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

OBJECTIVETo study the clinicopathologic features of collagen III glomerulopathy and its cause, pathogenesis and prognosis.

METHODSFive cases of collagen III glomerulopathy that collected from 2005 to 2014 were observed by renal biopsy. The morphologic characteristics were studied by light microscopy, immunofluorescence, immunohistochemical and electron microscopy.

RESULTSThe glomerular mesangium became expansion but no hypercellularity, basement membrane appeared thickened. The glomeruli showed collagen type III deposit by immunohistochemistry method, and collagen fibers increased by electron microscopy. The patients often show serious proteinuria, nephrotic syndrome and renal function damage.

CONCLUSIONSCollagen III glomerulopathy is an idiopathic glomerular disease, characterized by massive accumulation of collagen type III within the glomerular mesangial areas and basement membrane. Collagen III glomerulopathy is extremely rare. The etiology and pathogenesis may relate to the abnormality of collagen III gene. There is no specific treatment for it and its prognosis is poor.

Basement Membrane ; metabolism ; Biopsy ; Collagen Type III ; genetics ; metabolism ; Female ; Fluorescent Antibody Technique ; Glomerular Mesangium ; metabolism ; Humans ; Immunohistochemistry ; Kidney Diseases ; etiology ; pathology ; Kidney Glomerulus ; pathology ; Microscopy, Electron ; Prognosis ; Proteinuria ; diagnosis

In this paper, 2 cases of collagen Type Ⅲ glomerulopathy were analyzed. The clinical manifestations mainly included nephrotic syndrome, proteinuria, hypertension and renal dysfunction. One patient showed that the complement factor H-related protein 5 (CFHR5) gene was likely a disease-causing mutation. The pathological examination of renal tissues showed hyperplasia of mesangial matrix, sub-endothelial insertion, and double-track formation. Immunohistochemistry of Type III collagen was positive. Electron microscopy revealed that massive collagen fibers (40-70 nm in diameter) deposited in the mesangial matrix and basement membrane. As for the follow-up results, the normal renal function had kept steady and the proteinuria was moderate in 1 case treated with angiotensin Ⅱ receptor blocker. Due to other system disease, another case developed into acute kidney injury and then received hemodialysis. The clinical manifestations of collagen Type Ⅲ glomerulopathy was atypical, the light microscope pathological features were various, and the disease was mainly diagnosed by electron microscopy and immunohistochemistry.
Collagen Type III ; genetics ; Glomerular Mesangium ; Humans ; Kidney Diseases ; Kidney Glomerulus ; Proteinuria

OBJECTIVE: To investigate the relationship between the expression of nephrin and the infiltration of macrophages in renal tissues in patients with lupus nephritis (LN), and to provide the evidence of potential mechanism of podocyte injury in LN. METHODS: In the study, 60 patients who were first diagnosed with LN by pathology were selected including 38 active LN patients with r-SLEDAI≥4, and another 10 patients of normal renal tissue were excised as a normal control group. The renal tissue and podocyte injury were observed through light and transmission electron microscope. The expression of nephrin and the infiltration of macrophages (CD68+cells) in the renal tissue of the 60 LN patients and 10 normal cases were detected by immunohistochemical and immunofluorescence method. Different statistical analysis methods were used to analyze the correlation between the variables. Variance analysis was used for comparison among the groups, while LSD test was used for comparison between every two groups. Pearson correlation analysis was used to analyze the correlation between the variables. RESULTS: (1)Of all the LN patients, 24 h urinary protein [(3.94±1.76) vs. (1.56±0.68), P<0.05], erythrocyte sedimentation rate (ESR) [(79.83±6.3) vs. (40.1±10.5), P<0.05] and serum creatinine [(106.58±14.9) vs. (79.1±9.89), P<0.05] were significantly increased in active group than those in inactive group, while C3 [(0.34±0.12) vs. (0.78±0.11), P<0.05], C4 [(0.07±0.04) vs. (0.17±0.10), P<0.05 ] and eGFR [(62.42±5.16) vs. (81.33±4.53), P<0.05] were significantly decreased in active group. (2)Compared with the normal control group, the expression of nephrin in renal tissue of the LN patients was significantly decreased, and the expression of nephrin in the active patients was significantly lower than that in inactive group (P<0.05). (3)Compared with the normal control group, the number of infiltrated macrophages in the LN patients was significantly increased, especially in the active patients (P<0.05). Macrophages were mainly found in glomeruli. (4)There was a significant negative correlation between the expression of nephrin and macrophage infiltration in renal tissues of the LN patients (r=0.761, P<0.001). CONCLUSION Macrophage infiltration in renal tissues may be one of the potential mechanisms of podocyte injury in lupus nephritis.
Humans ; Kidney ; Kidney Glomerulus ; Lupus Nephritis ; Macrophages ; Podocytes

A study was performed on 60 patients, who were treated by Cockcroft- Gault, Jelliffe, Bjornsson and Gates formulas at Renal-Urinary Department of Hue Central hospital between March 2003 and May 2004. Among which, 30 patients suffered from chronic renal failure, 30 patients did not suffer from any renal disease. Results: in the patients without chronic renal failure, the mean of creatinine clearance was 107.55±11.68 ml/minute . In the patients with chronic renal failure, the mean of creatinine clearance was 12.35±13,15 ml/minute; Jelliffe: 15.57±14.47 ml/minute; Mawer: 11.41±13.26 ml/minute; Bjornsson: 15.89±14.43 ml/minute; Gates: 15.42±15.95 ml/minute.
Kidney Glomerulus ; Therapeutics

Transplant glomerulopathy is a late complication of renal transplantation. The characteristic morphology of transplant glomerulopathy includes thickening of glomerular capillary loops with double contour, and duplication of glomerular basement membrane on electron microscopy. Clinical and experimental evidences support the role of antibody-mediated immune mechanism in the development of transplant glomerulopathy. Antibody-induced endothelial cell injury is the key pathogenesis of transplant glomerulopathy. The evolution of transplant glomerulopathy in the context of immunologic injury is briefly reviewed.
Capillaries ; Endothelial Cells ; Glomerular Basement Membrane ; Graft Rejection ; Immunity, Humoral ; Kidney Glomerulus ; Kidney Transplantation ; Microscopy, Electron ; Transplants

Animals ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Glomerulonephritis ; drug therapy ; pathology ; Humans ; Kidney Glomerulus ; pathology ; Phytotherapy ; Podocytes ; pathology

Glomerulonephritis, Membranoproliferative ; Humans ; Kidney Glomerulus ; pathology

OBJECTIVEHepatitis B virus-associated membranous nephropathy (HBV-MN) is a disease characterized by podocytopathy. Podocyte is a terminally differentiated cell with limited capability of proliferation. Thus, damage of podocyte might result in decreased cell number, and then lead to the development of marked proteinuria and glomerulosclerosis. The present study aimed to investigate the changes of glomerular podocyte number in the children with hepatitis B virus-associated membranous nephropathy (HBV-MN), and their significance in the pathogenesis of HBV-MN.

METHODSPodocytes were identified through specific immunohistological staining of Wilms tumor gene protein 1 (WT1), a characteristic marker for podocyte nuclei, and podocyte numerical density (Nv), mean glomerular tuft volume (V) and the podocyte number per glomerulus (Npodo) were estimated through Weibel-Gomez method in 19 children with biopsy-proven HBV-MN and 8 children with thin basement membrane disease (control group), and analyses were made for possible correlation with clinical, serological and pathological data.

RESULTSAmong the 19 cases with HBV-MN, 3 showed microvillus-like foot process of podocytes, granular degeneration of podocyte were found in 4 cases, vacuolization in 1 case and podocyte detachment in 2 cases. Nv and Npodo were significantly decreased in children with HBV-MN compared with control group (t = 12.851, P = 0.0002 and t = 6.433, P = 0.0002, respectively). Moreover, the number of podocytes decreased more significantly in patients with stronger HBsAg deposition (> ++) than those with weak HBsAg deposition (< or = ++), P = 0.004, but no significant difference was found between patients with phase III or IV of HBV-MN and those with phase Ior II in podocyte number per glomerulus (P = 0.5262) and podocyte numerical density (P = 0.3564). Podocyte numerical density decreased more significantly in patients with massive proteinuria (> or = 2 g/24 h) than those with moderate proteinuria (< 2 g/24 h), P = 0.0488. The numbers of podocyte correlated significantly with serum levels of C(3) (r = 0.548, P = 0.028), but did not correlate with serum levels of albumin (r = -0.037, P = 0.891).

CONCLUSIONAll patients with HBV-MN showed podocyte damage and decreased number per glomerulus, which may play an important role in the pathogenesis of HBV-MN in children.

Cell Count ; Child ; Glomerulonephritis ; pathology ; Glomerulonephritis, Membranous ; complications ; virology ; Hepatitis B ; complications ; pathology ; Hepatitis B virus ; Humans ; Kidney Diseases ; pathology ; Kidney Glomerulus ; pathology ; Podocytes ; pathology ; Proteinuria ; pathology

The occurrence of immunoglobulin A nephropathy (IgAN) in patients with noninsulin dependent diabetes mellitus (NIDDM) is a rare event and of pathogenetic interest. It is not clear whether this is merely coincidence. We report here five patients with IgAN in NIDDM associated with or without diabetic glomerulosclerosis. All of the patients were Korean males. In three patients, diabetes mellitus was diagnosed at the same time with diagnosis of IgAN, and the known duration of the diabetes in the other two patients were three and seven years, respectively. There was no evidence of diabetic retinopathy in four patients, but it was found in one patient. In all cases, the diagnosis of IgAN was made by immunohistology.
Adult ; Biopsy ; Case Report ; Complement 3/analysis ; Diabetes Mellitus, Non-Insulin-Dependent/complications* ; Diabetic Nephropathies/pathology* ; Glomerular Mesangium/pathology ; Glomerulonephritis, IGA/pathology* ; Glomerulonephritis, IGA/etiology ; Human ; IgG/analysis ; Kidney Glomerulus/pathology ; Male ; Microscopy, Fluorescence ; Middle Age