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CRRAB 2 Week 2 > Renal Path: Tubulointerstitial Disease > Flashcards

Renal Path: Tubulointerstitial Disease Flashcards

1
Q

What are the two general mechanisms contributing to diseases of the tubules and interstitium? What form of disease do they each cause?

A
  1. ischemic/toxic injury to tubules = acute tubular necrosis

2. inflammatory reactions of the tubules and interstitium = tubulointerstitial nephritis

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2
Q

Acute tubular necrosis is the most common cause of what?

A

acute renal failure

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3
Q

Both ischemic and toxic acute tubular necrosis involve the formation of casts, but how do they differ in terms of the necrosis?

A

ischemic type has scattered necrosis throughout the nephron

toxic type has necrosis specifically in the proximal tubule (since that’s where the drugs will encounter the tubules first)

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4
Q

How can you get repair of acute tubular necrosis?

A

the necrosis that occurs doesn’t usually affect the basement membrane

the intact basement membrane is therefore able to secrete growth factor to help cells regenerate

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5
Q

Describe the pathogenesis of acute tubule necrosis.

A
  1. some form of endothelial injury occurs in the kidney
  2. the damaged cells will release cytokines which trigger a local inflammatory response
  3. intrarenal vasoconstriction actually occurs, decreaseing glomerular plasma flow and O2 deliver
  4. the dead cells slough off and obstruct the lumen
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6
Q

What are the pathways that lead to vasoconstriction in acute tubular necrosis?

A

the renin-angiotensin system
endothilin release by endothelial cells
decreased NO production

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7
Q

What will the pathology look like in acute tubular necrosis?

A

necrosis within the tubules
sloughing of the tubular cells
hyaline and granular casts
interstitial edema and incresaed lymphocytes

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8
Q

What additional microscopic finding might you see with toxic ATN?

A

ATN from ethylene glycol poisoning will have calcium oxalate crystals in the tubular lumens

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9
Q

What are the three stages of the ATN clinical course?

A
  1. initiation
  2. maintenance
  3. recovery
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10
Q

What happens initiation phase?

A

a slight decline in urine output and increased BUN, lasts for about 36 hours

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11
Q

What happens during the maintenance stage?

A

oliguria
salt and water overload with edema
increased BUN, hyperkalemia, metabolic acidosis
often requires dialysis

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12
Q

What happens during the recovery phase?

A

A steady increase in urine volume - actually a massive increase like 3 L/days

hypokalemia due to loss of K

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13
Q

What is the prognosis for nephrotoxic ATN? What about ATN related to shock/multiorgan failure?

A

nephrotoxic ATN has a 95% recovery rate if the patient survives the initial event

prognosis for ATN related to shock/organ failure is only 50% survival

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14
Q

What are the two main forms of tubulointerstitial nephritis? What characterizes each?

A

acute: with pMNs/Eos and edema
chronic: fibrosis and tubular atrophy

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15
Q

Clinically, what will tubulointerstitial nephritis present with?

A

polyuria
nocturia
metabolic acidosis

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16
Q

What is a common infectious cause of tubulointerstitial nephritis?

A

pyelonephritis

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17
Q

What is a common metabolic disease leading to TIN?

A

gout - urate buildup in the kidneys

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18
Q

What is a neoplasm common associated with TIN?

A

multiple myeloma

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19
Q

Acute pyelonephritis is a bacterial infection of the kidneys. What are some factors predisposing people to progress to chronic pyelonephritis?

A

structural issues - obstruction form BPH, tumor or stones

neurogenic bladder

vesiculoureteral reflux

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20
Q

What will the morphology be for acute pyelonephritis if you got a bopsy?

A

interstitial suppurative inflammation with PMNS

intratubular aggregates of neutrophils
tubular necrosis

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21
Q

How does an acute pyelonephritis heal microscopically

A

heals by scarring, with subsequent tubular atrophy and interstitial fibrosis with lymphocytes

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22
Q

If the issue is in part due to vesiculoureteral reflux, what parts of the kidney are most commonly affected?

A

the upper and lower poles (because thos eaer teh places where it’s most likely to reflux to)

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23
Q

What is a major complication of acute pyelonephritis that occurs mainly in diabetics of people with obstructions?

A

papillary necrosis

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24
Q

what does papillary necrosis look like?

A

gross: yellow necrosis at the papillary tips
micro: coagulative necrosis of th epapillary tips

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25
Q

What are two other complications of acute pyelonephritis that can happen in anyone?

A

pyonephrosis - kidney basically becomes a bag of pus

perinephric absces - suppurative inflammation extends TROUGH the renal capsule into the adjacent tissue (bad)

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26
Q

Why is CHRONIC pyelonephritis special in terms of what it does to the kidney?

A

it causes damage to the calyces (the only other thing that does that is analgesic nephropathy)

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27
Q

What will gross anatomy look like in chronic pyelo? Microscopically?

A

gross: irregularly scarred surface of kidney, discrete cortiomedullary scar overlying a blunted or deformed calyx
micro: focal tubular atrophy with other areas of dilated tubules. may see thyroidization and tubules filled with colloid casts

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28
Q

Pyelonephritis usually doesn’t affect the lgomerulus, but if it does, what’s the pattern?

A

focal segmental gomerulosclerosis

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29
Q

What are the three ways drugs can induce injury in the kidney?

A
  1. trigger an interstitial immunologic reaction
  2. cause acute tubular injury/acute renal failure
  3. slow injury to tubules over man years with resulting chronic renal insufficiency
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30
Q

For acute drug-induced interstitial nephritis, when is the onset?

A

usually about 15 days after exposure to the drug

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31
Q

What are the common symptoms of acute drug-induced interstiail nephritis?

A

fever, rash, eosinophilia, renal abnormalities

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32
Q

What will drug-induced acute interstitial nephritis look like microscopically

A
  1. interstitial edema and mononuclear cells (lymphocytes and macrophages)
  2. variable numbers of eosinophils and PMNs
  3. granulomas and giant cells will some drugs = methicillin, thiazides
  4. lyphocytes infiltrate tubular epithelium and cause necrosis
  5. normal glomeruli
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33
Q

True or false: the immune response is dose-dependent in acute drug-induced interstitial nephritis?

A

false - it’s idiosyncratic (not dose related)

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34
Q

How do the drugs seem to trigger an autoimmune response?

A

they act as haptens and bind covalently to a cytoplasmic or extracellular component of the tubular cells

this illicits the immune response (TYpe 4 HSR)

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35
Q

What is the main class of drugs to worry about for drug-induced acute intersitial nephritis?

A

NSAIDS

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36
Q

What are all the things NSAIDS can do bad to the kidney?

A
  1. acute renal failure - hemodynamically induced due to inhibition of vasodilatory prostaglandin synthesis
  2. acute hypersensitivity interstitial nephritis leading to ARF
  3. acue interstitial nephritis and MCD
  4. membranous glomerulonephritis
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37
Q

Describe acute uric acid nephropathy. Who does it usually occur in?

A

it’s from preipitation of uric acid crystals in the renal tubules resulting in obstruction and inflammation. leads to acute renal failure

usually in aptients with lymphomas undergoing chemotherapy or in patients with gout

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38
Q

Hoes does calcium contribute to TIN?

A

in hyperCa you get Ca stones and deposition to Ca which triggers inflammation in the tubules and interstitium

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39
Q

Why does multiple myeloma lead to TIN?

A

MM is a plasma cell neoplasm where you get polyclonal expansion of a light chain - either kappa or lambda (the Bence Jones proteins)

the light chains combine with tamm-horsfall proteins to form large tubular casts that cause obstruction an dperitubular inflammation

40
Q

Nephrosclerosis is very common. What is the gross finding with sclerosis of renal arterioles and small arteries?

A

normal to small kidneys wtih a surface that has a fine, even fgranularity to it - like sand paper

41
Q

What will you see microscopically in nephrosclerosis?

A

thickening and hyalinization fo the walls of the arterioles and msall arteries (hyalin arteriosclerosis) which narrows the vessel lumen

can get patchy ischemic atrophy with tubular atrophy and itnerstitial fibrosis and glomerularsclerosis in late disease

42
Q

In what patients is malignant nephrosclerosis more common?

A

more common in males, blacks and younger patients

43
Q

What do you get pathologically in malignant nephrosclerosis?

A

blood pressure is super superhigh which causes vascular damage to kidneys

vessels leak, endothelial cells die and platelets depotsit

fibrinoid necrosis of the essels with thrombosis

the kidney becomes ischemic and the rAAS system is activated

44
Q

What does the kidney look likeg rossy in malignant nephrosclerosis?

A

pinpoint petechial hemorrhages on the cortical surface (flea bitten)

45
Q

What does malignant nephrosclerosis look like microscopically?

A

fibrinoid necrosis of arterioles (eosinophilic material in blood vessel wall)

onion skinning of vessels = hyperplastic arteriolitis

46
Q

What are the clinical signs of malignant nephrosclerosis?

A

marked proteinuria and hematuria with rapid development of renal failure in a setting with other malingnat hypertension symptoms - HA, N/V, scotoma, etc.

47
Q

What percentage of HTN is caused by renal artery stenosis?

A

2-5%

but it’s important because if this is the cause, you can cure it

48
Q

What will the gross anatomy finding be in renal artery stenosis/

A

the ischemic kidney is small

49
Q

70% of renal artery stenosis is caused by what? How about the other 30%?

A

atheromatous plaques

fibromuscular dysplasia in young and middle aged women

50
Q

What will the ischemic kidney show microscopically? How about the unaffected kidney?

A

The affected kidney will atrophy

the unaffected kidney will who hyaline arteriolosclerosis because it’s subjected to the systemic hypertension

51
Q

What are the 4 categories of the thrombotic microangiopathies?

A

typical hemolytic uremic syndrome
atypical HUS
familial HUG
idiopathic thrombotic thrombocytopenic purpura

52
Q

What is the basic pathogenesis of the thombotic microsntiopathies?

A
  1. endothelial injury (multiple triggers, denuded endothelium reveals thombogenic tissue, reduced prostaglandin I2 and NO leads to vasoconstriciton)
  2. Platelet activation and aggregation
53
Q

75% of cases of typical HUS are caused by what?

A

intestinal infection by verocytotoxin-producin E.coli (0157:H7)

54
Q

What are the symptoms of typical HUS with e coli infection?

A 
sudden onset of bleeding = hematemesis or melena
oliguria
hematuria
MAHA 
with or without neurologic changes
55
Q

What does the verocytotoxin (shiga-like) toxin cause?

A

endothelial lysis, increased endothelin and decreased NO (leads to injury and vasoconstriction)

56
Q

What are thefour main entities that cause atypical HUS?

A

antiphospholipid syndrome

pregnancy = post-partum renal failure

vascular renal disease (like malignant HTN, systemic sclerosis, etc)

drug-related (esp chemotherapeutic and immunosuppressive drugs like cyclosporin)

57
Q

What percentage of HUS is familial?

A

5-10% have recurrent thromboses

58
Q

What is the inherited deficiency in familial HUS?

A

deficienty of complement regulatory protein Factor H, which trypically protects cells from uncontrolled complement activation

59
Q

What is the classic pentad of idiopathic TTP?

A 
fever
neurological symptoms
MAHA
thrombocytopenia
renal failure
60
Q

What is idiopathic TTP likely due to?

A

acquired or genetic defect in the protease that cleaves large von willbrand multimers (ADAMTS-13)

61
Q

Who is idiopathic TTP more common in?

A

women and those under 40

62
Q

What’s the treatment for i TTP?

A

plasma exchange and corticosteorids

63
Q

What do you see in gross anatomy for HUS/TTP?

A

pathy or diffuse renal cortical necrosis

64
Q

What do you see microscopically for HUS/TTP?

A

fibrinoid necrosis of arterioles with thrombi

65
Q

Why is the kidney aprticularly susceptible to infarct?

A

it’s an end-organ so it has limited collateral circulation and it gets 25% of the cardiac output

66
Q

Are most infarcts in the kidney secondary to emboli or thrombi?

A

emboli - left artial and ventricular thrombi post MI will embolize to the kidney

67
Q

What will you see on gross anatomy in a renal infarct?

A

acute - a solitary white wedge-shaped infarct

chronic - depressed, gray-white - scar in a V shape

68
Q

What will you see microscopically in a renal infarct?

A

ischemic coagulativ enecrosis

69
Q

What happens to the kidney in obstructive uropathy?

A

obstruction makes you more suscpetible to infection and stones

leads to hydronephrosis and renal atrophy

70
Q

What will you see in gross anatomy of obstructive uropathy?

A

hydronephrosis: dilation of the renal pelvis and calyces associated with atrophy of th ekidney due to obstruction of urine flow

slight to massive enlargement of the kidney

advanced idsease may leave the kidney a thin-walled cyst

71
Q

What will you see microsopically in obstructive uropathy?

A

interstitial inflammation leading eventually to fibrosis

tubular atrophy

72
Q

What are the two main benign renal tumors?

A

angiomyolipoma

oncocytoma

73
Q

What is an angiomyolipoma composed of?

A

blood vessels, smooth muscle and fat

74
Q

What are angiomyolipomas associated wtih?

A

tuberus sclerosis

75
Q

How is tuberous sclerosis inherited?

A

autosomal dominant

76
Q

What does an oncocytoma look like grossy? microscopically?

A

gross: mahogany brown
micro: large, eosinophilic cells with rounded nuclei. EM shows abundant mitochondria

77
Q

Where in the kidney do oncocytomas arise from?

A

the collecting ducts

78
Q

What is the most common malignant tumor of the kidney ina dults?

A

renal cell carinoma

79
Q

What patient groups get renal cell carcinoma most often?

A

elderly males with hx of smoking

80
Q

What syndrome is renal cell carcinoma associated with?

A

von hippel-lindau syndrome

81
Q

What is the gene that’s bad in von hippel-lindau?

A

on chromsome 3p

the VHL gene is a tumor suppressor gene that encodes a protein that’s part of the ubiquitin ligase compkex, so some proteins that increase transciption and promote angiogenesis are not degraded and you have uncontrolled cel growth

82
Q

What are some other symptoms of VHL besides renal cell carcinoma?

A

hemangioblastomas of the cerebellum and retina

renal cysts

83
Q

What is the most common type of renal cell carcinoma?

A

clear cell carcinoma

84
Q

What is the relationshi between clear cell carcinoma and VHL?

A

clear cell tumors show losses of chromosome 3p

85
Q

What do clear cell caricnomas look like grossly? micro?

A

gross: bright yellow tumor with or without necrosis
micro: solid or cystic growth pattern, polygonal cells with abundant CLEAR cytoplasm and prominent vasculture

86
Q

What kind of renal cell carinoma is NOT associated with 3p losses?

A

papillary carcinoma

87
Q

What will you see microscopically in papillary carcinoma?

A

cuboidal cells with a papillary growth pattern and foam cells within the papillary cores

88
Q

What is the type of renal cell carcinoma where microscopy shows vetegable-like cells with prominent cell membranes?

A

chromophobe carcinoma

89
Q

What blood vessel does renal cell carcinoma tend to invade?

A

tends to invade the renal vein - grows along it and may extend into the heart

90
Q

What is the classic presentation or renal cell carcinoma? Does this happen often?

A

flank pain, palpable mass, hematuria

not really - commonly asymptomatic for a long time and often high grade and metastatic at presentation

91
Q

Paraneoplastic syndromes are common with renal cell carcinoma. What symptoms can you get?

A 
polycthemia
hypercalcemia
hypertenison
hepatic dysfunction
feminization
masculinization
92
Q

Whats the treatment for renal cell carcinoma?

A

no drugs really work, so nephrectomy

93
Q

What type of carcinoma can occur in the renal pelvis?

A

urothelial carcinoma

94
Q

How do urothelial carcinomas present and why better prognosis than renal cell carinoma?

A

present early with hematuria - caught early!

95
Q

What will a urothelial carinoma look like microscopically?

A

like the bladder! transitional epithelium where it shouldn’t be

CRRAB 2 Week 2 (7 decks)

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