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73 m2. Serum albumin was low at 1.9 gm/dL and she was still severely nephrotic with MRIP UPC ratio ~23 but had no clinical uremia. Subsequently, five years after her initial presentation with us (08/2013) she was started on renal replacement therapy with hemodialysis in the context of a pregnancy, which she accepted only three times a week. She delivered a healthy female infant via C-section at 37 weeks of gestation and her post-operative course remained unremarkable. 3. Discussion The key feature of C1qNP is the presence of dominant or co-dominant staining for C1q component on immunofluorescence exam (1). In our case, both biopsy specimen has been processed in our hospital, using identical processing techniques on frozen tissues. Additionally, the resolution of electron-dense mesangial deposit on electron microscopy coincided with the immunofluorescence findings. Therefore, a variation of the processing technique (2) was unlikely to explain the observed phenomenon. Whether C1qNP is a distinct clinical entity from FSG remains uncertain and debated to some degree. It is usually a rare finding, diagnosed in http://www.selleckchem.com/products/Temsirolimus.html FSG with a generally favorable prognosis in minimal change disease (3,4) but not in others (5,6). The clinical dilemma of this potential overlap has been noted as far back as 1997 (7). Others have pointed out the potential overlay with past diagnosis of ��sero-negative lupus�� and the lack of reliable response to immune-modulating therapy (8). The disease may occur FGFR inhibitor in renal transplant recipients but may be missed if immune-fluorescence exams are not performed routinely. However, in renal transplant recipients, it is usually of no clinical consequences (9). Additionally, in renal transplant recipient, the possibility of C1q NP induction by BK virus nephropathy also has been raised (10). It may be coincidental to an unrelated process, such as diabetic nephropathy (11). Ideal treatment is not well defined and spontaneous improvement have been also observed (12). In a small pediatric cohort, disappearance of C1q deposit and emergence of focal sclerosis have already been documented after immunosuppressive therapy (prednisone, cyclosporine-A) (4,13). However, in another report of a single pediatric patient, the clinical improvement correlated with cessation of C1q deposition (14). Anecdotal evidence suggest efficacy of rituxamab (Rituxan?; monoclonal anti- CD 20 monoclonal antibody) in achieving remission in otherwise therapy-unresponsive cases (15). This case probes a very interesting clinical concept, i.e., whether biopsy-proven renal histological diagnoses remain stable over time.