Interstitial Nephritis (help with understanding)

[nature88]

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Can someone please explain to me the pathophysiology of interstitial nephritis...

I understand that it's inflammation of the interstitium (tissues surrounding the tubule) rather than the tubule itself. However if that's the case, why do we see increased eosinophils in the urine or increased BUN/Scr since it's not affecting the blood flow or the tubule?

It was explained to me that inflammation starts from things in the capillaries that leak out in interstitial space.Then protein logs clogging up the kidney, causing fluid not able to flow through. The latter part is where I get very confused. Because I see that it's inflammation of the tissues outside of the tubule, so everything should be working fine with the filtering in the tubule.

Thanks!

 

[Morsetlis]

Eos: They extravasate into the lumen.

Interstitial nephritis IS a type of tubulointerstitial nephritis. It DOES damage the tubules, but from within, not from without. Cytokines and granules from the T-cells and WBCs damage the tubular epithelium. The chronic type leads to interstitial fibrosis, scarring, and tubular atrophy. The acute kidney injury involves many causes (ATN, AIN, aGN) but lead to the same conclusion.The chronic pathway involves NFkB and TGF-b.

The unhealthy kidney retains wastes.

While the pathophys of AKI (-->ARF) more closely resembles classic ATN than AIN, the same principles remain:

Normal epithelium --> ischemic/toxic/allergic insult --> Acute inflammation (AIN: +Edema of interstitium +T-Cells +Eos) --> Loss of polarity --> Cell death and sloughing of epithelium --> Luminal obstruction and/or increased permeability --> Migration and dedifferentiation of viable cells --> Proliferation --> Reconstitution or Chronic inflammation.

Management involves withdrawal of offending agent, supportive care, steroid therapy.

http://www.aafp.org/afp/2003/0615/p2527.html
Medscape
Class notes

 

[nature88]

Thank you, Morsetlis, for your explanation!