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Renal Flashcards

1
Q

What part of the nephron is most susceptible to toxin damage?

A

The PCT

Acute tubular necrosis

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2
Q

What part of the nephron has a brush border?

A

PCT

For maximal reabsorption

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3
Q

Potter Syndrome

A

Babies can’t pee in utero

P: pulmonary hypoplasia
O: oligohydramnios
T: Twisted face
T: twisted skin
E: extremity defects (club feet)
R: renal failure in utero

**Caused by ARPKD, renal agenesis, obstructive uropathy

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4
Q

What is the hallmark of glomerular injury?

A

Proteinuria

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5
Q

What passes easier through the glomerulus: positive or negative charged particles?

A

Positive: the golmerular basement membrane carries a negative charge, which repels negatively charged particles

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6
Q

NSAID effects on kidney

A

Constriction of the afferent arteriole

Dec GFR
Dec RBF

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7
Q

ACE inhibitor effects on kidney

A

Dilation of the efferent arteriole

Dec GFR
Inc RBF

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8
Q

Ang II effects on the kidney

A

Constriction of the efferent arteriole

Inc GFR
Dec RBF

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9
Q

Where is glucose reabsorbed? How much is excreted in the urine?

A

100% is reabsorbed in the PCT

There should be no glucose in the urine – presence indicates diabetes

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10
Q

What section of the nephron is most permeable to water? Which sections are impermeable?

A

PCT = high permeability

TAL and DCT = no permeability

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11
Q

Electrolyte defect consequences of diabetes insipidus?

A

High excretion of water in the urine causes hypernatremia

Due to a problem with ADH (dec secretion or inc resistance)

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12
Q

What stimulates the release of renin from the JGA cells?

A

Low blood volume by baroreceptors
Low flow (dec Na in tubules)
Inc sympathetic activity (B1)

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13
Q

Acidosis and alkalosis effects on potassium levels

A

Acidosis causes hyperkalemia: H+ moves into cells to correct pH and K+ moves out of cells to maintain electroneutrality

Alkalosis causes hypokalemia: H+ moves out of cells to correct pH and K+ moves into cells to maintain electroneutrality

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14
Q

Insulin effects on potassium levels

A

Causes hypokalemia

Insulin activates Na/K ATPase which pumps K+ into cells

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15
Q

EKG changes: Hypokalemia

A

U waves

Flattened T waves

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16
Q

EKG changes: Hyperkalemia

A

Peaked T waves

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17
Q

What happens if you rapidly correct hypernatremia?

A

High to low your brain will blow

Cerebral edema

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18
Q

What happens if you rapidly correct hyponatremia?

A

Low to high your pons will die

Osmotic demyelination

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19
Q

Fanconi syndrome

A

PCT

Generalized reabsorptive defect: inc excretion of amino acids, glucose, HCO3 and phosphate

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20
Q

Bartter syndrome

A

TAL of loop of henle
Defect in NKCC2 cotransporter

Causes hypokalemia and metabolic alkalosis

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21
Q

Gitelman syndrome

A

DCT

Defect in Na/Cl cotransporter

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22
Q

Liddle syndrome

A

Collecting duct
Gain of function in ENaC channels

Causes hypokalemia and metabolic alkalosis
Treat with Amiloride

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23
Q

Black licorice effects

A

Contains glycyrrhetic acid – blocks the activity of 11B hydroxysteroid dehydrogenase

(normally 11B OHsteroid dehydrogenase breaks down cortisol before it can act on the mineralcorticoid receptor) – blocked activity causes inc mineralcorticoid receptor activity

Hypernatremia
Hypokalemia
Inc BP
Metabolic alkalosis

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24
Q

Metabolism of glutamine

A

In the PCT

Produces NH4 and HCO3 –> allows fro excretion of H+

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25
Q

Calculate anion gap

A

AG = Na - (Cl + HCO3)

Normal range: 8-12

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26
Q

Causes of metabolic acidosis with elevated anion gap

A

MUDPALES

Methanol
Uremia
DKA
Propofol
Alcoholic ketoacidosis
Lactic acidosis
Ethylene Glycol
Salicylates
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27
Q

Patient has respiratory alkalosis and metabolic acidosis wit elevated anion gap…

A

Salicylate overdose

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28
Q

Acid base: Opioid overdose

A

Respiratory acidosis

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29
Q

Acid base: pulmonary embolism

A

Respiratory alkalosis

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30
Q

Acid base: spironolactone

A

Metabolic acidosis

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31
Q

Acid base: Loop/thiazide diuretics

A

Metabolic alkalosis

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32
Q

Acid base: High altitude/hypoxemia

A

Respiratory alkalosis

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33
Q

Differential for intraabdominal tumor in children

A

Nephroblastoma (Wilms tumor): Kidney
Neuroblastoma: adrenal gland
Hepatoblastoma: liver

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34
Q

Muddy brown casts in urine = ?

Caused by what?
What portions of the nephron are particularly susceptible?

A

Acute Tubular necrosis

Caused by ischemia or toxicity

Ischemia: PCT and TAL of loop of henle
Toxicity: PCT

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35
Q

What can rhabdomylolysis do to the kidney?

A

Acute Tubular Necrosis

myoglobin is nephrotoxic

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36
Q

How does anemia occur in patients with renal disease?

A

Decreased production of EPO by the kidney

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37
Q

Nephrotic syndrome characterisitcs

A

Podocyte dysfunction

  1. Proteinura >3 g
  2. Hypoalbuminemia
  3. Edema
  4. Hyperlipidemia with lipiduria
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38
Q

Podocyte effacement seen on Electron Microscopy

A

Minimal change disease

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39
Q

Most common cause of nephrotic syndrome in kids

A

Minimal change disease - may be triggered by a recent infection, immunization or other immune stimulus

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40
Q

EM shows thickening of glomerular capillary loops with small spikes on the glomerular basement membrane

A

Membranous Nephropathy – immune complex deposition disease

Nephrotic presentation of SLE, can be associated with drugs or infections (hepatitis)

41
Q

Glomerular nodules and hyalinosis of arterioles seen on LM

A

Diabetic nephropathy

Kimmelstiel-Wilson lesions

42
Q

Starry night appearance on immunofluorescence

A

Post-strep glomerulonephritis (IgG, IgM, and C3)

43
Q

Large hump like subepithelial deposits on EM

A

Post-strep glomerulonephritis (IgG, IgM, and C3)

44
Q

What is the most common cause of glomerulonephritis?

A

IgA nephropathy

Usually presents following a URI

45
Q

Mesangial immune deposits

A

IgA nephropathy

46
Q

Tram track appearance of GBM

A

Membranoproliferative Glomerulonephritis

47
Q

which nephritic syndrome is associated with Hep B or Hep C

which nephrotic syndrome is associated with hep B or hep C?

A

Membranoproliferative Glomerulonephritis

Membranous Nephropathy

48
Q

Wire looping of capillaries seen on LM

A

Diffuse Proliferative Glomerulonephritis: SLE

“Wire lupus”

49
Q

Full house immunofluorescence

A

SLE: Diffuse Proliferative Glomerulonephritis

IgM, IgG, IgA C3, C1q, deposition

50
Q

What do horseshoe kidneys get trapped on during ascent?

A

Inferior mesenteric artery

51
Q

Acute interstitial nephritis:

Causes and presentation

A

Acute interstitial renal inflammation
→ associated with drugs (PCNs, NSAIDs, Thiazides, Rifampin, sulfonamides, diuretics, etc)

patients present with fever, skin rash, and eosinophilia

52
Q

What part of the nephron causes alkalinization of the urine when acted on by an antidiuretic?

A

PCT: Acetazolamide

53
Q

Hartnup disease

A

Autosomal recessive
Deficiency of amino acid transporters in the PCT and in enterocytes – increased excretion and reduced absorption of amino acids

Deficiency of tryptophan causes niacin deficiency and symptoms of pellagra – dermatitis, diarrhea, and dementia

54
Q

Most common kidney stone presentation

A

calcium oxalate stone in a patient with hypercalcuria and normocalcemia

55
Q

Coffin lid shaped crystals

A

Ammonium magnesium sulfate (struvite)

Precipitates due to high pH (urease positive bugs like proteus mirabilis)

56
Q

Rhomboid shaped crystals

A

Uric acid

Precipitates due to low pH

57
Q

Hexagonal shaped crystals

A

Cysteine

Precipitates due to low pH

58
Q

Envelope shaped crystals

A

Calcium oxalate

Precipitates due to hypocitraturia

59
Q

What else should you see in someone with cystinuria?

A

AR defect in cysteine reabsorbing PCT transporter causing cytinuria –> leads to poor absorption of cysteine, ornithine, lysine, and arginine

(COLA)

60
Q

Origin of renal cell carcinoma

A

PCT

61
Q

Origin of renal oncocytoma

A

Collecting duct

62
Q

Calculation of RPF and RBF

A

RPF = PAH clearance = (urine PAH x urine flow rate)/plasma PAH

RBF = RPF/(1 - Hct)

63
Q

Macula densa

A

Patch of columnar epithelium that senses the composition of fluid in the DCT

64
Q

Filtration fraction calculation

A

FF = GFR/RPF

65
Q

What is the result of acute tubular necrosis?

A

Usually spontaneously resolves – re-epthelialization of the tubules

66
Q

Acetazolamide

A

Carbonic anhydrase inhibitor

Acts on the PCT

67
Q

What is the effect of loop diuretics on renal perfusion?

A

Loop diuretics (like Furosemide) induce the expression of COX and increase prostaglandin synthesis –> dilation of the afferent renal arteriole

68
Q

What diuretic could you give to someone to relieve their hypercalcemia?

A

Loop diuretic like Furosemide (increases calcium excretion)

69
Q

What diuretic can help promote bone strength and decrease kidney stone formation?

A

Thick ascending limb diuretics (thiazides)

Promote the uptake of calcium
Dec absorption of Na increases the positive charge gradient, so more calcium is absorbed

70
Q

If a patient is has a sulfa allergy, what loop diuretic can you not give them? What should you give them instead?

A

Furosemide (sulfonamide loop diuretic)

Give them Ethacrynic Acid (nonsulfonamide loop diuretic)

71
Q

Which diuretic can cause lithium toxicity?

A

Thiazides

72
Q

What labs do thiazides increase?

A 
hyperGLUC
hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia
73
Q

Where does ADH act? What is the mechanism of action?

A

ADH binds to V2 receptor (G coupled protein) → inc cAMP and activation of PKA → PKA activation stimulated AQP2 that is stored in vesicles to shuttle it to the apical membrane → inc AQP2 causes inc H2O reuptake → concentrated urine

74
Q

Patient presents with hematuria, proteinuria, oliguria, inc BUN and hypertension. What do they have?

A

Nephritic syndrome

Immune complex mediated disease

75
Q

60-40-20 rule of distribution of water

A

o Total body water = 60%
o Intracellular fluid = 40%
o Extracellular fluid = 20%

76
Q

Renal cell carcinoma is associated with which gene mutation?

A

Deletion on chromosome 3 (VHL)

Von Hippel Lindau

77
Q

Von Hippel Lindau

A

Mutation or deletion of VHL gene on chromosome 3

Characterized by cerebellar hemangioblastoma, renal cell carcinomas, and pheochromocytomas

Renal cell carcinoma is the major cause of death

78
Q

Where do uric acid crystals precipitate during tumor lysis syndrome? Why here?

A

These crystals precipitate in an acidic environment and the lowest pH along the nephron is found in the distal tubules and collecting ducts – these segments of the nephron can be obstructed

79
Q

Renal biopsy shows crescent formation in glomeruli?

A

Rapidly progressive glomerulonephritis

ANCA positive

80
Q

What are the two most important buffers in urine? What is their function?

A

NH3 and HPO4^2-
o The kidney utilizes acid buffers to trap H+ and allow the excretion of much larger amounts of acid without markedly lowering urinary pH
o HPO4^2- is a titratable acid that combines with H+ to form H2PO4^-
o NH3 is generated by the proximal tubular cells via metabolism of glutamine and combines with H+ to form NH4+
o These are elevated during DKA! Allows for excretion of acid

81
Q

What diuretic can cause ototoxicity?

A

Furosemide (loop diuretics)

Usually resolves after med discontinuation

82
Q

c-ANCA vs p-ANCA

A

c-ANCA: target antigen is proteinase 3

p-ANCA: target antigen is MPO

83
Q

Patient presents with history of vision problems, glomerulonephritis, and deafness. What do you suspect?

Inheritance?
Mechanism of action?

A

Alport Syndrome

X linked dominant

Mutation in type IV collagen –> thinning and splitting of glomerular basement membrane

Generally have eye and ear problems as well

84
Q

Renal Osteodystrophy: caused by?

Calcium
Phosphate
PTH
Calcitriol

A

Complication of chronic kidney disease

Calcium: dec
Phosphate: inc (less is filtered due to dec GFR)
PTH: inc (due to dec calcium)
Calcitriol: dec (injured kidney cannot activate vitamin D)

85
Q

Effects of citrate on calcium oxalate stone formation

A

Citrate will bind to free (ionized) calcium and prevent it from precipitating

Give citrate or thiazide diuretics in the tx of calcium stones

86
Q

Acid Base: Vomiting

A

Metabolic alkalosis (due to loss of gastric H+)

87
Q

Acid-base: diarrhea

A

Metabolic acidosis ( due to loss of GI HCO3-)

88
Q

Chronic kidney hypoperfusion results in hyperplasia and hypertrophy of which cells?

A

The juxtaglomerular cells (modified smooth muscle cells that are part of the afferent arteriole)

89
Q

Blood supply to different parts of the ureter

A

o Proximal: renal artery
o Middle: multiple anastamoses
o Distal: superior vesicle artery

90
Q

Non lactose fermenting cause of UTI

A

Pseudomonas

91
Q

What should you consider in a patient who has been taking Naproxen daily for 3+ months?

A

Chronic interstitial necrosis – NSAIDs can cause damage over time to the kidneys

92
Q

What do positive nitrates in urine indicate?

A

Presence of gram negative bacteria, like E coli

93
Q

What is the most common site of obstruction (hydronephrosis) in fetus?

A

The uteropelvic junction, as this is the last area to canalize during development

94
Q

Which cells in the kidney are responsible for activation of vitamin D? Using what enzyme?

A

The PCT cells

1a hydroxylase

95
Q

renal disease in paroxysmal nocturnal hemoglobinuria is caused by?

A

Lysis of iron-containing RBCs leads to inc iron deposition in the kidney (hemosiderosis) which can interfere with PCT function and cause interstitial scarring and cortical infarcts

96
Q 
Precipitate in high or low pH?
Calcium
Uric acid
Ammonium magnesium (struvite)
Cysteine
A

Calcium: high pH
Uric acid: low pH
Ammonium magnesium (struvite): high pH
Cysteine: low pH

97
Q

Patient presents with signs of ATN (proximal tubular cell ballooning and vacuolar degeneration in a patient with acute renal failure) and is found to have oxalate crystals in the tubular lumen

A

Indicative of ethylene glycol poisoning (seen as suicide – antifreeze – or due to alcohol abuse)

98
Q

How does renal artery stenosis lead to HTN?

A

Renal artery stenosis causes decreased perfusion to the kidney. This causes the kidney to release more renin, which is then used to eventually form Ang II –> inc BP

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