Beta 2-microglobulin as an indicator of interstitial cell infiltration in IgA nephropathy.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to H Nihei.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Proximal and distal sodium reabsorption values were calculated from lithium clearance in 63 patients with renal diseases, 13 cirrhotic patients with ascites and 12 control subjects. In the patients with renal diseases, fractional excretion of lithium (FELi) and fractional proximal reabsorption of sodium (FPRNa) were not changed in patients whose glomerular filtration rate (GFR), was over 30 mL/min, but FELi was increased and FPRNa was decreased when the GFR was lower than 30 mL/min. Moreover, fractional distal reabsorption of sodium (FDRNa) was decreased in patients whose GFR was under 40 mL/min. These results indicate that proximal tubular function is well adapted to the degree of renal function even if the etiologies of renal diseases are different. Five patients with nephrotic syndrome (minimal change type) were subjected to lithium clearance method before and after steroid treatment. FPRNa in nephrotic patients was reduced after the treatment, though there was no significant difference in FDRNa. In cirrhotic patients, FELi, FPRNa and FDRNa did not differ from the values in the control subjects, which were not influenced by the decrease in GFR. Thus, the reduction of FPRNa with GFR which was observed in renal disease, was absent in liver cirrhosis. In conclusion, these data indicate that renal adjustment of sodium excretion in chronic renal disease at first takes place in the distal parts of the nephron and later in the proximal tubule, and in addition, that in appropriate reabsorption of sodium from the proximal tubule probably plays a role in ascites formation in cirrhotic patients.
Explore the source record for details and available documents.
The present study was designed to identify the mechanism of increased oxidant stress in the rat model of anti-glomerular basement membrane nephritis. Sixty-three Sprague-Dawley rats were injected with nephrotoxic serum and evaluated 1 to 24 hours later. In these rats, CeCl3 deposition, an index of hydrogen peroxide production, was observed on the surfaces of glomerular endothelial cells and polymorphonuclear leukocytes, whereas no such depositions were observed in controls. Renal cortical level of lipid peroxidation products (phosphatidylcholine hydroperoxide) was significantly (p < 0.05) elevated at one hour after the injection and remained elevated at least for 24 hours. Protein levels of glomerular Mn-superoxide dismutase (SOD) decreased from 1.55 +/- 0.38 microgram/mg protein to 0.67 +/- 0.18 microgram/mg protein at one hour and normalized by 12 hours after the injection. The activity of the enzyme showed a similar trend. In contrast, Mn-SOD mRNA increased 3.4-fold at 3 hours after the injection. In situ hybridization showed increased Mn-SOD mRNA expression in glomeruli. Cu/Zn-SOD mRNA expression was transiently suppressed. These results indicated that both increase in local production of reactive oxygen species (ROS) and reduction in antioxidant enzyme activities are responsible for the enhanced oxidant stress in the heterologous phase of anti-glomerular basement membrane nephritis. The paradoxical increase in Mn-SOD mRNA expression indicates that the posttranscriptional down regulation of Mn-SOD (i.e., reduction in protein and activity) and the increased ROS may activate transcription of the gene.
We report a case of aortitis syndrome, in which carotid ultrasonography was a useful approach for the diagnosis. A 21-year-old woman was admitted to our hospital for persistent fever. No specific physical findings or laboratory abnormalities were observed except high fever and marked increase of erythrocyte sedimentation rate and c reactive protein. Since clinical trial of antibiotics and antituberculosis agents resulted in no effectiveness, prednisolone was started, but the effect was limited. After that, she complained of the neck pain, and vascular murmur became apparently audible at the pain site. Ultrasonography of the carotid artery revealed the smooth lumen and homogeneous, non-hyperechoic intimal thickening. Then aortography confirmed the diagnosis of aortitis syndrome. Cyclophosphamide combined with steroid therapy diminished the disease activity. In this case, carotid ultrasonography gave us the important information to enforce the aortography. If ultrasonography of the carotid artery has been popularized for aortitis syndrome, and its findings have been standardized, non-invasive diagnosis of this disease will be taken a step forward.
The present study was designed to investigate the role of intercellular adhesion molecule (ICAM)-1 in the interaction between glomerular endothelial cells (GEN) and granulocytes. Expression of ICAM-1 was promoted after stimulation with tumor necrosis factor (TNF)-alpha. This effect was dose- and time-dependent. Granulocytes attached to GEN in accordance with the increased expression of ICAM-1 on the cells stimulated with TNF-alpha. In addition, the adhesion of granulocytes to activated GEN with TNF-alpha stimulated specific [51Cr] release from the monolayers. Furthermore, monoclonal antibodies to TNF-alpha dose-dependently inhibited the adhesion of granulocytes to activated GEN. In summary, ICAM-1 is related to the glomerular endothelial cell injury induced by granulocytes activated with TNF-alpha, suggesting that ICAM-1 may play a role in the initiation of certain types of glomerulonephritis with granulocyte infiltration.
These experiments were performed in an attempt to determine whether chronic stimulation of glomerular endothelial cells with recombinant human erythropoietin would alter mesangial cell proliferation. Glomerular endothelial cells in culture incubated with various concentrations of erythropoietin for up to 4 days exhibited dose-dependent endothelin-1 production. Moreover, the conditioned medium from erythropoietin-stimulated glomerular endothelial cells enhanced [3H]thymidine incorporation into mesangial cells. This enhancement was significantly attenuated in the presence of a endothelin A receptor antagonist, BQ-123. These results suggest that endothelin-1 mediates erythropoietin-stimulated glomerular endothelial cell-dependent mesangial cell proliferation, resulting in the progression of glomerulonephritis.
Explore the source record for details and available documents.
We conducted these experiments to determine whether glomerular endothelial cells (GEN) may play a role in the regulation of glomerular mesangial cells (GMC) growth. When GMC were separately co-cultured with GEN for 24 h, [3H]thymidine incorporation into GMC increased by 22%. In addition, when GMC were co-cultured with GEN for 4 days, the GMC count increased statistically. Conditioned medium (CM) was obtained from confluent GEN monolayers and tested for its effect on GMC growth. When CM was mixed with RPMI 1640 medium containing fetal calf serum (final concentration: 10%), GMC growth was potentiated in a dose-dependent manner. This stimulatory effect of CM from GEN cultures was inhibited by the addition of anti-human platelet-derived growth factor (PDGF) antibody. However, antibodies against interleukin 1-beta, tumor necrosis factor-alpha and endothelin-1 did not affect the stimulatory effect of CM. Moreover, the modulator contained in CM was stable at 100 degrees C, and pH 2.5 at 22 degrees C for 30 min. When treated with 2 mM mercaptoethanol, this activity was almost completely lost. These findings suggest that GEN promote GMC growth in co-culture systems, without direct contact, by means of a PDGF-like substance.
The study of the current status of renal replacement therapy in Japan is based on the analysis of data from the registry reports for regular dialysis therapy and kidney transplantation. The total number of patients receiving regular dialysis therapy was 123,926 at the end of 1992: 117,809 (95.1%) on hemodialysis and 6,117 (4.9%) on peritoneal dialysis. The primary diseases of newly accepted patients were chronic glomerulonephritis (42.2%), diabetic nephropathy (28.4%), nephrosclerosis (5.9%), polycystic kidney disease (2.7%), chronic pyelonephritis (1.6%), and others. The number of kidney transplant patients in Japan was 8,384 at the end of 1991: 6,154 (73.4%) received a living donor transplantation and 2,230 (26.9%) received a cadaver donor transplantation. Overall 5-year survival rates of dialysis patients were 60.4%: 69.7% for chronic glomerulonephritis, 41.7% for diabetic nephropathy, 39.6% for nephrosclerosis, 73.6% for diffuse polycystic kidney disease, and 66.6% for chronic pyelonephritis. The causes of death of dialysis patients were heart failure (31.1%), cerebrovascular accident (13.6%), infectious diseases (11.3%), malignancies (7.1%), cachexia/uremia (6.7%), myocardial infarction (5.8%), and others. The gross mortality rate of dialysis patients was increased in cases of less than 4 hours of the average length of each dialysis session, less than 4% and more than 9% of the average weight loss during each dialysis session, less than 1.0 of Kt/V, and less than 0.9 and more than 1.7 g/kg/d of protein catabolic rate. Overall 5-year patient and graft survival rates of kidney transplant patients since 1964 were 82.7% and 60.3%: 84.4% and 65.0% in living donor cases, and 77.4% and 46.2% in cadaver donor case, respectively. Those since 1983 were 90.1% and 68.2%: 91.3% and 72.6% in living donor cases, and 87.8% and 59.3%, respectively. Graft survival rates were superior in cases treated with combined steroid, cyclosporine and azathioprine or mizoribine, to those treated with other immuno-suppressive regimens, and they decreased as the number of HLA-A, -B and -DR increased.
Peroxidation of cell membrane (phosphatidylcholine hydroperoxide, PCOOH) was quantitatively assessed using a chemiluminescence-HPLC system to clarify whether haemodialysis patients are damaged by oxidative stress. Patients were divided into two groups, one dialysed with conventional cellulose membranes, and the other with cellulose triacetate for 3 months, subsequently followed by a crossover study of each membrane for 3 more months. The mean value of PCOOH in haemodialysis patients was 508.5 +/- 208.7 pmol/ml (P < 0.01 vs normal controls), which showed a statistically insignificant tendency to increase during each haemodialysis session of 4 h. Two years after commencing haemodialysis, PCOOH was maintained within almost the same range, but significantly greater than normal. There was no significant tendency between an index of aortic sclerosis and plasma PCOOH. However, three patients using conventional cellulose membranes died of myocardial infarction. Plasma PCOOH increased after the commencement of haemodialysis. This tendency was more notable in patients using conventional cellulose membrane compared to the cellulose triacetate. Cellulose triacetate, which we thought to be more biocompatible, did not necessarily produce lipid peroxide. We conclude that it is very important to check production of oxygen radicals when developing new membranes.
Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) who developed carpal tunnel syndrome (CTS) were retrospectively studied in 143 centers in Japan. Among the total 5,050 patients undergoing CAPD between 1980 and 1993 only 7 patients (0.14%) given CAPD developed CTS. Five of these 7 patients treated solely with CAPD developed CTS 12-108 months after starting CAPD. The remaining 2 patients who were initially treated with HD for 7-9 years and then switched to CAPD developed this complication 9 years after starting CAPD. All 7 patients were women, ranging in age from 32 to 70 (average 52) years. We detected the presence of amyloid deposits in 2 of 5 specimens and beta 2-microglobulin in 2 of 4 specimens from these patients. It was concluded that CAPD minimizes the emergence of CTS although constant surveillance is necessary to detect CTS in patients during CAPD.
Explore the source record for details and available documents.
To investigate the physiological role of a kidney-specific chloride channel (ClC-K1), we sought to determine its exact localization by immunohistochemistry and its functional regulation using Xenopus oocyte expression system. The antiserum specifically recognized a 70-kD protein in SDS-PAGE of membrane protein from rat inner medulla and an in vitro translated ClC-K1 protein. Immunohistochemistry revealed that ClC-K1 was exclusively localized to the thin limb of Henle's loop in rat inner medulla. In comparison with the immunostaining with anti-aquaporin-CHIP antibody that only stains the descending thin limb of Henle's loop (tDL), ClC-K1 was found to be localized only in the ascending limb (tAL) which has the highest chloride permeability among nephron segments. Immunoelectron microscopy confirmed that the staining of ClC-K1 in tAL was observed in the region of both apical and basolateral plasma membranes. Expressed chloride current in Xenopus oocytes by ClC-K1 cRNA was regulated by extracellular pH and extracellular calcium. Furosemide inhibited the expressed current (Ki = 100 microM), whereas N-ethyl-maleimide stimulated the current. These functional characteristics were consistent with the in vitro perfusion studies of chloride transport in tAL. The localization and the functional characteristics described here indicate that ClC-K1 is responsible for the transepithelial chloride transport in tAL.
Adhesion of lymphocytes to glomerular endothelial cells might be a critical step in the development of acute and chronic glomerulonephritis. The protective effect of anti-CD11a and anti-intercellular adhesion molecule (ICAM-1) antibodies on the cytotoxity elicited by phorbol 12-myristate 13-acetate (PMA)-stimulated lymphocytes was investigated by using cultured bovine glomerular endothelial cells (GEN). Both anti-CD11a and CD18 antibodies inhibited GEN injury induced by the activated lymphocytes in a dose-dependent manner. In addition, both antibodies also inhibited the adhesion of the activated lymphocytes to the GEN monolayers. These results suggest that it is important for activated lymphocytes to bind to GEN via adhesion molecules for cytotoxity to be produced by the activated lymphocytes.
A 48-year-old woman with nephrotic syndrome underwent renal biopsy. Light microscopy showed nodular sclerosis and thickening of the glomerular capillary wall. Immunoglobulins (Ig) G, especially IgG2, IgM, IgA, C3, C1q were detected along the glomerular capillary walls by immunofluorescent microscopy. Electron microscopy revealed that fibrillar materials of about 25 nm were accumulated in the subepithelial area of the glomerular basement membrane. These materials were negative for Congo-red staining. Neither cryoglobulinemia nor paraproteinemia including light chains was found. This case was diagnosed as membranous nephropathy by clinical findings and pathological examinations, and seemed to be a case of fibrillary glomerulonephritis.
We report here two cases of mixed cryoglobulinemia showing renal involvement associated with hepatitis C virus (HCV) infection. The subjects were 62- and 63-year-old males. Both patients presented with purpura on the legs, which was diagnosed as allergic vasculitis by skin biopsy. Case 1 followed a clinical course of progressive nephrotic syndrome with mild hematuria. He also had diabetes mellitus and hypertension. In contrast, case 2 showed only mild hematuria without proteinuria at the time of the renal biopsy. Both cases had immunological disarrangements, such as severe hypocomplimentemia and seropositive rheumatic factor. Recently, it was reported that patients with type II mixed cryoglobulinemia had HCV seropositivity, and revealed membranoproliferative glomerulonephritis. These facts strongly suggested that renal lesions are the result of direct damage mediated by cryoglobulinemia and an activated complement pathway through an immune complex mechanism related to HCV.