My opinion is that we should have always in mind dr Robert Colvin studies and the need to differentiate several conditions. Indeed Tx glomerulopathy may be a useful term to hid our unability to rtecognize the true condition.

a) CNI nephrotoxicity?

b) Hypertension related damage?

c) Viral (BKV) disease?

d) True chronic rejection?

e) Other?

thank you very much for your contributions

Are you able to provide any other information on the cases? This may assist with some of us then being able to provide you with additional information. For example age of recipients, time point post transplantation that the glomerulopathy was diagnosed, any other associated clinical  signs or laboratory findings and outcomes of any treatments administered.

thank you very much for your interest.

A 49 years old female patient with primary renal disease was polycystic kidney disease. she received a two matched cadaveric kidney from a 40 years old female donor 8 years ago. Her PRA class I & II titers were negative before transplantation. The first six years period was uneventful with SCr:1.0mg/dl and a maintenance therapy of 5 mg/d prednisolone , 360 mg /d mycophenolate sodium  and 1 mg /d tacrolimus. Tacrolimus level was 3-5 ng/mL the last 2 years peroid.  Serum creatinine was gradually increased the last 1,5 years peroid (from 1 to 1.6 mg/dL). Proteinuria was increased from 0,4 gram/day to 2,3 gram/day the last 1 year period.  Her   urinary findings were nonspesific. In the sixth year of transplant, serum creatinin was 2,3 mg/dL and proteinuria 2,3 gram/day. Renal biopsy was demonstrated C4d and IF (5 glomerul) negative,  mild chronic changes as IFTA (10-15%) and glomerulosclerosis (10%), arteriolar hyalinosis (ah1) and arterial intimal fibrosis (cv1), segmental sclerosis (10%),   all non-sclerotic glomeruli (30 glomerul) were  extensive duplication of GBM, increased MM.  PRA Class I was positive (6%, DSA negative) and II was negative.

Maybe this presentation may be useful

Thank you very much for your answer 

Have you tested for presence of nonHLA antibodies? 

Thank you very much 

But nonHLA antibodies have never been tested.

Difficult management problem. Not sure that there is any evidence for altering this patients immunosuppressive medications allowing for the fact that the biopsy findings also has elements of chronic change.

Thank you very much for your answer

Agree with previous opinions, not sure if increasing immunosupression will be of any benefit. Try to rescue the remaining viable tissue and buy some time before it fails. Would suggest keeping TACROLIMUS blood level around 5, rule out BKV associated nephropathy " although it is less likely giving the remote time of transplant and the low level of Tacrolimus in blood, follow renal diet " Salt and Protein restriction". Would starting counseling for re-transplant. One last option would be a single run of steroid pulse " if no other contraindication" - won't hurt.

Do you have any information about g and ptc scores?

thank you very much for your question

g:0 and ptc:1

Therefore, signs of immunologic activity/inflammation are limited. I agree with previous comments that there is little argument to increase immunosuppression.

Trasplante glomerulopathy is an histologic form of AbMR. The main target is the endothelial cell. This is the reason that explain its similarities with MAT. The prognistic is to bad and the gaft is losting in 90%. The close relationship with TMA approach to similar treatment with blocking the Complemet cascade.

Thank you  very much för your comment   but cost is too important problem för complemet cascade inh. treatment. 

Yes, it's allrigth But the another treatment way should be plasma replacement to block the circulantes Abs....,and it's also expensive...

His kidney function was excellent  for the first 6 years

Is there a possibility that he stopped his medication or that his medication was precipitously reduced 1.5 years ago?

thank you very much for your answer.

Apologize for my late respond

this patient is health care workers

so his medication was stopped by herself.

but we reduced gradually her drug dossage  because of  recurrent lung infection disease.