Tubulointerstitial Pathology Flashcards
What’s a simple way to distinguish between acute interstitial nephritis (AIN) and chronic interstitial nephritis in histology?
Acute: inflammation dominates.
Chronic: collagen/fibrosis and tubular atrophy.
Can the tubular epithelial cells be damaged in interstitial nephritis (AIN)?
Yes - the presence of inflammation in the interstitium distinguishes it from ATN.
H&E of a AIN caused by drug/toxin?
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.)
What do you see in the urinalysis of AIN?
Sterile pyuria, eosinophils, proteinuria, +/- hematuria.
Clinical presentation of AIN?
Fever, rash.
CBC: +/- eosinophilia.
Chem: rise in Cr, metabolic acidosis.
What is a cause of acute papillary necrosis?
What other bad thing can be caused by this same underlying cause?
Chronic analgesic abuse.
Can also lead to urothelial carcinoma.
What has hyperuricemia got to do with interstitial nephritis?
Uric acid crystals can precipate as tophi in tubules/interstitium -> lots of inflammation.
Anything that causes hypercalciuria can cause Ca++ deposition in the kidney tubules or interstitium… which causes interstitial nephritis.
Yeah. HyperPTH, multiple myeloma (via lymphotoxin), Vit D overdose, and bone metastases are some examples.
What functions does nephrocalcinosis impair?
Can cause defects in concentrating urine.
Can cause RTA.
Review: 3 types of cause of too much oxalate in urine?
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)
What kind of histological changes will ethylene glycol ingestion -> hyperoxaluria produce?
“vaculolar changes” (dilated tubular cells) with oxalate crystals.
Pyelonephritis is caused by a bacterial infection.
2 ways that the bacteria get there?
Ascending infection - from urine reflux.
Hematogenous.
Acute pyelonephritis in histology?
pus everywhere
Common cause of chronic pyelonephritis?
Reflux
3 criteria for a diagnosis of chronic pyelonephritis?
- Irregular scarring.
- Chronic inflammation / fibrosis.
- Distortion of calcyces.
What can develop if the immune system fails to clear the bugs causing pyelonephritis?
Xanthogranulomatous pyelonephritis (akin to TB, bacteria are walled off in granulomas)
Chronic reflux / pyelonephritis results in what distinctive pattern of scarring?
(why does this happen?)
Polar scarring.
(The papillae at the poles drain multiple collecting ducts… and… the infection seems to prefer compound papillae… (low yield facts))
What does end stage chronic tubulointerstitial nephritis look like on histology?
There’s so much necrosis/scarring in the tubules that they look like thyroid lacunae -> “thyroidization”.
Other than xanthogranulomatous pyelonephritis, what’s a cause of granulomas in the kidney?
(and it’s one that doesn’t have necrosis)
Sarcoidosis - involves many systems.
What does IgG4-related disease do to the kidney?
Dense, whorled fibrosis in multiple organs (kidney, pancreas, gall bladder, lung…)
Multiple myeloma causes paraprotein to appear in urine, but can all that protein damage the kidney?
Yep. Light chain can precipitate in tubules (casts with fracture lines), and incite matrix deposition.
In order of most to least common, causes of AIN?
Drugs/toxins.
Pyelonephritis / crystals.
Weird stuff like sarcoidosis, paraprotein.
