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Renal Pathology > Tubulo-Interstitial Diseases > Flashcards

Tubulo-Interstitial Diseases Flashcards

1
Q

What are the 2 broad groups of conditions?

A
  1. Acute tubular necrosis
    • ischaemic or toxic necrosis of tubular cells
  2. Tubulointerstitial nephritis
    - more commonly just “interstitial” nephritis
    - inflammatory reactions involving the tubules and/or interstitium
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2
Q

What does acute tubular necrosis cause?

A

acute renal failure

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3
Q

What is acute tubular necrosis characterized by?

A
  • characterized by acute destruction of tubular
    epithelial cells
  • most commonly secondary to ischaemia, but
    can also be due to direct toxic cell damage
  • potentially reversible, since tubular cells can
    regenerate given time
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4
Q

Acute tubular necrosis due to ischemia is caused by?

A
  1. “shock” (rapid uncompensated fall in systemic BP)
    e. g. in trauma, burns, falciparum malaria, pancreatitis, sepsis, DIC, blood transfusion reactions etc OR
    2) reduction in intrarenal blood flow (RPGN, acute interstitial nephritis, urinary obstruction)
    - remember, tubular blood flow is from post-glomerular capillary bed - and tubules are metabolically very active, thus susceptible to ischaemia
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5
Q

Which heavy metals cause cause ATN?

A

Pb, Au, As, Cr etc

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6
Q

Which organic solvents cause ATN?

A

CCl4, chloroform

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7
Q

Which drugs cause ATN?

A

antibiotics (espec gentamicin), anti-viral agents, NSAIDs, mercurial diuretics

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8
Q

Name toxins that cause ATN?

A
  1. iodinated contrast agents used for X rays
  2. pesticides
  3. glycols – ethylene glycol (“antifreeze”)
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9
Q

Describe the macro morphology of ATN?

A

Pale swollen edematous kidney, blurred cortico-medullary junction

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10
Q

Describe the micro anatomy of ATN?

A
  1. focal tubular epithelial necrosis and apoptosis
  2. basement membrane rupture
  3. interstitial edema
  4. epithelial regeneration
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11
Q

Distribution of tubular damage depends on?

A

cause

  1. ischaemic type - any part of nephron
  2. toxic type - only proximal tubules
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12
Q

Why does distribution of tubular damage depend on cause?

A
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13
Q

What are the effects of ATn?

A
  1. initial (~ 36 hrs) (usually missed) – slight increase in urine output and rise in serum urea
  2. oliguric – urine output 400 ml or less/day, so water, Na+ and K+ retention, rising urea, metabolic acidosis – danger of pulmonary oedema & cardiac dysrhythmias
  3. diuretic – urine output above normal, so loss of water, Na+ & K+ – danger of dehydration
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14
Q

What are the effects of ATn?

A
  1. initial (~ 36 hrs) (usually missed) – slight increase in urine output and rise in serum urea
  2. oliguric – urine output 400 ml or less/day, so water, Na+ and K+ retention, rising urea, metabolic acidosis – danger of pulmonary oedema & cardiac dysrhythmias
  3. diuretic – urine output above normal, so loss of water, Na+ & K+ – danger of dehydration
    - complete recovery possible
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15
Q

Describe the pathogenesis of the 3 phases ATN?

A

initial – tubular cells begin to lose concentrating ability
oliguric – tubular epithelium lost, and so is reabsorption of most of glomerular filtrate
diuretic – regenerating epithelium does prevent much reabsorption, but can’t yet concentrate
- once concentrating ability restored, complete return to normal

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16
Q

What is renal cortical necrosis?

A

the destruction of cortical tissue resulting from renal arteriolar injury and leading to chronic kidney disease

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17
Q

What are the causes of renal cortical necrosis?

A
  • A severe effect of shock on the kidneys than ATN produces

- also caused by rapid uncompensated fall in systemic BP (“shock”)

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18
Q

Describe the pathogenesis of renal cortical necrosis?

A

hypotension is so severe that renal blood flow is diverted into medullary vasa recta away from cortex

  • whole cortex becomes infarcted
  • irreversible
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19
Q

What is tubulointerstitial nephritis?

A

inflammation that affects the tubules of the kidneys and the tissues surrounding them (interstitial tissue)
- this disorder may be caused by diseases, drugs and toxins that damage the kidneys

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20
Q

Describe primary tubulointerstitial nephritis?

A

lacks significant glomerular or vascular injury

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21
Q

Describe secondary tubulointerstitial nephritis?

A

due to glomerular disease, systemic or vascular disorders

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22
Q

Describe acute tubulointerstitial nephritis?

A

interstitial edema, neutrophils, focal tubular necrosis

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23
Q

Describe chronic tubulointerstitial nephritis?

A

mononuclear inflammation, interstitial fibrosis, tubular atrophy

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24
Q

Describe symptoms of acute drug induced TIN?

A
  1. Onset 15 days after exposure (not dose related)

2. Rash, fever, eosinophilia, hematuria, mild proteinuria; 50% have rising creatinine or acute renal failure

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25
Q

Which drugs cause acute drug induced TIN?

A

synthetic penicillins, rifampin, thiazides, phenylbutazone, cimetidine

26
Q

Describe the pathophysiology of acute drug induced TIN?

A

possibly a delayed (type IV) hypersensitivity reaction, due to hapten like effect of drug, which binds to tubular epithelium, making it immunogenic

27
Q

What is the treatment for acute drug induced TIN?

A

stop taking offending drug

28
Q

Describe the micro anatomy of acute drug induced TIN?

A

edematous interstitium containing abundant eosinophils and neutrophils, lymphocytes, macrophage

29
Q

What is analgesic abuse nephropathy?

A

Chronic renal disease due to excessive intake of analgesics

30
Q

What causes analgesic abuse nephropathy?

A

Due to phenacetin plus aspirin, caffeine, acetaminophen, codeine

31
Q

What is the epidemiology of analgesic abuse nephropathy?

A

80% women

32
Q

Consequences of analgesic abuse nephropathy?

A

Cannot concentrate urine, renal stones, anaemia due to RBC damage from phenacetin metabolites

33
Q

What is the long term risk of analgesic abuse nephropathy?

A

papillary urothelial carcinoma of renal pelvis
- important cause of papillary necrosis &
sloughing

34
Q

State causes of papillary necrosis?

A
  1. analgesic abuse nephropathy
  2. diabetes mellitus
  3. obstruction
  4. sickle cell disease
35
Q

What is acute pyelonephritis?

A

Acute suppurative (pus forming) infection of kidney collecting system

36
Q

What are the causes of acute pyelonephritis?

A

urinary tract infection (UTI), obstruction, instrumentation, vesicoureteral reflux, pregnancy

37
Q

Describe the epidemiology of acute pyelonephritis?

A

common in women, usually ages 1-40

38
Q

Acute pyelonephritis is associated with?

A

diabetes or immunocompromised

39
Q

What is a bacterial urinary tract infection?

A

due to colonization of distal urethra and introitus by coliform bacteria plus upward spread via instrumentation or catheterization

40
Q

UTIs are most common among?

A

women

41
Q

Why are UTIs most common in women?

A

short urethra, no anti-bacterial prostatic fluid, hormonal changes, sex-related trauma

42
Q

How does bacteria in a UTI spread?

A
  1. Ascending route most common

2. hematogenous spread of bacteria to kidney

43
Q

What is vesicoureteral reflux?

A

a condition in which urine flows backward from the bladder to one or both ureters an sometimes to the kidneys

44
Q

What causes vesicoureteral reflux?

A
  1. short intravesical ureter

2. spinal cord injuries

45
Q

What are the signs and symptoms of vesicoureteral reflux?

A
  1. sudden onset of costovertebral angle pain,

2. symptoms of systemic infection or urinary tract infection, pyuria, WBC casts

46
Q

What is the treatment for the signs and symptoms of vesicoureteral relux?

A

antibiotics usually cause symptoms to disappear in a few days

47
Q

Persistent bacteriuria as a symptom of vesicoureteral reflux is associated with?

A

obstruction, diabetes, immunocompromised

48
Q

What are the complications of acute pyelonephritis?

A
  1. Papillary necrosis: more common in diabetes and urinary tract obstruction
  2. Pyonephrosis: total or almost complete obstruction prevents drainage of pus
  3. Perinephric abscess: extension of pus through the renal capsule into adjacent tissue
49
Q

Gross morphology of acute pyelonephritis?

A

focal abscesses or wedge-shaped areas of suppuration

50
Q

Micro morphology of acute pyelonehritis?

A

patchy suppurative inflammation, primarily cortical, with edema, neutrophils in interstitium and tubular lumina, and tubular necrosis

51
Q

What does chronic pyelonephritis cause?

A
  1. end stage kidney/chronic renal failure
  2. renal cause of secondary hypertension
  3. association with vesicoureteral reflux
    - due to “incompetent vesicoureteral valve”
    - aka “short intravesical ureter”
52
Q

Pathogenesis of chronic pyelonephritis?

A
  • urine refluxes into ureter during micturition
  • but reflux into renal parenchyma essential for pyelonephritis to develop
  • structure of papillae at renal poles (“refluxing papillae”) promotes this – so chronic pyelonephritis is common at the poles
53
Q

What is the clinical course of chronic pyelonephritis?

A
  1. often insidious
  2. acute recurrent pyelonephritis
    - back or loin pain, fever, frequent bacteriuria and/or pyuria
  3. hypertension
54
Q

Describe obstructive uropathy?

A
  • Increases susceptibility to infection

- chronic obstruction causes hydronephrosis

55
Q

What are the congenital causes of obstructive uropathy?

A

urethral strictures, meatal stenosis, bladder neck obstruction, ureteropelvic junction narrowing, vesicoureteral reflux

56
Q

What are the causes of acquired obstructive uropathy?

A

stones, prostatic hypertrophy, tumors, inflammation, sloughed papillae or blood clots, normal pregnancy, uterine prolapse or cystocele, neurogenic ureter/bladder

57
Q

What is the main symptom of obstructive uropathy?

A

pain - due to distention of collecting system or renal capsule

58
Q

What is hydronephrosis?

A

cystic dilation of renal pelvis and calyces associated with progressive atrophy of kidney due to obstructive uropathy

59
Q

Gross morphology of hydronephrosis?

A

calyceal dilation

cortical rim thins out due to atrophy

60
Q

Micro morphology of hydronephrosis?

A

interstitial inflammatory infiltrate;
cortical atrophy,
diffuse interstitial fibrosis,
blunting of calyces

61
Q

What are urothiasis (stones)?

A

Due to supersaturation of stone constituents, decreased urine volume or deficiency of crystal inhibitors in urine
80% unilateral, usually in calyces, pelvis, bladder
- 5-10% of Americans, men age 20-30 most common

62
Q

Describe the different types of kidney stones?

A
  1. Calcium oxalate/phosphate (75%): due to hypercalciuria, hypercalcemia, hyperoxaluria (in vegetarians with oxalate rich diet)
  2. Struvite (triple stones, magnesium ammonium phosphate, 15%): due to urea-splitting bacteria (Proteus, Staphylococcus); produce staghorn calculi
  3. Uric acid (6%): due to hyperuricemia, chemotherapy for leukemia

Renal Pathology (3 decks)

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