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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
Which drugs cause acute drug induced TIN?
synthetic penicillins, rifampin, thiazides, phenylbutazone, cimetidine
26
Describe the pathophysiology of acute drug induced TIN?
possibly a delayed (type IV) hypersensitivity reaction, due to hapten like effect of drug, which binds to tubular epithelium, making it immunogenic
27
What is the treatment for acute drug induced TIN?
stop taking offending drug
28
Describe the micro anatomy of acute drug induced TIN?
edematous interstitium containing abundant eosinophils and neutrophils, lymphocytes, macrophage
29
What is analgesic abuse nephropathy?
Chronic renal disease due to excessive intake of analgesics
30
What causes analgesic abuse nephropathy?
Due to phenacetin plus aspirin, caffeine, acetaminophen, codeine
31
What is the epidemiology of analgesic abuse nephropathy?
80% women
32
Consequences of analgesic abuse nephropathy?
Cannot concentrate urine, renal stones, anaemia due to RBC damage from phenacetin metabolites
33
What is the long term risk of analgesic abuse nephropathy?
papillary urothelial carcinoma of renal pelvis - important cause of papillary necrosis & sloughing
34
State causes of papillary necrosis?
1. analgesic abuse nephropathy 2. diabetes mellitus 3. obstruction 4. sickle cell disease
35
What is acute pyelonephritis?
Acute suppurative (pus forming) infection of kidney collecting system
36
What are the causes of acute pyelonephritis?
urinary tract infection (UTI), obstruction, instrumentation, vesicoureteral reflux, pregnancy
37
Describe the epidemiology of acute pyelonephritis?
common in women, usually ages 1-40
38
Acute pyelonephritis is associated with?
diabetes or immunocompromised
39
What is a bacterial urinary tract infection?
due to colonization of distal urethra and introitus by coliform bacteria plus upward spread via instrumentation or catheterization
40
UTIs are most common among?
women
41
Why are UTIs most common in women?
short urethra, no anti-bacterial prostatic fluid, hormonal changes, sex-related trauma
42
How does bacteria in a UTI spread?
1. Ascending route most common | 2. hematogenous spread of bacteria to kidney
43
What is vesicoureteral reflux?
a condition in which urine flows backward from the bladder to one or both ureters an sometimes to the kidneys
44
What causes vesicoureteral reflux?
1. short intravesical ureter | 2. spinal cord injuries
45
What are the signs and symptoms of vesicoureteral reflux?
1. sudden onset of costovertebral angle pain, | 2. symptoms of systemic infection or urinary tract infection, pyuria, WBC casts
46
What is the treatment for the signs and symptoms of vesicoureteral relux?
antibiotics usually cause symptoms to disappear in a few days
47
Persistent bacteriuria as a symptom of vesicoureteral reflux is associated with?
obstruction, diabetes, immunocompromised
48
What are the complications of acute pyelonephritis?
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
Gross morphology of acute pyelonephritis?
focal abscesses or wedge-shaped areas of suppuration
50
Micro morphology of acute pyelonehritis?
patchy suppurative inflammation, primarily cortical, with edema, neutrophils in interstitium and tubular lumina, and tubular necrosis
51
What does chronic pyelonephritis cause?
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
Pathogenesis of chronic pyelonephritis?
- 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
What is the clinical course of chronic pyelonephritis?
1. often insidious 2. acute recurrent pyelonephritis - back or loin pain, fever, frequent bacteriuria and/or pyuria 3. hypertension
54
Describe obstructive uropathy?
- Increases susceptibility to infection | - chronic obstruction causes hydronephrosis
55
What are the congenital causes of obstructive uropathy?
urethral strictures, meatal stenosis, bladder neck obstruction, ureteropelvic junction narrowing, vesicoureteral reflux
56
What are the causes of acquired obstructive uropathy?
stones, prostatic hypertrophy, tumors, inflammation, sloughed papillae or blood clots, normal pregnancy, uterine prolapse or cystocele, neurogenic ureter/bladder
57
What is the main symptom of obstructive uropathy?
pain - due to distention of collecting system or renal capsule
58
What is hydronephrosis?
cystic dilation of renal pelvis and calyces associated with progressive atrophy of kidney due to obstructive uropathy
59
Gross morphology of hydronephrosis?
calyceal dilation | cortical rim thins out due to atrophy
60
Micro morphology of hydronephrosis?
interstitial inflammatory infiltrate; cortical atrophy, diffuse interstitial fibrosis, blunting of calyces
61
What are urothiasis (stones)?
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
Describe the different types of kidney stones?
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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