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PATH: Tubulointerstitial Disease Flashcards

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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
What parts of the nephron have the highest energy demands?
straight PT and the TALH
26
Where is most of the blood in the medulla concentrated?
around the medullary TALH
27
What is the most hypoxic part of the kidney?
the medulla (10 mmHg pO2 compared to 50 mmHg pO2 in the cortex)
28
What is a major target of hypoxic injury in the kidney?
outer medulla (where straight PT and TALH are located!)
29
Why are renal tubular epithelial cells highly vulnerable to hypoxic injury?
they are UNABLE to perform anaerobic metabolism!
30
Why is the inner medulla less vulnerable to hypoxic injury than the outer medulla?
its structures have less metabolic demands (ex. loop of Henle is all passive diffusion)
31
When is serum potassium a medical emergency?
when plasma concentration is > 7 mmol/L
32
What is the key determinant of whether an ATN patient needs dialysis?
potassium level
33
How do you treat someone with K+ > 7 mmol/L?
``` IV calcium gluconate IV insulin (+ glucose) ```
34
What is the MOA of calcium gluconate?
antagonize membrane depolarization and protects against arrhythmias within 1-3 minutes after administration
35
What is the MOA of IV insulin + glucose?
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
What is pyelonephritis?
renal parenchymal and pelvic inflammation due to bacterial infection (usually ascending from the bladder)
37
What are the main types of bacteria that cause ascending pyelonephritis?
E. coli | Proteus mirabilis
38
How does the bacteria get from the urethra/bladder to the kidneys?
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
What is the other way (not ascending) that pyelonephritis can occur?
hematogenous spread
40
What is the main type of bacteria that causes hematogenous pyelonephritis?
staph aureus from long-indwelling catheters
41
What is the characteristic pathology of Pyelonephritis?
intense neurtophilic infiltration with liquefactive necrosis leading to abscess formation
42
What is pyonephrosis?
pus fills and distends the renal calyces, pelvis, and ureter
43
What is a perinephric abscess?
spread of necrotizing infection through the renal capsule and into fat
44
What is papillary necrosis? When is it most commonly seen?
Intense infection of the papillary tip--most commonly seen in diabetics
45
What is emphysematous pyelonephritis?
gas production by infecting organisms
46
What is characteristic pathology of chronic tubular necrosis?
inflammation (lymphocytes and plasma cells in the interstitium), fibrosis, atrophic and distended tubules that look like thyroid follicles (thyroidizaiton)
47
What are the S/S of pyelonephritis?
Dysuria, frequent urination, suprapubic pain, hematuria, fever, chills, vomiting, CVAT, spesis, turbid urine with pus, renal abscesses on imaging
48
What is the treatment for Pyelonephritis?
drainage of pus from abscesses, antibiotics, supportive care
49
What is a potential complication of Pyelonephritis?
recurrence may lead to scarring that depresses the cortical surface!
50
What are the two possible causes of AIN?
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
What is a type I immune response?
eosinophils, neurtophils, IgE
52
What is a type IV immune response?
macrophages, giant cells, granulomas
53
When do you see symptoms of AIN? What are they?
around 15 days after exposure to drug--> oliguria, fever, eosinophilia (23%), skin rash, hematuria
54
What are the clinical signs of AIN?
Increased serum creatinine, mild-moderate proteinuria, WBC, RBC and white cell casts in urine, urine EOSINOPHILS
55
How do you treat AIN?
withdrawal medication, dialysis (40%)
56
What is analgesic nephropathy?
rare, seen in elderly females with long-term combination analgesic use (chronic interstitial nephritis with papillary necrosis)
57
What is the mutation seen in AD (adult) PCKD?
mutation in polycystin-1 (85%) or polycystin-2 --need a 2nd hit!
58
What does the mutation of polysystin cause in AD PCKD?
Ciliopathy with defective mechanosensing of urine flow with dysregulation of cell adhesion
59
What is the mutation seen in AR (childhood) PCKD?
Mutation in fibrocystin (protein in cilia of tubular epithelial cells)
60
What is the pathology of AD PCKD?
cysts can form at any level along the nephron--kidney gradually enlarges due to huge cysts
61
What is the pathology of AR PCKD?
numerous small cysts replace normal tissue durin fetal like, kidneys cannot produce aminotic fluid
62
Why is the oligohydramnios fatal for infants?
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
What are the clinical features of AD PCKD?
``` 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
What is the treatment/prognosis of AD PCKD?
dialysis or transplant around the age of 50
65
What is another name for nephronophthisis?
medullary cystic disease complex
66
Who gets nephronophthisis?
Children (AR disease) MOST COMMON CAUSE OF ESRD in children!
67
What is the pathology of nephronophthisis?
Small kidneys numerous small cysts at CMJ chronic tubulointerstitial nephritis Fibrosis
68
What is medullary sponge kidney?
Relatively common condition characteried by the formation of cysts in the medulla (usually asymptomatic!)

Renal (12 decks)

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