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Renal > PATH: Tubulointerstitial Disease > Flashcards

PATH: Tubulointerstitial Disease Flashcards

1
Q

What is the most common cause of acute kidney injury?

A

ischemia

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2
Q

What is the most common histopathologic counterpart to actue kidney injury?

A

acute tubular necrosis

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3
Q

What are the common signs of acute kidney injury (plasma wise)?

A

Increase in Creatinine, BUN, and (usually) urea

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4
Q

What accounts for over 80% of acute kidney injury?

A

acute tubular necrosis

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5
Q

What are the underlying mechanisms for ATN?

A

Ischemia (75%)
Nephrotoxins
Urinary tract obstruction, glomerulonephritis, etc. (uncommon)

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6
Q

What is the most common cause of ischemia-induced ATN?

A

shock (septic)

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7
Q

Ischemia-induced ATN usually spares what portion of the kidney?

A

glomeruli (unless cortical necrosis which irreversibly kills glomeruli)

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8
Q

What is the most common nephrotoxin that leads to ATN?

A

radio contrast dye

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9
Q

True or false: ATN is reversible?

A

True! Though the tubular epithelial cells die, the basement membrane is preserved (contains stem cells) that can regenerate epithelial cells and restore the tubule fully (in 3-6 weeks)

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10
Q

What are the molecular mechanisms to injury in a post-ischemic kidney?

A

1) Arteriole vasoconstriction in response to increased tissue levels of endothelin, AngII, TXA2, PG, etc.
2) Decreased arteriole vasodilation in response to Ach, bradykinin, decreased NO.

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11
Q

Why do you see more vasoconstriction and less vasodilation in ATN?

A

Release of vasoactive cytokines (TNF-alpha, IL-1-beta, endothelin, etc.) during leukocyte mediated injury to endothelium

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12
Q

Ischemia can also lead to what sort of epithelial state?

A

pro-inflammatory and pro-coagulant

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13
Q

Why does edema occur in ATN? What does it cause?

A

Edema occurs due to inflammation and loss of tubular epithelial funciton (causing congestion that could compress and add to the regional hypoxia)

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14
Q

What does a gross kidney with ATN look like?

A

Enlarged, pale cortex, congested medulla near CMJ

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15
Q

What is the difference between ATN due to calcineurin toxicity and due to ethylene glycol toxicity under the microscope?

A

Ethylene glycol toxicity will have the cytoplasmic vacuolizaiton but will also have formation of oxalate crystals (translucent, wedge-shaped) in the tubular lumen

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16
Q

What are two early microscopic findings in ATN?

A

blebbing and loss of the brush border

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17
Q

What does later ATN look like microscopically?

A

Cogulative necrosis, epitehlial cells slough into lumen (becoming casts), and apoptosis occurs.

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18
Q

Other than “muddy brown casts,” what other type of casts may be seen in ATN?

A

Myoglobin casts (darkly eosinophilic) if necrosis of skeletal muscle precipitates into the renal tubule

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19
Q

What will the urinalysis of ATN show?

A 
Low urine output
Low urine specific gravity
Low urine osmolarity
High urine Na+ concentration
Muddy brown casts
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20
Q

True or false: people with ATN will be hypertensive.

A

FALSE: not hypertensive (probably in shock)

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21
Q

True of false: people with ATN will be in metabolic acidosis.

A

True!

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22
Q

True or false: people with ATN will be hyperkalemic.

A

True! (and possibly hyponatremic)

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23
Q

How do you treat ATN?

A

Dialysis (but must first treat shock or whatever disease is going on!)

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24
Q

What supplies blood to the renal medulla?

A

vasa recta

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25
Q

What parts of the nephron have the highest energy demands?

A

straight PT and the TALH

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26
Q

Where is most of the blood in the medulla concentrated?

A

around the medullary TALH

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27
Q

What is the most hypoxic part of the kidney?

A

the medulla (10 mmHg pO2 compared to 50 mmHg pO2 in the cortex)

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28
Q

What is a major target of hypoxic injury in the kidney?

A

outer medulla (where straight PT and TALH are located!)

29
Q

Why are renal tubular epithelial cells highly vulnerable to hypoxic injury?

A

they are UNABLE to perform anaerobic metabolism!

30
Q

Why is the inner medulla less vulnerable to hypoxic injury than the outer medulla?

A

its structures have less metabolic demands (ex. loop of Henle is all passive diffusion)

31
Q

When is serum potassium a medical emergency?

A

when plasma concentration is > 7 mmol/L

32
Q

What is the key determinant of whether an ATN patient needs dialysis?

A

potassium level

33
Q

How do you treat someone with K+ > 7 mmol/L?

A 
IV calcium gluconate 
IV insulin (+ glucose)
34
Q

What is the MOA of calcium gluconate?

A

antagonize membrane depolarization and protects against arrhythmias within 1-3 minutes after administration

35
Q

What is the MOA of IV insulin + glucose?

A

Works within 30 minutes to directly activate Na+/H+ exchanger int he collecting duct that moves sodium into the cell to fully activate the sodium potassium pump (shunts K+ into the cell)

36
Q

What is pyelonephritis?

A

renal parenchymal and pelvic inflammation due to bacterial infection (usually ascending from the bladder)

37
Q

What are the main types of bacteria that cause ascending pyelonephritis?

A

E. coli

Proteus mirabilis

38
Q

How does the bacteria get from the urethra/bladder to the kidneys?

A

vesicoureteral reflex (bladder gets over-distended with infected urine and if the patient tried to forcefully urinate, it can force the valves open and the infected urine can wash back up into kidney

39
Q

What is the other way (not ascending) that pyelonephritis can occur?

A

hematogenous spread

40
Q

What is the main type of bacteria that causes hematogenous pyelonephritis?

A

staph aureus from long-indwelling catheters

41
Q

What is the characteristic pathology of Pyelonephritis?

A

intense neurtophilic infiltration with liquefactive necrosis leading to abscess formation

42
Q

What is pyonephrosis?

A

pus fills and distends the renal calyces, pelvis, and ureter

43
Q

What is a perinephric abscess?

A

spread of necrotizing infection through the renal capsule and into fat

44
Q

What is papillary necrosis? When is it most commonly seen?

A

Intense infection of the papillary tip–most commonly seen in diabetics

45
Q

What is emphysematous pyelonephritis?

A

gas production by infecting organisms

46
Q

What is characteristic pathology of chronic tubular necrosis?

A

inflammation (lymphocytes and plasma cells in the interstitium), fibrosis, atrophic and distended tubules that look like thyroid follicles (thyroidizaiton)

47
Q

What are the S/S of pyelonephritis?

A

Dysuria, frequent urination, suprapubic pain, hematuria, fever, chills, vomiting, CVAT, spesis, turbid urine with pus, renal abscesses on imaging

48
Q

What is the treatment for Pyelonephritis?

A

drainage of pus from abscesses, antibiotics, supportive care

49
Q

What is a potential complication of Pyelonephritis?

A

recurrence may lead to scarring that depresses the cortical surface!

50
Q

What are the two possible causes of AIN?

A

1) Drugs acting as hapten to bind to tubular epithelial cells and elicit a type I and type IV immune response
2) Mutli-organ autoimmune inflammatory disease like lupus

51
Q

What is a type I immune response?

A

eosinophils, neurtophils, IgE

52
Q

What is a type IV immune response?

A

macrophages, giant cells, granulomas

53
Q

When do you see symptoms of AIN? What are they?

A

around 15 days after exposure to drug–> oliguria, fever, eosinophilia (23%), skin rash, hematuria

54
Q

What are the clinical signs of AIN?

A

Increased serum creatinine, mild-moderate proteinuria, WBC, RBC and white cell casts in urine, urine EOSINOPHILS

55
Q

How do you treat AIN?

A

withdrawal medication, dialysis (40%)

56
Q

What is analgesic nephropathy?

A

rare, seen in elderly females with long-term combination analgesic use (chronic interstitial nephritis with papillary necrosis)

57
Q

What is the mutation seen in AD (adult) PCKD?

A

mutation in polycystin-1 (85%) or polycystin-2 –need a 2nd hit!

58
Q

What does the mutation of polysystin cause in AD PCKD?

A

Ciliopathy with defective mechanosensing of urine flow with dysregulation of cell adhesion

59
Q

What is the mutation seen in AR (childhood) PCKD?

A

Mutation in fibrocystin (protein in cilia of tubular epithelial cells)

60
Q

What is the pathology of AD PCKD?

A

cysts can form at any level along the nephron–kidney gradually enlarges due to huge cysts

61
Q

What is the pathology of AR PCKD?

A

numerous small cysts replace normal tissue durin fetal like, kidneys cannot produce aminotic fluid

62
Q

Why is the oligohydramnios fatal for infants?

A

the fetus needs to “breathe amniotic fluid” for lungs to develop and needs normal developing kidneys to produce the fluid–the infant will undergo immediate respiratory failure at birth!

63
Q

What are the clinical features of AD PCKD?

A 
flank pain/dragging sensation in abdomen
 may be in severe pain due to hemorrhage/obstruciton
gross hematuria may occur
HTN
UTI
Cysts form in liver
Cerebral vascular aneurysms
64
Q

What is the treatment/prognosis of AD PCKD?

A

dialysis or transplant around the age of 50

65
Q

What is another name for nephronophthisis?

A

medullary cystic disease complex

66
Q

Who gets nephronophthisis?

A

Children (AR disease) MOST COMMON CAUSE OF ESRD in children!

67
Q

What is the pathology of nephronophthisis?

A

Small kidneys
numerous small cysts at CMJ
chronic tubulointerstitial nephritis
Fibrosis

68
Q

What is medullary sponge kidney?

A

Relatively common condition characteried by the formation of cysts in the medulla (usually asymptomatic!)

Renal (12 decks)

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