Tubulointerstitial Pathology Flashcards

0
Q

What’s a simple way to distinguish between acute interstitial nephritis (AIN) and chronic interstitial nephritis in histology?

A

Acute: inflammation dominates.
Chronic: collagen/fibrosis and tubular atrophy.

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1
Q

Can the tubular epithelial cells be damaged in interstitial nephritis (AIN)?

A

Yes - the presence of inflammation in the interstitium distinguishes it from ATN.

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2
Q

H&E of a AIN caused by drug/toxin?

A

Inflammatory infiltrate with lymphocytes and macrophages in the interstitium (spreading the tubules apart).
Some infiltration of the tubule epithelium can be seen.
But sometimes it’s a PMN/eosinophil/plasma cell pattern.
And sometimes there are giant cells…
(so…. yeah. Inflammation in the interstitium.)

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3
Q

What do you see in the urinalysis of AIN?

A

Sterile pyuria, eosinophils, proteinuria, +/- hematuria.

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4
Q

Clinical presentation of AIN?

A

Fever, rash.
CBC: +/- eosinophilia.
Chem: rise in Cr, metabolic acidosis.

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5
Q

What is a cause of acute papillary necrosis?

What other bad thing can be caused by this same underlying cause?

A

Chronic analgesic abuse.

Can also lead to urothelial carcinoma.

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6
Q

What has hyperuricemia got to do with interstitial nephritis?

A

Uric acid crystals can precipate as tophi in tubules/interstitium -> lots of inflammation.

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7
Q

Anything that causes hypercalciuria can cause Ca++ deposition in the kidney tubules or interstitium… which causes interstitial nephritis.

A

Yeah. HyperPTH, multiple myeloma (via lymphotoxin), Vit D overdose, and bone metastases are some examples.

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8
Q

What functions does nephrocalcinosis impair?

A

Can cause defects in concentrating urine.

Can cause RTA.

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9
Q

Review: 3 types of cause of too much oxalate in urine?

A

Primary (congenital disorder in oxalate handling).
Enteric (fat malabsorption… FFAs chelate Ca++ so it can’t chelate oxalate)
Acute (ethylene glycol, excess consumption of oxalate-containing foods)

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10
Q

What kind of histological changes will ethylene glycol ingestion -> hyperoxaluria produce?

A

“vaculolar changes” (dilated tubular cells) with oxalate crystals.

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11
Q

Pyelonephritis is caused by a bacterial infection.

2 ways that the bacteria get there?

A

Ascending infection - from urine reflux.

Hematogenous.

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12
Q

Acute pyelonephritis in histology?

A

pus everywhere

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13
Q

Common cause of chronic pyelonephritis?

A

Reflux

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14
Q

3 criteria for a diagnosis of chronic pyelonephritis?

A
  1. Irregular scarring.
  2. Chronic inflammation / fibrosis.
  3. Distortion of calcyces.
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15
Q

What can develop if the immune system fails to clear the bugs causing pyelonephritis?

A

Xanthogranulomatous pyelonephritis (akin to TB, bacteria are walled off in granulomas)

16
Q

Chronic reflux / pyelonephritis results in what distinctive pattern of scarring?
(why does this happen?)

A

Polar scarring.
(The papillae at the poles drain multiple collecting ducts… and… the infection seems to prefer compound papillae… (low yield facts))

17
Q

What does end stage chronic tubulointerstitial nephritis look like on histology?

A

There’s so much necrosis/scarring in the tubules that they look like thyroid lacunae -> “thyroidization”.

18
Q

Other than xanthogranulomatous pyelonephritis, what’s a cause of granulomas in the kidney?
(and it’s one that doesn’t have necrosis)

A

Sarcoidosis - involves many systems.

19
Q

What does IgG4-related disease do to the kidney?

A

Dense, whorled fibrosis in multiple organs (kidney, pancreas, gall bladder, lung…)

20
Q

Multiple myeloma causes paraprotein to appear in urine, but can all that protein damage the kidney?

A

Yep. Light chain can precipitate in tubules (casts with fracture lines), and incite matrix deposition.

21
Q

In order of most to least common, causes of AIN?

A

Drugs/toxins.
Pyelonephritis / crystals.
Weird stuff like sarcoidosis, paraprotein.