Authors’ reply

Sir,

We have read the comments[1] offered on our article. We agree completely that collapsing glomerulopathy (CG) may finally be accepted as a distinct entity with no relation to focal and segmental glomerulosclerosis (FSGS). We would like to clarify that the global sclerosis in the article refers to obsolescent glomeruli and not to global collapse. We did not observe global collapse in any of our cases. Systemic lupus erythematosus was excluded on the basis of clinical and serological features in the case with immune complex deposition.

We agree that a short follow-up period may be an additional factor for the favorable outcome in our study. However, a study by Stokes et al.[2] showed high frequency of graft failure within 3–4 months of diagnosis of CG. In comparison to these results, our patients had a favorable outcome.

It is somewhat difficult to clearly outline the etiologic factors of CG in our cases. Vascular lesions definitely play a role in the pathogenesis of CG by causing ischemia and glomerular collapse, as has been described in native kidneys as well. Other factors such as viral infections and drug toxicities may also be involved.

Although serum creatinine in 5 cases (cases 2, 3, 6, 7, 8) was less than 2.0 mg/dL, there was a significant rise from the baseline creatinine value. Proteinuria we agree is moderate to severe.

We thank the authors for pointing out the discrepancies in numbers at certain places and regret the typographical errors. The correct duration is of post-transplant duration and follow-up are 12–98 and 3–12 months, respectively. The follow-up creatinine values ranged between 1.4 and 2.1 mg/dL.