Objective: Renal Cell Carcinomas include about 2-3 % of adults neoplasms and 90-95 % of all renal tumors. In many cases, it is possible to distinguish. RCC subtypes on the basis of hematoxylin-eosin staining alone. However, overlapping morphologic features pose some difficulties in making a proper diagnosis. To render an accurate diagnosis, additional methods like immunohistochemichal staining against C-Kit have been recommended. Method: We reviewed 65 cases of RCC diagnosed during 9 years. Formalin fixed, paraffin embedded specimens was available in 65 cases. The expression of C-kit was evaluated using immunohitochemistry. Results: Six cases of 39 clear cell type (15.4 %), 8 of 13 papillary type (61.5 %), and 11 of 11 chromophobe type (100 %) were positive for C-kit that considering Chi-Square test there is significant relevation between RCC's subtypes and C-Kit expression (P: 0.001). From 8 cases with renal vein invasion, 3 showed positive expression of C-Kit (37.5 %) and in 55 cases with no venous invasion, C-kit expression was detected in 22 (38.6), so no significant relation was found between renal vein invasion and C-kit expression. Conclusion: The expression of C-Kit in RCC may have diagnostic significance. Objective: IgG4-RSD shows abundant IgG4-positive plasma cells, diffuse fibrosis, and increased serum IgG4 levels. Although IgG4-RSD typically results in autoimmune pancreatitis (AIP), any organ may be involved. Thus, IgG4-RSD TIN often goes unrecognized in the absence of AIP. This is an IgG4-RSD TIN case with mediastinal lymph node and pulmonary involvement. Method: A 73-year-old male presented with rapidly progressive renal failure, hypergammaglobulinemia, hypocomplementemia, and enlarged mediastinal lymph nodes and bilateral pulmonary nodules on CT. Renal and mediastinal lymph node biopsies were performed and IgG4 IHC was done on both after standard techniques. Results: The renal cortex and medulla showed diffuse interstitial fibrosis with tubular atrophy and abundant plasma cells (25 IgG4-positive cells/HPF), numerous lymphocytes and some eosinophils. IF showed IgG, C3, kappa, and lambda granular deposits in tubular basal membranes and Bowmann capsules. Lymph node follicular and paracortical hyperplasia with abundance of mostly IgG4positive plasma cells was seen. An IgG4-RSD diagnosis was rendered and high serum IgG4 levels were demonstrated. Steroid therapy resulted in lymph node and lung nodule reduction. Conclusion: TIN with abundant plasma cells and diffuse interstitial fibrosis, especially if accompanied by hypergammaglobulinemia, hypocomplementemia, or extrarenal involvement, should suggest IgG4-RSD and prompt serum IgG4 level determination and renal IgG4 IHC. Objective: A 39-year-old woman was admitted for chronic renal failure. Clinical examination was normal. Biological explorations showed creatinin clearance around 55 ml/min, tubular proteinuria with Bence Jones κ protein. Serum immunoelectrophoresis identified abnormal monoclonal immunoglobulin G and κ-light chains (LC). Bone marrow histology was normal. Method: Kidney biopsy revealed diffuse intracytoplasmic vacuoles in the proximal tubules resembling osmotic nephrosis. Distal tubules, glomeruli, vessels and interstitial compartment were normal. Immunofluorescence (including anti-κ and -λ staining) was negative. Electronic microscopy (EM) revealed intracytoplasmic immunoglobulinic crystals containing κ LC inside the vacuoles, leading to the diagnosis of Light Chain Proximal Tubulopathy (LCPT). Results: LCPT is a rare complication of dysglobulinemia. It may be associated with crystals within the cytoplasm of proximal, less frequently distal, tubular cells, consisting more frequently in κ LC. Rarely, diffuse tubular vacuolization is present, often indistinguishable from osmotic nephrosis. In our case, there was no proximal tubular dysfunction and immunofluorescence was negative. The first evocated diagnosis by light microscopy was "osmotic nephrosis". However, we failed to identify any causal factor. Finally, the diagnosis was performed by immunoEM. Conclusion: In conclusion, before a picture of osmotic nephrosis without obvious cause, EM and immunoEM may be helpful for the diagnosis of LCPT, often revealing a dysglobulinemia.