Biopsy ; methods ; Glomerulonephritis, IGA ; pathology ; Humans ; Kidney ; pathology ; Kidney Diseases ; pathology ; Lupus Nephritis ; pathology

Carcinoma, Renal Cell ; classification ; genetics ; pathology ; Humans ; Kidney Neoplasms ; classification ; genetics ; pathology ; World Health Organization

Biopsy, Needle ; methods ; China ; Humans ; Kidney ; pathology ; Kidney Diseases ; pathology ; Kidney Neoplasms ; pathology ; Specimen Handling

Animals ; Biopsy ; Disease Models, Animal ; Fluorescent Antibody Technique ; Glomerulonephritis, Membranoproliferative ; pathology ; Humans ; Kidney ; pathology ; Kidney Diseases ; pathology ; Plastic Embedding

Humans ; Immunoglobulin Light Chains ; genetics ; immunology ; Immunoglobulin kappa-Chains ; genetics ; immunology ; Kidney ; immunology ; metabolism ; pathology ; Kidney Diseases ; immunology ; pathology ; therapy ; Mutation ; Transforming Growth Factor beta ; metabolism

OBJECTIVETo observe the transdifferentiation of renal tubular epithelial cells in tubulointerstitial fibrosis.

METHODSThe renal tubulointerstitial fibrosis model in Wistar rats was established by unilateral renal vein ligature. The rats were kept 25 days after renal vein ligature. The kidneys were dissected every 5 days by killing 5 rats. The morphological changes of the kidney were observed by light microscopy, electron microscopy, polarizing microscopy and immunohistochemistry method.

RESULTSThe histological changes showed tubular atrophy and disappearance, widening of intertubular spaces with increased lymphocytes and mononuclear cells infiltration and fibrosis. The CK marker in injured and atrophic epithelial cells gradually weakened, but the alpha-SMA, vimentin, TGF-beta(1), collagen I and III showed gradually stronger positivity for immunohistochemistry. Some interstitial cells became positive for CK. Electron microscopy revealed decreased mitochondria, increased endoplasmic reticulum and microfilament of the tubular epithelial cells which merged into the interstitium. During the early stage of tubulointerstitial fibrosis, there was proliferation of type III collagen and then followed by type I collagen at later stage when observing the Sirius Red stained sections under the polarizing microscope.

CONCLUSIONTubular epithelial cells can transdifferentiate to fibroblasts during the process of tubulointerstitial fibrosis.

Actins ; analysis ; Animals ; Cell Differentiation ; Collagen ; analysis ; Epithelial Cells ; cytology ; Fibrosis ; Immunohistochemistry ; Keratins ; analysis ; Kidney Tubules ; chemistry ; pathology ; ultrastructure ; Male ; Rats ; Rats, Wistar

Aged ; Diagnosis, Differential ; Fibronectins ; metabolism ; Glomerulonephritis, Membranoproliferative ; pathology ; Humans ; Immunohistochemistry ; Kidney Diseases ; metabolism ; pathology ; Kidney Glomerulus ; metabolism ; pathology ; ultrastructure ; Male ; Microscopy, Electron

Aristolochic Acids ; adverse effects ; Child ; Drugs, Chinese Herbal ; adverse effects ; Female ; Humans ; Male ; Nephrosis ; chemically induced

Adult ; Biopsy, Needle ; Diagnosis, Differential ; Humans ; Kidney ; pathology ; Kidney Diseases ; pathology ; therapy ; Male ; Nephritis, Interstitial ; pathology ; Renal Dialysis ; Sarcoidosis ; pathology ; therapy ; Tuberculosis, Renal ; pathology

OBJECTIVETo study the clinicopathologic features of membranous nephropathy coexisting with IgA nephropathy.

METHODSThe renal biopsies performed in Peking University First Hospital during the period from January, 1998 to April, 2006 were retrospectively reviewed. The clinicopathologic features of 11 cases of membranous nephropathy coexisting with IgA nephropathy were studied. Electron microscopy with immunogold labeling for IgG and IgA were also performed.

RESULTSThe mean age of patients was 39.9 years. The male-to-female ratio was 1:2.9. The patients mainly presented with proteinuria. Proteinuria of nephrotic level was seen in 7 cases (63.6%). Seven cases also had associated microscopic hematuria. None of them showed evidence of renal insufficiency. Cases with secondary diseases, such as hepatitis virus infection and systemic lupus erythematosus, were excluded from the study. Histologically, vacuolation and thickening of glomerular basement membrane was seen. There was also mild mesangial hypercellularity and increase in mesangial matrix. Occasional glomeruli with crescent formation were identified in 2 cases. Immunofluorescence study showed granular staining for IgG and C3 along glomerular capillary walls, in addition to clumps of IgA deposits in mesangium. Electron microscopy revealed subepithelial and mesangial electron-dense deposits. Immunogold labeling showed IgG and IgA localized in the subepithelial and mesangial deposits respectively.

CONCLUSIONMembranous nephropathy coexisting with IgA nephropathy possesses the clinicopathologic features of both components. It might be caused by independent occurrence of the two entities.

Adult ; Female ; Glomerular Basement Membrane ; immunology ; pathology ; ultrastructure ; Glomerular Mesangium ; immunology ; pathology ; ultrastructure ; Glomerulonephritis, IGA ; complications ; immunology ; pathology ; Glomerulonephritis, Membranous ; complications ; immunology ; pathology ; Humans ; Immunoglobulin A ; metabolism ; Immunoglobulin G ; metabolism ; Kidney Glomerulus ; immunology ; pathology ; ultrastructure ; Male ; Middle Aged ; Retrospective Studies