Objective: To study the relationship between monocyte/macrophage(MC/MP) accumulation and tubulointerstitial fibrosis.Methods: The renal tubulointerstitial fibrosis model in Wistar rats was established by unilateral renal vein ligature. The rats were fed for 25 days. The kidneys were obtained every 5 days by killing the rats. The morphological changes of tubulointerstitial fibrosis were observed by light microscopy with HE,PAS, PASM and Masson staining. Immunohistochemistry and double immunohistochemistry were used to observe MC/MP accumulation and proliferation. In situ hybridization and immunochemistry were used to observe MCP 1 and M CSF expression in experimental renal tissue. The MCP 1 protein expression was inspected by Western blot. All the data were analyzed statistically.Results: The pathological changes of tubulointerstitial fibrosis were typical. There were many MC/MPs accumul sated in the interstitial space at the early stage and some of them were PCNA positive. At the late stage both accumulation and proliferation of MC/MPs were decreased. The portion of monocyte proliferation was high correlated with the MC/MP accumulation. In situ hybridization showed the positive signals of MCP 1 and M CSF were mainly located in the cytoplasm of degenerated tubular epithelium and they were strong at the early stage, weak at the late stage. MCP 1 by immunochemistry and Western blot were consistent with in situ hybridization. The MC/MP accumulation was high correlated with the expression of MCP 1 and tubular epithelium degeneration. The portion of monocyte proliferation was high correlated with the expression of M CSF.Conclusion:There was obvious accumulation of MC/MP at the early stage of tubulointerstitial fibrosis. The accumulation came from infiltration and proliferation which were regulated by degenerated tubular epithelial cells producing MCP 1 and M CSF. MC/MP accumulation was highly correlated with tubular degeneration. MC/MP promoted tubulointerstitial fibrosis and damaged tubular epithelium by secreting a variety of cytokines.

Objective: To detect the localization of HBV DNA in kidneys of HBV-associated glomerulonephritis, and investigate the pathogenesis of HBV-associated glomerulonephritis. Methods: 45 cases of renal biopsy specimens (38 cases had glomerular deposition of HBV antigens, 7 cases were negative for serologic and histologic HBV antigens) were examined for HBV DNA by in situ hybridization (ISH) and in situ PCR (IS-PCR). Results: The positive rate of HBV DNA in renal biopsy was 71% (27/38) in patients with glomerular deposition of HBV antigens. HBV DNA was found in 19 cases (19/26, 73%) of HBV-associated glomerulonephritis; and in 8 cases (8/12, 67%) of IgA nephropathy and lupus nephritis with glomerular deposition of HBV antigens. HBV DNA was detected mainly in the cytoplasm of tubular epithelia with ISH; IS-PCR showed that HBV DNA was localized not only in cytoplasm of tubular epithelia, but also in nuclei of tubular epithelia, in nuclei and cytoplasm of glomerular epithelia and mesangial cells, and in GBM. Conclusion: Our study suggested the presence of HBV infection and replication in glomerular cells and renal tubular epithelia, indicating an etiologic role of HBV in HBV-associated glomerulonephritis.

China ; Humans ; Kidney ; pathology

To report a Chinese female adult suffering with lipoprotein glomerulopathy. Methods Light , electron microscopy and immunofluorescence were performed with renal tissue from biopsy. Results Mass proteinuria and nephrotic syndrome were seen as clinical features in this patient. Obvious expansion of glomerular capillary cavities, full of positive sudan 3 lipoprotein thrombi, was observed. Electron microscopy demonstrated cavities were full of various foaming lipid deposition in cluster and layer arrangement. Repeat renal biopsy after two months found expansive cavities decreased remarkably and lipoprotein thrombi were replaced by mesangial proliferation and sectional sclerosis gradually. Conclusion This case is diagnosed by pathology.

To investigate the location of Epstein-Barr virus (EBV) in renal tissues of patients with interstitial nephritis(IN). Methods By in situ hybridization. EBER1 was detected in renal tissues of 12 IN patients and 10 patients with minimal change nephropathy (MCN) as control group. Results EBER1 was found positive in 3 renal tissues of IN patients. It mainly distributed in the nuclei of renal tubular cells, infiltration cells and glomerular cells and 10 MCN patients were all negative. Conclusion EBV infection may play an important role in the pathogenesis of IN. In different types of IN, EBV infection may play different role.

To explore the relationship between eosinophilic hyperplasia lymphogranuloma (ELG) and nephrotic syndrome (NS). Methods 3 cases of ELG associated with NS were collected. The specimen of ELG and renal biopsy were confinned by pathological method, and clinical characteristic, therapeutic course and follow up were summarized. Results Two cases were ELG associated with minimal changes disease (MCD), another was early membranous nephropathy (MN) . ELG and NS were cured by prednisone therapy. Conclusion About 12% of ELG may be associated NS. The pathogenesis of ELG, MCD and MN are similar, and curative effect occured by same therapy. Suggesting that, they are identical allergic disease caused by one pathogeny.

Objective To investigate the role of transmission electron microscopy (TEM) on the diagnosis of cryoglobulinemia related glomerulonephritis. Methods Sixteen cases which showed glomerular organized deposits by TEM in the renal biopsy specimens were collected in our hospital during last six years. Their clinical data, renal pathological features and ultrastructural morphology were analysed. Results Four cases had positive serum cryoglobulin were diagnosed as cryoglobulinemia related glomerulonephritis. Serum cryoglobulin was not available in the other 12 cases, who were suspected as cryoglobulinemia related glomerulonephritis. All patients had proteinuria with microscopic hematuria,and some cases had nephrotic syndrome, hypertension and mild to moderate renal insufficency. The main pathological pattern was membranoproliferative glomerulonephritis.Endocapillary proliferation with an infiltration of monocytes was observed in these cases. Glomerular subendothelial deposits and intraluminal thrombi was their prominent features. Organized electron-dense deposits were identified by TEM, whose deposits organized into microtubular, fibrillary, crystalline-like and granular structures, and were demonstrated mainly in glomerular subendothelia and capillary lumen. Most of cases were considered as cryoglobulinemia related glomerulonephritis by the ultrastructural findings of glomerular organized deposits. Conclusion Glomerular organized deposits identified by TEM provide important diagnostic implications for cryoglobulinemia related glomerulonephritis.

Objective To investigate the elinicopathoiogical features of Castleman disease with kidney injury. Methods Clinicopathological data of 10 Castleman disease patients with kidney injury from Peking University First Hospital and China-Japan Friendship Hospital were analyzed retrospectively. All the cases received biopsies of lymph node and kidney. Their renal tissues were examined by light microscopy, immunofluorescence and electron microscopy. Results Ten patients were all male with mean age (493:14) years. They presented edema and proteinuria, with mean urinary protein at (2.79±3.56) g/24 h, including one nephrotie syndrome (NS). Hematuria occurred in 8 cases, acute renal insufficiency in 6 cases, hypertension in 4 cases. Most of the patients had fever, fatigue, anorexia, weight loss, increased ESR and CRP, hypergammaglobulinaemia and decreased complements. Other abnormalities included anemia, thrombocytopenia, pleural effusion, hepatomegaly, splenomegaly, hypothyroidism, etc. Two cases demonstrated POEMS syndrome, one presented Sjogren syndrome. The enlargement of multiple cervical, axillary and inguinal lymph nodes were identified in all the patients. The pathological patterns of lymph node were plasma cell type in 4 cases, hyaline-vascular type in 3 cases, and mixed type in 3 cases. Pathological examination of renal biopsy showed thrombotic microangiopathy in 5 cases, crescentic glomerulonephritis in 2 cases, renal amyloidosis, minimal change disease and chronic tubular interstitial nephropathy in 1 case respectively. After immunosupressive reagents or COP therapy, lymph nodes became smaller, systemic symptoms were alleviated, proteinuira was decreased or disappeared, and renal function was recovered in most of patients. Conclusions Castleman disease with kidney injury manifests various symptoms with high prevalence of renal insufficiency and multiple systemic damage. Renal lesions present many patterns of pathological change with a higher frequency of thrombotic microangiopathy. It is necessary to examine the lymph nodes by ultrasound, radiology or biopsy for the patients of renal diseases with multiple systemic symptoms.

Objective To analyze the clinical and pathological characteristics of ANCA associated systemic vasculitis(AASV) with immune complex deposition in kidney and compare with that of pauci-immune AASV. Methods Patients with AASV, admitted in our hospital in last 5 years, were retrospectively studied. The clinical and pathological characteristics were compared between patients with immune complex deposition and patients with pauci-immune deposition. Results There were eitht patients with immune complex deposition (five with IgM deposition, two with IgA deposition and one with IgG deposition) and 32 patients with pauci-immune deposition. There was no significant difference in age, gender, type of ANCA, interval between onset of vasculitis and renal biopsy, clinical manifestations and short-term renal survival rate between the two groups. Patients with immune complex deposition had a higher predromal infection rate ( P

ObjectiveTo investigate the clinical significance and histological origin of glomerular epithelial proliferative lesion in patients with focal segmental glomerulosclerosis (FSGS). MethodsSeventy-four patients with idiopathic FSGS hospitalized in Peking University First Hospital from Jan. 2000 to Dec.2005 were enrolled in this study. Patients were classified into two groups according to with or without glomerular epithelial proliferative lesion. Estimation of active and chronic pathological scores was carried out using a semi-quantitative grade system by two pathologists. Clinical and pathological characteristics were compared between two groups. Immunohistochemical studies were performed to analyze the histological origin of glomerular epithelial proliferative lesion. ResultsThirty-one patients with glomerular epithelial proliferative lesion showed shorter interval from presentation to biopsy (P<0.05), higher percentage of nephrotic syndrome (NS) (P<0.05), higher frequency of segmental glomerulosclerosis(P<0.05), higher pathological active scores (P<0.05) and lower pathological chronic scores (P<0.05)as compared to 43 patients without glomerular epithelial proliferative lesion. Twenty-nine patients were followed up and renal survival rate in patients with glomerular epithelial proliferative lesion (39.7%) was significantly lower than that in patients without glomerular epithelial proliferative lesion (83.3%) (P=0.049). The frequency of glomerular epithelial proliferative lesion and the serum creatinine (Scr) level at biopsy were independent predictors of ESRD (OR value was 1.204, 1.008 respectively ). Glomerular epithelial proliferative lesion did not express mature podocyte markers including WT-1 and pedocalyxin, but stained positive for PCNA, PAX-2 and CK-8. ConclusionsGlomerular epithelial proliferative lesion represents the pathological change of acute stage and active lesion of FSGS, and also may be the pathological marker of severe clinical presentation and worse renal survival. Glomerular epithelial proliferative lesion may be derived from proliferation of parietal epithelial proliferation or de-differentiated podocytes.