To determine prospectively the prevalence of mitral, aortic, tricuspid, and pulmonary regurgitation in normal persons, 211 consecutive, apparently healthy volunteers were examined with a color Doppler flow imaging system. The subjects were divided into five age groups (group 1, 6-9 years old; group 2, [10][11][12][13][14][15][16][17][18][19]
In the present study, two series of experiments were done with PAN nephropathy rats given fibroblast growth factor 2 (FGF2) or FGF2 neutralizing antibodies. In the first series of experiments, a dose of 10 micrograms of FGF2 (FGF2 group), 40 micrograms of an FGF2 neutralizing antibody (Anti-FGF2 group) or an equal volume of physiological saline (Control group) was administered for four days after PAN injection. Urinary protein increased more in the FGF2 group than in the other two groups. PCNA (+) glomerular cells were found in decreasing order in groups FGF2, Control and Anti-FGF2. Most of the PCNA (+) cells were podocytes and epithelial cells of Bowman's capsule. Staining for desmin, a marker of podocyte injury, was significantly reduced in the Anti-FGF2 group. Glomerular adhesive lesions were found in decreasing order in groups FGF2, Control and Anti-FGF2. The second series of experiments was designed to study the effects of FGF2 neutralizing antibody (40 micrograms for 5 days after PAN injection, in MoAb group) on severely damaged podocytes caused by repeated (two courses) injections in the PAN nephropathy rats. The results were the same as those in series 1. An increase in urinary protein excretion was observed in both groups, but on the 40th day, the level of proteinuria in the MoAb group decreased abruptly. It was observed that the MoAb group had few adhesive glomeruli compared to the IgG group (administration of mouse IgG) and the PCNA (+) epithelial cells of Bowman's capsule were also few. It was supposed that FGF2 would promote the formation of adhesive lesions by stimulating the proliferation of podocytes and epithelial cells of Bowman's capsule. Additionally, FGF2 itself was thought to impair podocytes because of the increasing desmin score and proteinuria.
Summary:A 64-year-old woman underwent an ileocecal resection for ileus. The specimen revealed a diffuse large B cell lymphoma. The diagnosis was stage IIA non-Hodgkin's lymphoma. She received chemotherapy with the CHOPetoposide regimen, resulting in partial remission. Highdose etoposide was used for PBSC mobilization before auto-PBSCT. Conditioning was ranimustine, carboplatin, etoposide and cyclophosphamide. Her renal function deteriorated gradually, starting 3 months post-PBSCT. Eight months post-transplant, serum creatine concentration was 7.1 mg/dl, and BUN was 59.2 mg/dl. Her hemoglobin concentration decreased to 5.3 g/dl, with no evidence of hemolysis. Renal biopsy revealed fibrous crescent formations in glomeruli, and mononuclear cell infiltration in interstitial spaces. Renal injury in this patient differs from BMT nephropathy, which is similar to hemolytic uremic syndrome, and represents another type of late renal injury after PBSCT. Keywords: crescentic glomerulonephritis; PBSCT; nonHodgkin's lymphoma Transplantation of either allogeneic or autologous hematopoietic stem cells can be complicated by renal failure from a variety of causes. These complications include not only early but also late renal injury characterized by a syndrome similar to hemolytic uremic syndrome (HUS). [1][2][3][4][5] We report another type of late renal injury, crescentic glomerulonephritis, which developed more than 3 months after auto-PBSC transplantation (T) for non-Hodgkin's lymphoma. Case reportA 64-year-old woman, who underwent an ileocecal resection for ileus due to an iliocecal tumor, was diagnosed with non-Hodgkin's lymphoma (diffuse large B cell type). She was referred to us in April 1996. Multiple enlarged intraperitoneal lymph nodes were observed during the operation. Her clinical stage was IIA, according to the Ann Arbor system. At the time of diagnosis, renal involvement with lymphoma was not detected, and no abnormal findings were seen on urinalysis or renal function tests. 6 She received the CHOP-etoposide regimen, consisting of doxorubicin 50 mg/m 2 on day 1, cyclophosphamide, 750 mg/m 2 on day 1, vincristine, 1.4 mg/m 2 on day 1, etoposide, 100 mg/m 2 on days 1-3 and prednisolone 60 mg/m 2 on days 1-4 repeated every 3 weeks. After five cycles of chemotherapy, she had achieved only partial remission. She therefore received high-dose etoposide (etoposide 500 mg/m 2 , days 1-3), to collect PBSC. Subsequently, PBSCT (CD34 8 × 10 6 /kg, CFU-GM 15 × 10 5 /kg) was performed after a conditioning regimen (ranimustine 200 mg/m 2 , days Ϫ8 and Ϫ3; carboplatin, 300 mg/m 2 , days Ϫ7 to Ϫ4; etoposide 500 mg/m 2 , days Ϫ6 to Ϫ4; and cyclophosphamide 50 mg/kg, days Ϫ3 and Ϫ2). 7 Her serum creatinine (Cr) concentration rose to 1.8 mg/dl (normal range 0.4-0.8 mg/dl) on day 1 (before the conditioning chemotherapy, her serum Cr was 0.5 mg/dl and her Cr clearance was 63.8 ml/min), then returned to baseline on day 6. A complete response was confirmed after Figure 1 Histopathological findings of the biopsied kidney (PAS stain, × 400...
Abstract. Cultured, rat glomerular podocytes were examined by electron microscopy and immunohistochemistry in order to determine their origin. The outgrowth of polygonal cells was noted first. Large arboroid ceils were occasionally observed around the polygonal cells. Immunostaining of these large arboroid cells for the intermediate filament proteins showed an intensely positive reaction for vimentin, whereas cytokeratin was not detected. In the polygonal cells, however, both cytokeratin and vimentin were sometimes detected. Although scanning electron microscopy did not detect any specific irregularities in podocytes on the surface of the glomerulus, developing polygonal cells were observed. Both transmission and scanning electron microscopies revealed the polygonal cells to be similar to Bowman's capsule epithelial cells in situ. The vascular poles of the cultured glomeruli were always in contact with the culture dish. A residual Bowman's capsule was also observed. These results suggest that polygonal cells originate from the epithelial cells of the residual Bowman's capsule, whereas large arboroid cells arise from podocytes.
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