Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of cell-mediated immunity in glomerular injury has been extensively studied, but the precise mechanism remains obscure. This study was undertaken to determine whether the homologous glomerular basement membrane (GBM) combined heterogeneous anti-GBM antibody would induce cell-mediated immunity. Wistar-Kyoto rats were divided into three groups; group I rats were immunized with homologous GBM antigen that was derived from Masugi nephritis and emulsified in complete Freund's adjuvant (CFA); group II rats were immunized with homologous GBM antigen that was derived from normal rats and emulsified in CFA; group III rats were immunized with CFA only. Group I rats demonstrated proteinuria on days 7 and 10 after immunization. Histologically, mesangial cell proliferation and cell infiltration were observed in the glomeruli. No changes in tubulointerstitial tissue. CD4-positive cells, CD8-positive cells and macrophages were found in the glomeruli, and mononuclear cells were found in the glomerular capillary lumen. Group II and Group III rats demonstrated no proteinuria and no histological changes. These findings indicated that the altered GBM obtained antigenicity and induced cell-mediated immunity in the glomeruli.
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PMID:[Studies on cell-mediated immunity (CMI) in the glomeruli: immunization with GBM antigen from Masugi nephritis in Wistar-Kyoto rats]. 813 54

Glomerular and interstitial leukocyte subpopulations were analyzed in renal biopsies from 18 patients with IgM mesangial proliferative glomerulonephritis (IgM MPGN), 19 patients with minimal change nephrotic syndrome (MC) and 10 patients with immune-negative mesangial proliferative glomerulonephritis (IN MPGN), by immunoperoxidase techniques with monoclonal antibodies. Mesangial cell proliferation was strongly correlated with absolute numbers of intraglomerular T lymphocytes (r = 0.71; p < 0.01) in IgM MPGN, but not in MC or IN MPGN. Significant differences were found in the numbers of macrophages, CD4- and CD8-positive glomerular cells (Student's t test p < 0.01, 0.05 and 0.01, respectively) in IgM MPGN, but not in MC or IN MPGN. The numbers of CD45-, CD3- and CD8-positive cells also differed in each patient group (ANOVA p < 0.01, 0.05 and 0.05, respectively), the greatest and smallest values appearing in IgM MPGN and MC, respectively. Multiple regression test showed initial proteinuria values in IgM MPGN to be closely dependent on the density of neutrophils, macrophages, T and B lymphocytes and CD4 cell inflammatory infiltrates (r2 = 0.92; p < 0.01). At the end of the follow-up, proteinuria in IgM MPGN, but not in MC or IN MPGN, was dependent on T cell infiltrate (r2 = 0.97; p < 0.01). Our findings suggest that proteinuria in IgM MPGN results from local mesangial damage rather than from the effects of a soluble circulating factor, as has been proposed for MC. The clinical and immunohistochemical differences observed between these two processes support the notion that they should be considered as separate entities.
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PMID:Mononuclear cell subsets in IgM mesangial proliferative glomerulonephritis. A comparative study with minimal change nephrotic syndrome and immunonegative mesangial proliferative glomerulonephritis. 824 83

A 26-year-old male was admitted to our hospital having suffered from subfever, sterile pyuria and renal insufficiency for 1 year. There had been no apparent hematuria/proteinuria, and evidence of infection, allergy or intoxication was not demonstrated. Open renal biopsy revealed severe tubulointerstitial changes with granuloma accompanied by neither caseous necrosis nor giant cells. Infiltrating cells mostly consisted of CD4 and CD8 T cells, and some proximal tubular cells presented MHC class II antigen. Following the negative culture of biopsied specimen for acid-fast bacilli, diagnosis of idiopathic granulomatous tubulointerstitial nephritis was made, and steroid therapy was started. Two months later, pyuria disappeared and renal function improved significantly, proving the effectiveness of steroid on idiopathic granulomatous tubulointerstitial nephritis.
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PMID:Steroid-responsive renal insufficiency due to idiopathic granulomatous tubulointerstitial nephritis. 834 85

Four cases of idiopathic acute tubulointerstitial nephritis (TIN) associated with uveitis (so-called TINU syndrome) were experienced between 1986 and 1990. Patients' ages ranged from 14 to 42 years old and three were female and one was male. All cases showed general symptoms, such as general malaise, anorexia and weight loss. All patients had initially TIN and became ill uveitis four to eight months after the onset of TIN. All cases had mild proteinuria, mild anemia, the lower serum levels of potassium, hyper gamma-globulinemia and the reduced glomerular filtration rate with the increased beta 2-microglobulin in urine and serum. All renal biopsies specimens showed mild edema and diffuse infiltration of inflammatory mononuclear cells in the interstitium without any glomerular or vascular abnormalities. Furthermore, numerous CD4 positive cells, CD8 positive cells and CD11c positive cells were seen in the interstitium. Of four patients, three cases were treated with both oral administration and eye drop of prednisolone (PSL), another one case was therapied with eye drop PSL only. In all cases TIN had good prognosis, but two patients had recurrences of uveitis. All patients underwent tissue typing for HLA-A, B, C and DR antigens. Three patients had identical HLA-Cw3 and all four cases revealed identical HLA-A24(9). These results suggest that immunological mechanism, especially cell-mediated, and HLA system may play an important role in the occurrence of TINU syndrome.
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PMID:[HLA tissue types in patients with acute tubulointerstitial nephritis accompanying uveitis]. 837 85

The role of P-selectin in T-lymphocyte accumulation and injury was studied in delayed-type hypersensitivity (DTH) responses in the skin and glomeruli of rats. Sprague Dawley rats were sensitized to sheep globulin and challenged 5 days later in the skin by subcutaneous injection and simultaneously in glomeruli by intravenous injection of a subnephritogenic dose of sheep anti-rat glomerular basement membrane globulin. This resulted in cutaneous and glomerular T lymphocyte-dependent macrophage influx and injury characteristic of DTH. Up-regulation of P-selectin expression on endothelial cells was observed in both inflammatory lesions. Treatment of rats with anti-CD5 antibody immediately prior to antigen challenge prevented the development of injury as assessed by measurement of proteinuria and skin swelling, as well as local T cell and macrophage accumulation in the glomerulus and in the skin, but did not block up-regulation endothelial cell P-selectin. Treatment with anti-CD4 antibody produced similar results. Blocking P-selectin in vivo with a functionally inhibitory antibody prevented development of proteinuria and skin swelling following antigen challenge. Local accumulation of T cells and macrophages was markedly attenuated in glomeruli and the skin and up-regulation of endothelial cell P-selectin was prevented. These data demonstrate that P-selectin is locally up-regulated on endothelial cells in T cell-dependent glomerular and cutaneous inflammation and suggests a pivotal functional role for P-selectin in local T cell recruitment and subsequent injury in DTH.
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PMID:P-selectin directs T lymphocyte-mediated injury in delayed-type hypersensitivity responses: studies in glomerulonephritis and cutaneous delayed-type hypersensitivity. 861 18

We studied the expression of adhesion molecules on infiltrating leukocytes and tubular cells in chronic tubulointerstitial nephritis associated with puromycin aminonucleoside (PA) nephrosis. Rats received injections of PA (2 mg/100 g body wt) weekly for the first 3 weeks and every other week thereafter. Rats were killed at 0, 3, 5, 8, and 12 weeks after the start of injections. From the third to the fifth week, the initial infiltrating cells in interstitial tissue were mainly CD4+ T lymphocytes. At the fifth week, ICAM-1, CD44, and hyaluronate were expressed on infiltrating cells in interstitial tissue. At the eighth week, the number of infiltrating cells reached a peak and consisted of T lymphocytes (CD4, CD8) and macrophages (ED1, MHC class II, CD11b, and CD18). The severity of interstitial infiltration was correlated with the degree of proteinuria and with ICAM-1 expression. Our results suggest that CD4+ T lymphocytes may contribute to the production of initial tubular injury. Expression of ICAM-1 helps mononuclear cells migrate to the interstitium. In addition, expression of CD44 and hyaluronate may play important roles in the chronicity of tubulointerstitial nephritis.
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PMID:The relationship of adhesion molecules and leukocyte infiltration in chronic tubulointerstitial nephritis induced by puromycin aminonucleoside in Wistar rats. 863 80

Chyluria is the passage of chylus into urine resulting in fistulization through the lymphatic system and the urinary system. This rare condition is usually caused by filaria infestation or malformations, neoplasia or trauma. We report a case of a 18-year-old man. The patient presented milky urine which had appeared after angiography following minor leg trauma. Physical examination revealed asymmetry of the face and cutaneous dyschromia. Blood tests revealed hypogammaglobulinemia and altered CD4/CD8 ratio (0.6). Urine tests showed proteinuria (30 mg/dl), lipiduria (triglycerides 750 mg/dl) and density of 1025. Renal function was normal. Abdomen computed tomography and urography were normal. Cystoscopy revealed the presence of milky urine in the bladder and selective catheterization revealed that the origin was the right ureter alone. Ascendent pyelography did not reveal any malformation of the urinary tract; but after this the chyluria spontaneously disappeared. The patient was rehospitalized 3 months later for recurrence. Lymphography was then performed and revealed a dilated lymphatic network with minute lacunar images projecting into the right kidney. Chyluria again disappeared spontaneously and recurred sporadically over the next two years in a patient who remained in good physical condition. The etiology of chyluria in a patient without filaria infestation is problematic, particularly when the most common causes (tuberculosis, neoplasia, trauma) are excluded as in our case. The asymmetry of the face, together with cutaneous dyschromia and the presence of a subarachnoidea cyst in the right temporal region suggested our patient had multiple congenital malformations.
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PMID:[Intermittent chyluria in a young man]. 872 1

In rats, transient prophylactic anti-CD4 therapy with the nondepleting mAB RIB5/2 prevents acute rejection of MHC-mismatched allografted kidneys and induces long-lasting unresponsiveness. However, little is known about long-term benefits of this prophylactic anti-CD4 regimen. Here we report experimental results of permanently accepted rat renal allografts after prophylactic anti-CD4 treatment in regard to signs of chronic rejection. Kidneys from Wistar Furth donors were orthotopically grafted into bilateral nephrectomized BDIX recipients under the cover of anti-CD4 treatment (20 mg/kg b.w). Kidney function was serially monitored by measurement of serum creatinine and urine protein excretion. After 100 or 300 days respectively renal allografts were harvested, histologically and immunohistologically assessed and intragraft cytokine gene expression determined. Serum creatinine increased in few allografted rats. 30% of the 300-day-old grafts had an increased proteinuria and higher degrees of glomerular sclerosis. In these grafts cellular infiltration was more pronounced. However, no activated leukocytes (IL-2 receptor positive) were detected. Correspondingly, intragraft gene expression of CD3, IL-10 and IFN gamma was low. The results of our study indicate that a prophylactic anti-CD4 regimen diminishes chronic rejection to a level comparable to isografted or naive mass-reduced or ischemic kidneys. Thus, the signs of chronic rejection observed seem to be mainly caused by alloantigen-independent processes.
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PMID:Assessment of chronic rejection in permanent accepted renal allografts in anti-CD4 treated rats. 873 73

Glomerular and interstitial leukocyte infiltrates were studied by indirect immunoperoxidaze technique using monoclonal antibodies against all leukocytes, pan-T lymphocytes, helper/inducer CD4 cells, suppressor/cytotoxic CD8 cells, pan-B lymphocytes, monocytes/macrophages and polymorphs in 23 renal biopsy samples obtained from children with minimal change disease (MCD). The cases were classified on the basis of light, electron microscopy and immunofluorescence. Nephrotic syndrome was steroid-sensitive in 15 patients (group I) and steroid-resistant in 8 subjects (group II). Both groups did not differ in the type or number of glomerular immune cells, quantified as immunopositive cells per glomerular cross section. Intraglomerular cellular infiltrates were mainly constituted of monocytes/macrophages; among T lymphocytes T helper/inducer cells predominated over T cytotoxic/suppressor cells. Enumeration of interstitial immune cells showed significantly higher number of all leukocytes and T lymphocytes, quantified as immunopositive cells/mm2, in steroid-resistant group. T helper/inducer cells predominated over T cytotoxic/suppressor cells in the renal interstitium in steroid-responsive and in steroid-resistant MCD. The leukocyte infiltrates did not correlate with a degree of proteinuria at the tine of biopsy and with the renal cortical interstitial volume in both studied groups. Our data suggest, that steroid resistance in minimal change nephropathy in children seems to be related to interstitial T lymphocytes.
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PMID:Monoclonal antibody analysis of glomerular and renal interstitial immune cells in steroid-resistant and steroid-responsive minimal change disease in children. 891 22

MRL/lpr mice develop lymphoproliferation and accelerated autoimmune glomerulonephritis from which they ultimately die. To investigate the role of IFN-gamma in the manifestation of the disease, we generated MRL/lpr mice lacking the IFN-gamma receptor (MRL/lpr gammaR -/-). The absence of IFN-gamma signaling had no effect on generalized lymphoproliferation, expansion of CD4- CD8- double-negative T cells, or hypergammaglobulinemia. By contrast, glomerulonephritis as detected by proteinuria and histology was absent in MRL/lpr gammaR -/- mice. While serum IgG1 anti-dsDNA Abs were increased in all three strains of MRL/lpr mice (gammaR +/+, +/-, -/-), those of the IgG2a and IgG3 isotypes were low in MRL/lpr gammaR -/- mice. Immune complexes and C3 deposition were dramatically reduced in the glomerular capillaries of MRL/lpr gammaR -/- mice compared with MRL/lpr gammaR +/+ and +/- mice. Therefore, IFN-gamma plays a key regulatory role in the development of nephritis in MRL/lpr mice. Low levels of IFN-gamma-dependent IgG2a and IgG3 autoantibodies in MRL/lpr gammaR -/- mice might protect them from the pathogenic features of IgG3 cryoglobulins and complement-activating IgG2a and IgG3.
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PMID:IFN-gamma is essential for the development of autoimmune glomerulonephritis in MRL/Ipr mice. 916 71


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