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Renal by Minnie: AH Version > Renal SAS/Review > Flashcards

Renal SAS/Review Flashcards

1
Q

The tonicity of the filtrate exiting the loop of Henle and entering the distal convoluted tubule is:

A. Hypotonic

B. Isotonic

C. Hypertonic

A

A. Hypotonic

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2
Q

A 32 year-old man presents for evaluation of hematuria found on a routine work physical. He thinks he has been told of blood in urine samples in the past. He is feeling well and does not take any medications.

  • BP 145/90 HR 80, exam unremarkable
  • Serum Cr 1.5, Albumin 4.0
  • Urinalysis: 1+ protein, + dysmorphic RBCs

Which of the following is most likely diagnosis?

A. IgA nephropathy

B. Post-infectious glomerulonephritis

C. Minimal change disease

D. Membranous nephropathy

A

A. IgA nephropathy

Nephritic picture: Dysmorphic RBCs, 1+ protein isn’t that much (not nephrotic range) => IgA or Post-infectious GN

No preceding illness, recurrent blood in urine, white adult male = more likely IgA

(but IgA can also occur during or right after an infection)

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3
Q

What defines orthostatic tachycardia?

A

>30 BPM increase in pulse when going from lying down to sitting or standing

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4
Q

What is the equation for a patient’s water deficit?

Why would we need to calculate this?

A

We need to know the water deficit so we can treat hypernatremia

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5
Q

Which one of the following scenarios is most likely to lead to volume loss primarily from the extracellular fluid space?

  1. High fever
  2. Car accident in which there is injury to the spleen with resultant bleeding
  3. Bikram yoga (profuse sweating)
A

b. Car accident in which there is injury to the spleen with resultant bleeding

Blood loss is isotonic = lost from ECF

Sweat is hyoptonic = lost from both ECF and ICF
(Lost from ECF, then fluid moves ICF -> ECF, continues)

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6
Q

Why do NSAIDS increase a person’s risk of AKI?

A

NSAIDS inhibit prostaglandins

  • -> Cannot dilate the afferent arteriole to increase perfusion to the glomerulus through autoregulation
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7
Q

In a patient with primary hyperparathyroidism (excess production of PTH), predict the following levels: serum calcium, serum phosphorus, urinary phosphorus

  1. High serum calcium, high serum phosphorus, high urinary phosphorus
  2. High serum calcium, low serum phosphorus, high urinary phosphorus
  3. High serum calcium, high serum phosphorus, low urinary phosphorus
  4. High serum calcium, low serum phosphorus, low urinary phosphorus
A

b. High serum calcium, low serum phosphorus, high urinary phosphorus

PTH inhibits phosphorous reabsorption in the kidney tubule

PTH stimulates 1,25-hydroxy-D3 production -> Ca2+ absorption in the GI tract

PTH stimulates Ca2+ reabsorption in the kidney tubule

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8
Q

Choose high or low for each blank

_________ NaCl delivery to the macula densa stimulates tubuloglomerular feedback and __________ NaCl delivery to the macula densa stimulates renin secretion.

A

High** NaCl delivery to the macula densa stimulates tubuloglomerular feedback and **low NaCl delivery to the macula densa stimulates renin secretion.

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9
Q

Why does hyperkalemia occur in response to acidosis?

A

Cellular buffering of H+ moves H+ intracellularly, and K+ extracellularly

-> Hyperkalemia

In RTA or diarrhea, the same thing happens but we lose a lot of K+ in the urine or poop, resulting in hypokalemia

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10
Q

What kind of AKI does rhabdomyolysis cause?

What urinalysis findings are consistent with this diagnosis?

A

Intrinsic AKI

  • Muscle injury/cell lysis
    • -> Myoglobin release
    • -> Toxic to renal tubules
    • -> Intrinsic AKI

Urinalysis findings

  • Dipstic + for blood but no RBCs
    • “Tea/cola-colored urine”
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11
Q

What key findings are characteristic of hepatorenal syndrome?

A

Hepatorenal syndrome = renal vasoconstriction in the setting of advanced liver disease and normal kidneys

  • Liver damage
    • Alcoholism
    • Jaundice
  • Urine Na < 10
  • Confusion
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12
Q

Are ACE inhibitors more likely to cause hypokalemia or hyperkalemia?

A

Hyperkalemia

Anything that decreases Na+ reabsorption in the collecting duct can cause hyperkalemia

  • ACE inhibitor or ARB
  • MRA
  • Low flow

Decreased Na+ reabsorption = Decreased K+ secretion -> Hyperkalemia

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13
Q

What laboratory findings are consistent with acute interstitial nephritis?

A

Urinalysis shows…

  • WBC, WBC casts
  • Urine eosinophils

History of antibiotic use w/allergic reaction (rash) is common

Note: Post-infectious GN will have RBCs and RBC casts. If a person had a recent streptococcal infection treated w/ antibiotics, look at casts to determine whether AIN (WBC, WBC casts) or postinfectious GN (RBC, RBC casts)

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14
Q

A 5-year old boy is brought for evaluation with new onset of abdominal swelling. His mother first noticed 2 weeks ago. She has also noticed swelling in his feet and around his eyes. You perform urine tests in the office:

  • Urinalysis - 3+ protein, no blood, no RBCs, no casts
  • Urine protein to urine Cr ratio – 5 grams
  • Serum albumin 2.8 mg/dL (low)

If you were to perform a kidney biopsy, what would you expect to see?

  1. Subepithelial deposits (humps) on electron microscopy
  2. Nodular sclerosis on light microscopy (Kimmelsteil-Wilson nodules)
  3. Linear staining of glomerular basement membrane on immunoflurosescence
  4. Podocyte foot process fusion on electron microscopy
A

d. Podocyte foot process fusion on electron microscopy

This is most likely minimal change disease

Subepithelial humps = PIGN

Linear IgG GBM staining = Anti-GBM (RPGN Type I)

Nodular sclerosis = diabetic nephropathy

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15
Q

Choose the correct pair of urinary abnormality with the most likely diagnosis:

A. Urine sodium <20; urinary obstruction

B. FENa >1%; prerenal kidney injury

C. Muddy brown casts; acute tubular necrosis

D. Waxy hyaline casts; glomerulonephritis

A

C. Muddy brown casts; acute tubular necrosis

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16
Q

Why do some blood pressure medications decrease GFR?

A

ACE inhibitors and ARBs inhibit the RAAs

They decrease GFR by causing efferent arteriole vasodilation

  • RAAs ususally causes efferent arteriole constriction through the effects of angiotensin II
  • Medications that inhibit the RAAs inhibit efferent arteriole constriction
17
Q

Describe the differences between RTA types 1, 2, and 3

A
  • Type 1
    • Distal tubule
    • Cannot secrete H+
    • Hypokalemic
    • Severe acidosis - Urine pH >5.5
  • Type 2
    • Proximal tubule
    • Cannot reabsorb HCO3- (Bicarb wasting)
    • Hypokalemic
  • Type 3
    • Collecting tubule
    • Decreased ammonia genesis
    • Decreaed H+ secretion
    • Hyperkalemic
    • Mild acidosis - Urine pH usually <5.5
18
Q

Which of the following would support a diagnosis of acute kidney injury?

  1. Urine output of 1L in next 12 hours
  2. Kidney ultrasound without evidence of hydronephrosis
  3. Chemistry panel with Cr of 1.8 mg/dL
A

c. Chemistry panel with Cr of 1.8 mg/dL

Definition of AKI = one of the following:

  • Rise in serum Cr
    • >0.3 mg/dL in 48 hours
    • Rise 1.5x above baseline in the peceding 7 days
      • In the real world, you usually have to estimate baseline Cr
  • Decreased urine output
    • <0.5 mg/Kg/hour for 6+ hours
19
Q

What is normal for daily urinary creatinine excretion?

A
  • Males excrete 20-25 mg/Kg/day of creatinine
  • Females excrete 15-20 mg/Kg/day of creatinine
20
Q

How does GFR change during RTA?

A

GFR does not change!

Renal function is normal except for the defect in urine acidification

Proximal tubule: Bicarbonate wastage

Distal tubule and collecting duct: Cannot secrete H+

21
Q

A new class of medications has recently been released for the treatment of diabetes mellitus known as SGLT2-inhibitors. They act to inhibit the Na/glucose co-transporter in the proximal tubule. What are the predictable side effects of these medications?

A

Increased glycosuria

Osmotic diuresis -> dehydration

22
Q

Which type of RTA results in the most severe acidosis?

A

Distal tubule RTA

Cannot secrete H+

Urine pH always >5.5

23
Q

What GFR is indicative of ESRD?

A

GFR <15 mL/min

24
Q

A genetic mutation is discovered that leads to activation of the epithelial sodium channel (ENaC) in the cortical collecting duct. Predict the blood pressure and serum potassium levels of affected patients.

A

Increased blood pressure

Decreased serum K+

In the cortical collecting duct:

Increased Na+ reabsorption -> Increased K+ secretion

25
Q

What conditions are associated with membranous nephropathy?

A
  • Hep B, Hep C
  • Membranous Lupus Nephritis (Class V)
  • Solid tumors

Membranous nephropathy is the most common nephrotic syndrome in caucasian males

26
Q

Which of the following is NOT a component of the glomerular permeability barrier?

A. Glomerular capillary endothelial cells

B. Negatively charged glycosaminoglycans

C. Mesangial cells

D. Visceral epithelial cells (podocytes)

A

C. Mesangial cells

27
Q

What is the minimal amount of daily urine production required to excrete a typical solute load?

A

500 mL

28
Q

Your patient is started on an antibiotic for a urinary tract infection called trimethoprim-sulfa. You remember learning that trimethoprim blocks tubular secretion of creatinine. What will happen to your patient’s serum creatinine level after starting this new antibiotic?

A

Serum creatinine will increase

29
Q

Where in the kidney is creatine secreted?

By which transporters?

A

Proximal tubule

Organic cation transporters

30
Q

A 65 year-old man with history of hypertension, type II diabetes, and CAD returns to clinic for follow-up of his stage IV chronic kidney disease. His recent serum creatinine has been 3.0 mg/dL.

Under which law might a Nephrologist’s compensation by Medicare be reduced as a result of having such patients with high blood pressure?

A. Social Security Act

B. Affordable Care Act

C. Medicare Access and CHIP Reauthorization Act (MACRA)

D. High Value Care Act

A

C. Medicare Access and CHIP Reauthorization Act (MACRA)

31
Q

A 30 year old woman is brought to the ER by her family due to new onset of confusion. Has previously been very healthy and does not take any medications. They have also noticed new bruising on her legs and arms.
Initial labs demonstrate a hemoglobin of 6 g/dL (normal 12-15 g/dL), platelets of 12K (normal 150-350K), and serum Cr of 3.2 mg/dL.

Which test would help to distinguish between TTP and atypical HUS?

A. ADAMTS13 level

B. LDH

C. Peripheral smear (looking for schistocytes)

D. Haptoglobin

A

A. ADAMTS13 level

Low ADAMTS13 = diagnostic of TTM

Peripheral smear showing schistocytes would be predicted in aHUS or TTM, and would not distinguish between the two

32
Q

Which of the following electrolyte abnormalities is somebody with ESRD predisposed to?

A. Hypercalcemia

B. Hyperphosphatemia

C. Hyperkalemia

D. B and C

E. All of the above

A

D. B and C

Kidneys cannot excrete phosphate and potassium from the diet

Not at risk for hypercalcemia - 1,25 Hydroxy-D3 is low due to renal dysfunction (and increased FGF-23 secretion), resulting in decreased Ca2+ absorption and reabsorption

33
Q

What ECG changes would we expect in hyperkalemia?

A

Tall T wave

Shortened QT interval

Decreasedd ST segment

V-fib if very severe

34
Q

You are seeing a patient in urgent care with new onset of leg cramps. Basic labs are performed and are normal outside of the following values:

Potassium 2.9 mg/dL (normal 3.5-5.0 mg/dL)
Calcium 10.6 mg/dL (normal 8.5-10.4 mg/dL)

He tells you that he was started on a new blood pressure medication a few weeks ago, but he cannot remember the name of the medication. His new medication is most likely…

A. Spironolactone

B. Hydrochlorothiazide

C. Amiloride

D. Furosemide

A

B. Hydrochlorothiazide

Thiazide diuretics cause low K+ and high Ca2+

Spironolactone and amiloride are K+ sparing

Furosemide causes low K+ and low Ca2+

35
Q

For a patient with new swelling in her legs, blood pressure at home has running higher – usually 160s/90s, and 10 lbs of weight gain in the last week, which of the following would you predict?

A. High serum sodium level (hypernatremia)

B. Elevated plasma renin level

C. Positive total body sodium balance

D. High serum potassium level (hyperkalemia)

A

C. Positive total body sodium balance

(B. elevated plasma renin is also “kind of right” - However, she is not showing signs of low EBV. If she had low EBV + edema, we would definitely expect high renin)

Any patient with volume overload will have a positive total body sodium balance (but not necessarily a high concentration)

Labs will only tell us about concentration - need to use physical exam findings to see volume overload, which indicates positive total body sodium balance

36
Q

Opiates are likely to contribute to which cause of AKI?

A

Postrenal AKI

Opiates contribute to urinary retention

37
Q

Prerenal AKI that continues for long enough will develop into…

A

Acute Tubular Necrosis

Due to ischemia, tubule epithelial cells become damaged and die :(

Post-renal injury that goes on for a long time can also cause ATN

38
Q

Which risk factor is correctly paired with mechanism for causing hyperkalemia?

  1. Hyperglycemia; transcellular shift
  2. ACE inhibitor; increased intake
  3. Volume depletion; cell breakdown
  4. Rhabdomyolysis; decreased excretion
A

Hyperglycemia; transcellular shift

  • ACE inhibitor -> Decreased K+ excretion
    • Decreased Na+ reabsorption in collecting tubule
    • -> Decreased K+ secretion
  • Volume depletion -> Decreased K+ excretion
    • Decreased flow
    • -> Decreased Na+ reabsorption in collecting tubule
    • -> Decreased K+ secretion
  • Rhabdomyolysis -> Decreased K+ excretion
    • Myoglobin is toxic to tubules
39
Q

What are the major risk factors for progression of CKD?

A
  • Elevated Cr
  • Proteinuria
  • HTN
  • Evidence of fibrosis on kidney biopsy

Renal by Minnie: AH Version (27 decks)

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