Difference between revisions of "Medical kidney diseases"

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Medical kidney diseases (view source)

Revision as of 17:40, 4 November 2011

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→‎Transplant: split-out into a separate article
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*Normal.
*Normal.


=Transplant=
=Renal transplant pathology=
===General===
{{Main|Renal transplant pathology}}
Rejection can be:
*Acute.
*Chronic.
*Acute-on-chronic.


====Acute====
*Acute rejection.
*Acute rejection has a standardized classification ''Banff classification''.<ref name=pmid9987096>{{cite journal |author=Racusen LC, Solez K, Colvin RB, ''et al.'' |title=The Banff 97 working classification of renal allograft pathology |journal=Kidney Int. |volume=55 |issue=2 |pages=713–23 |year=1999 |month=February |pmid=9987096 |doi=10.1046/j.1523-1755.1999.00299.x |url=http://www.nature.com/ki/journal/v55/n2/full/4490631a.html}}</ref>
*Chronic rejection.
 
*[[Polyomavirus]].
Diagnosis of acute rejection requires:
*[[Transplant glomerulopathy]].
#Serology.
*Calcineurin-inhibitor toxicity.
#IHC (C4d).
#*This is somewhat debated.
#Morphology.
 
===Predictors===
*Associated with C4d+ IHC.<ref name=pmid1747954>Vascular deposition of complement-split products in kidney allografts with cell-mediated rejection. Feucht HE, Felber E, Gokel MJ, Hillebrand G, Nattermann U, Brockmeyer C, Held E, Riethmüller G, Land W, Albert E. Clin Exp Immunol. 1991 Dec;86(3):464-70. PMID 1747954.</ref>
*Mean graft survival is ~4 years for C4d+ interstitial capillaries vs. ~8 years for C4d- renal grafts.<ref name=pmid11135088>Impact of humoral alloreactivity early after transplantation on the long-term survival of renal allografts. Lederer SR, Kluth-Pepper B, Schneeberger H, Albert E, Land W, Feucht HE. Kidney Int. 2001 Jan;59(1):334-41. PMID 11135088.</ref>
 
===Polyomavirus===
*This bad-boy is associated with failure of transplanted kidneys.<ref name=pmid216990>{{cite journal |author=Mackenzie EF, Poulding JM, Harrison PR, Amer B |title=Human polyoma virus (HPV)--a significant pathogen in renal transplantation |journal=Proc Eur Dial Transplant Assoc |volume=15 |issue= |pages=352–60 |year=1978 |pmid=216990 |doi= |url=}}</ref>
*Treatment: reduce immunosuppression.<ref name=Nickeleit>Nickeleit, Volker; Singh, Harsharan K. Polyomavirus Allograft Nephropathy: Clinico-Pathological Correlations. URL: [http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=eurekah&part=A74503#A74539 http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=eurekah&part=A74503#A74539]. Accessed on: 8 November 2010.</ref>
 
Microscopic features:<ref name=Nickeleit/>
*Ground glass-like nuclear inclusions.
*Nuclear enlargement.
 
===Transplant glomerulopathy===
Microscopic:
*Tram-tracking of basement membrane.
 
DDx (tram-tracking):
*[[MPGN]].
*[[Thrombotic microangiopathy]] (TMA).
 
===Calcineurin-inhibitor toxicity===
*Calcineurin-inhibitors (e.g. cyclosporine,<ref name=pmid10354295>{{cite journal |author=Zarifian A, Meleg-Smith S, O'donovan R, Tesi RJ, Batuman V |title=Cyclosporine-associated thrombotic microangiopathy in renal allografts |journal=Kidney Int. |volume=55 |issue=6 |pages=2457–66 |year=1999 |month=June |pmid=10354295 |doi=10.1046/j.1523-1755.1999.00492.x |url=}}</ref>, tacrolimus<ref name=Ref_FoRP203>{{Ref FoRP|203}}</ref>) toxicity can induce a [[thrombotic microangiopathy]].
*Hyaline arteriopathy with a peripheral and nodular distribution (chronic toxicity).


=See also=
=See also=
Michael
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