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Renal > Tubulointerstitial Diseases I/II > Flashcards

Tubulointerstitial Diseases I/II Flashcards

1
Q

What is ATN? How does it present?

A

subset of AKI, representing the worst cases

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2
Q

What are the common causes/types of acute tubular necrosis (ATN)?

A
  1. Ischemic (~75% of ATN cases; usually ischemia is due to shock–esp septic shock)
  2. Nephrotoxins (radio contrast)
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3
Q

What is the gross pathology of ATN?

A
  1. Enlarged (up to 30% larger than normal)
  2. Pale cortex
  3. Congested medulla, especially at cortico-medullary junction
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4
Q

The portions of the renal tubules most vulnerable to acute ischemic necrosis are:
(Why these portions?)

A

(1) Proximal straight tubule and
(2) Ascending thick limb of the loop of Henle

*these are the 2 parts of the tubule in the outer medulla at corticomedullary junction, which is the area that becomes congested in ATN

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5
Q

What are 2 early ischemic change noted in the microscopy pathology of renal tubules?

A
  1. Blebbing of luminal side of cell membranes

2. Diffuse edema of tubular cells (seen as vacuolization of cytoplasm

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6
Q

What 5 microscopic pathologic findings are seen in ATN?

A
  1. loss of brush borders
  2. flattening of epithelium
  3. necrosis & sloughing of epithelial cells
  4. formation of proteinaceous casts
  5. apoptosis
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7
Q

What casts are seen in ATN? Why is finding these casts significant?

A

pigmented, brownish, coarsely granular casts (“muddy brown”)

they can be used to diagnose ATN

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8
Q

The apoptotic renal tubular epithelial cells are most likely have decreased cytoplasmic activity of:

A

BCL2

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9
Q

Vacuolization and calcium oxalate are related to ingestion of what substance?

A

Ethylene glycol

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10
Q

What is the immediate treatment for potassium over 7 mmol/L?

A 
Intravenous calcium gluconate
Intravenous insulin (+ glucose)
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11
Q

What causes the cortical hemorrhages present in ATN?

A

when cells undergo ischemia/necrosis, dead cells of basement membrane slough off into the tubular lumen. This creates an obstruction. This (somehow) leads to hemorrhage, and more cells are damaged by the ROS involved in reperfusion

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12
Q

When is ATN a medical emergency?

A

when K is >7

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13
Q

How is ATN reversible and necrotic simultaneously?

A

ATN is reversible at the level fo the patient, even though the individual cells which are affected die

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14
Q

Gross pathology of acute pyelonephritis?

A

Areas of dark red congestion
Areas of light tan suppurative inflammation
Some necrosis
Some abscesses may form

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15
Q

Microscopic pathology of acute pyelonephritis?

A

Congestion with some mild hemorrhage

Heavy infiltration by leukocytes

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16
Q

Acute pyelonephritis is characteristically abscessing because it produces:

A

Liquefactive necrosis

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17
Q

Microscopic Pathology of Renal Abscesses:

A

severe acute inflammation
necrosis
no liquefaction

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18
Q

Why are renal abscesses so blue under the microscope?

A

Nuclear debris from breakdown of dead cells, especially neutrophils.

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19
Q

What are possible complications of acute pyelonephritis?

A
  1. pyelonephrosis
  2. perinephric abscesses
  3. acute papillary necrosis
  4. healing by scar formation and calyx deformation
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20
Q

Learning gross pathology of kidneys will be most helpful for future

A

radiologists

you never know what bizarre questions he’ll ask

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21
Q

Pyelonephritis can cause

A
  1. necrosis

2. subsequent scarring, which visible on the cortical surface

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22
Q

What are 2 sources of infection causing pyelonephritis? What bacteria is usually responsible?

A

from bladder
blood
E. Coli

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23
Q

Gross Pathology of Chronic Pyelonephritis:

A

scarring, causing depression of cortical surface

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24
Q

Microscopic Pathology of Chronic Pyelonephritis:

A
  1. inflammation (lymphocytes & plasma cells), primarily interstitial
  2. fibrosis
  3. tubules distended (with inspissated urine)
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25
Q

What is the relationship between
acute interstitial nephritis (AIN)
and drug reactions?

A

Drug reactions are a subset/cause of AIN, accounting for 75% of cases of AIN
(note: most drug rxns do not cause AIN)

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26
Q

What are common findings in interstitial nephritis (microscopically?)

A
  1. edema

2. presence of lymphocytes, macrophages, neutrophils and eosinophils

27
Q

What is analgesic nephropathy? What causes it?

A

form of chronic interstitial nephritis which can progress to papillary necrosis

long term combination analgesic use
(usually in elderly females)

28
Q

How does adult polycystic kidney disease affect the kidneys?

A

Slowly expanding cysts compress nml tissue and cause ischemic atrophy, which leads to

  1. ciliopathy
  2. defective mechanosensing of urine flow
  3. dysregulation of cell adhesion
29
Q

Adult Polycystic Kidney Disease is autosomal (dominant/recessive), while the childhood form is autosomal (dominant/recessive).

A

dominant

recessive

30
Q

What mutations are involved in developing AD Polycystic Kidney Disease?

A

mutations in polycystin-1 (85%) or polycystin-2

*note: 2 hit genetics (inherited AD but took a second mutation to form cyst)

31
Q

Where along the nephron do cysts form in AD Polycystic Kidney Disease?

A

anywhere

32
Q

What are common symptoms/characteristics of AD Polycystic Kidney Disease?

A
  1. very enlarged kidneys
  2. flank pain
  3. intermittent gross hematuria
  4. hypertension (75% of pts)
  5. possible cyst formation in liver
  6. cerebral vascular aneurysms (30% pts)

Note: onset around 30 y/o, transplant/dialysis around 50 y/o

33
Q

How does AR Polycystic Kidney Disease affect the kidneys?

A

Numerous small cysts replace normal tissue during fetal life
usually leads to untreatable resp failure at birth due to pulmonary hypoplasia (abn kidneys cannot produce the amniotic fluid needed for lung development)

34
Q

What mutation is involved in developing AR Polycystic Kidney Disease?

A

fibrocystin (which has some unknown function in cilia of tubular epithelial cells)

35
Q

How does AR Nephronophthisis - Medullary

Cystic Disease Complex affect the kidneys?

A
  1. Small kidneys with numerous small cysts at the corticomedullary junction
  2. chronic tubulointerstitial nephritis and fibrosis
    * this is the most common genetic cause of ESRD in kids
36
Q

In Nephronophthisis - Medullary

Cystic Disease Complex, what genes are mutated?

A

9+ genes for cilia components

37
Q

What is Medullary Sponge Kidney?

A

characterized by cysts in the medulla, which are usually benign

38
Q

How do AKI and ATN present?

A
  1. increased creatinine
  2. increased BUN
  3. oliguria or anuria
  4. hyperkalemia
  5. hyponaturemia
  6. nausea, vomiting
  7. bleeding due to platelet dysfunction
39
Q

Renal ischemia usually spared what portion of the nephron?

A

glomeruli

except in cortical necrosis, which is irreversible

40
Q

T/F: The renal medulla is hypoxic under normal circumstances.

A

T

41
Q

Why is vasodilation decreased in post-ischemic arterioles?

A

damaged endothelial cells produce less NO and other vasodil substances

42
Q

Ischemia causes a pro-______ and pro-_____ state.

A

inflammatory

coagulant

43
Q

How does the epithelium further cause damage to ischemic tubules?

A

generate pro-inflmm and chemotactic cytokines (TNF-A, IL1, TGF-B, IL6, IL8, MCP1, RANTES, ENA78)

44
Q

Pyelonephritis is most common in (males/females) up to 1 year of age, (males/females) from 1-50y/o, and (males/females) after the age of 50.

A

males
females
equal in both

45
Q

What is pyelonephrosis?

A

infected pus fills/distends renal calyces, pelvis and ureter

46
Q

What is a perinephric abscess?

A

necrotizing infection that spreads through the renal capsule into the fat surrounding kidney

47
Q

What is the classic triad of drug-induced interstitial nephritis?
What are the other common symptoms?

A

fever, rash, eosinophilia
*eosinophilia is highly specific for this

new-onset azotemia with oliguria
elevated creatinine
urinary eosinophils

48
Q

What is a concurrent mechanism?

A

urine concentration mechanism created by flow of fluid back up a loop with surrounding hyperosmolarity driving water out and not letting it back into urine

49
Q

In pre-renal AKI, the FENa is __% and the urine Na conc is ____.

A

<20

50
Q

In ATN, the FENa is __% and the urine Na conc is ____.

A

> 2%

>40

51
Q

In pre-renal AKI, the urine osmolality is ___; in ATN the urine osmolality is ____.
*Why?

A

> 500 (pre-renal AKI must conserve Na)

~300 (water and Na loss)

52
Q

What part of the nephron is damaged by aminoglycosides, and by what mechanism?

A

PT; drugs remains in the renal cortex’s endosomes and lysosomes, which causes damage after ~1week (once it reaches cytosol)

53
Q

How does contrast affect the kidneys?

A

initially, increases renal blood flow

Prolonged effects:
renal artery vasoconstriction
reduced renal blood flow
shunts blood from medulla to cortex
causes increase in creatinine in 2-3days
54
Q

What appears in the urine in contrast-induced nephropathy?

A

coarse granular casts

renal tubular epithelial cells

55
Q

What drugs cause acute drug-induced interstitial nephritis?

A 
synthetic penicillins
rifampin, cipro
diuretics (thiazides)
NSAIDs
Allopurinol
**occurs ~15d after drug exposure
56
Q

What is the triad of symptoms in acute drug-induced interstitial nephritis? (What are other abnormalities?)

A

rash, fever, eosinophilia

hematuria, proteinuria, leukocyturia, increasing creatinine or acute renal failure

57
Q

4 causes of papillary necrosis:

A

diabetes mellitus
analgesic nephropathy
Sickle-cell
obstruction

58
Q

What abnormalities are present in Aristolochic nephropathy, and what causes this?

A

chronic/extensive interstitial fibrosis and tubular atrophy, mostly in the cortex
(*glomeruli are spared)

Aristolochic acid forms covalent adducts with DNA, which causes vessel wall lesions (and ischemia/fibrosis)

59
Q

Aristolochic nephropathy has a high incidence of:

A

cellular atypia and urothelial (transitional cell) carcinoma in renal pelvis,, ureter and bladder

60
Q

Acute uric acid nephropathy occurs secondary to:

A

lymphoma, leukemia, myeloproliferative disorders, tumor cell lysis syndrome
(overproduction of uric acid, which ppt’s in CD)

61
Q

Chronic uric acid nephropathy is due to:

A

deposition of monosodium urate crystals into the (acidic) DT, CD and interstitium

*causes cortical atrophy and scarring

62
Q

What causes nephrocalcinosis?

A

hypercalcemia-induced kidney stones and calcium deposition in kidneys which may lead to obstructive atrophy of nephrons and secondary interstitial fibrosis and inflammation
(caused by milk-alkali syndrome, vitD intoxication, malignancy, multiple myeloma, hyperparathyroidism)

63
Q

By what mechanism does nephrocalcinosis develop?

A

first: distorts mitochondria in tubular epithelial cells
next: calcium deposits appear within mitochondria, cytoplasm and basement membrane
ultimately: calcified cellular debris causes obstructive nephron atrophy and interstitial fibrosis –> renal failure

64
Q

What causes acute phosphate nephropathy?

A

accumulations of calcium phosphate crystals which precipitates in tubules due to too much oral phosphate solutions (colonoscopy prep)

**renal insufficiency occurs several weeks after exposure, and patients only partial recover

Renal (33 decks)

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