

77
Q

How would multiple myeloma affect GFR and filtration fraction?

A

Multiple myeloma would increase plasma osmolarity —> decreased GFR but no change in plasma renal flow – therefore decreased filtration fraction

Renal (28 decks)

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