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)

Adult female (NZB/NZW)F1 hybrid mice with documented autoimmune glomerulonephritis resembling systemic lupus erythematosus were treated with fractionated total lymphoid irradiation (TLI), a modification of the radiotherapeutic regimen currently used for the treatment of Hodgkin disease. After TLI, proteinuria subsided in all mice that had undergone radiotherapy, and the mean survival increased from 359 days in untreated controls to 545 days. It is suggested that TLI should be further investigated as a new approach for immunoregulation of autoimmune disorders.
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PMID:Successful treatment of autoimmune disease in (NZB/NZW)F1 female mice by using fractionated total lymphoid irradiation. 29 44

The incidence of asymptomatic proteinuria in young healthy men entering the army service in Singapore was 0.94%; 0.56% had intermittent orthostatic proteinuria and 0.38% with persistent proteinuria. Renal biopsies from 45 cases with persistent proteinuria and 10 cases with orthostatic proteinuria were studied by light microscopy, electron microscopic and immunofluorescent antibody techniques. Three cases with orthostatic proteinuria showed a minimal lesion ('Nil'), and 7 a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity. Focal and segmental capillary loop changes were seen in two cases. No immunoglobulin deposits were found in orthostatic proteinuria. A raised anti-streptolysin O titer was found in 3 cases. 13.3% of cases with persistent proteinuria showed a minimal lesion ('Nil'); 66.6% a minimal lesion with increased centrilobular mesangial matrix and mild focal and segmental mesangial hypercellularity: Focal global sclerosis, focal segmental sclerosing glomerulonephritis and diffuse proliferative GN (mesangial hypercellularity) were each found in 6.7% of patients in this group. Focal and segmental changes in capillary loops were found in 30% of cases. Changes in visceral epithelium such as the appearance of cytoplasmic swelling, vesicles and dense aggregates, and areas of focal foot process fusion were common findings. Mesangial deposits of IgA were found in 34.3%, with an IgA-IgG-beta1C globulin combination in 28.6% of cases. IgM-beta1C globulin was present in 5.7% of cases with persistent proteinuria. Early complement components, C1q and C4, and IgA secretory piece were absent. A raised antistreptolysin O titer was found in 25% of cases. The changes inthe glomeruli may represent the end or healing stages of an early bout of glomerulonephritis. Changed hemodynamic responses on assuming an upright position may play a role in the loss of protein across the glomerular basement membrane in patients with orthostatic proteinuria.
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PMID:Glomerular lesions in patients with asymptomatic persistent andorthostatic proteinuria discovered on routine medical examination. 31 47

The incidence and early recurrence after transplantation prove the specificity of the appearance of an electron dense alteration of kidney basement membrane often called dense intra-membranous deposit disease. Three new cases with dense deposit disease affecting the original kidneys have been followed-up after transplantation for periods ranging from 4 to 8 years and illustrate the natural history of the recurrence. Serial kidney biopsies showed the predominance of dense deposits near the mesangial area and the vascular pole. These deposits were also seen in some tubular basement membranes. Absence of cell proliferation was noted in all biopsies performed. Immunofluorescence studies revealed fixation of C3 alone. Histological signs of recurrence are compatible with the absence of clinical and biological signs. Transient or permanent proteinuria and microhematuria were common findings. Serum complement levels, measured after transplantation, were low in all three cases. Despite recurrence of the original glomerulonephritis, long-term survival of the graft was commonly observed, two cases being followed-up for 7 and 8 years. Patients with dense intra-membranous deposits glomerulonephritis should not be excluded from a transplantation program. One of the three cases reported here illustrates the exceptional association of recurrence of dense intramembranous deposits, de novo membranous glomerulonephritis and chronic rejection.
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PMID:Dense deposit disease: long term follow-up of three cases of recurrence after transplantation. 31 48

Three children with cyanotic congenital heart disease who developed transient proteinuria and edema are described. One died of an intercurrent illness but the other two are now well. Renal biopsy findings in all three children demonstrated a mesangial proliferative glomerulonephritis on light microscopy. An unusual ultrastructural appearance of localized electron-dense thickening of the basement membrane of the capillary loops was seen in all three and collagen fibers were present in the mesangium of two. There was slight fusion of foot processes in two specimens and marked fusion in the third. Immunofluorescence in two patients demonstrated IgM staining in both and fibrin in one. The cause of the glomerular lesions is unknown but, among the many possible factors involved, anoxia and increased venous pressure may be important.
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PMID:Nephropathy in cyanotic congenital heart disease. 31 49

The kidneys of three patients who died of pneumonia due to Klebsiella pneumoniae were studied at autopsy by light and immunofluoerescent microscopy. One had no clinical evidence of renal disease; two had only microscopic hematuria and mild proteinuria. Light microscopy revealed focal proliferative glomerulonephritis in all three cases. Also in all three, immunofluorescent microscopy revealed a granular deposition of capsular polysaccharide antigens of Klebsiella pneumoniae in association with immunoglobulins and complement components in the mesangium and along the glomerular basement membrane. Furthermore, the glomerular bound immunoglobulins were eluted and demonstrated to contain antibodies specific to a capsular polysaccharide antigen of Klebsiella pneumoniae isolated from each patient. These findings may illustrate that the capsular polysaccharides of Klebsiella pneumoniae are antigenic, and that the immune complex deposition in the kidney during infection with this agent can be associated with renal morphological changes. Whether or not clinical evidence of nephritis occurs may depend on the characteristics of the infection and the host factors.
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PMID:Immune complex glomerulonephritis associated with Klebsiella pneumoniae infection. 32 Nov 71

Detailed immunopathologic studies of early or silent renal alterations in systemic lupus erythematosus have been sparse. The renal biopsies of 16 lupus patients with normal renal function, including 8 with hematuria and/or proteinuria of recent onset, and 8 without clinically detectable renal disease were investigated by light, immunofluorescence, and electron microscopy. Immunoglobulins, complement components, and electron-dense deposits were detected in glomeruli of all patients, regardless of morphologic appearance or lack of clinical evidence of renal involvement. Features of membranous glomerulonepritis were observed in 4 patients with substantial proteinuria. In the remaining 12 patients, including 3 with hematuria and 4 with slight proteinuria, either minimal glomerular alterations or features of mesangial proliferative glomerulonephritis were seen. Transformation of the original disease was demonstrated in 3 of 3 patients rebiopsied within 2 years. The significance of these findings is discussed in relation to a) the spectrum of clinical and immunopathologic alterations in lupus nephritis and b) transformation of the original disease.
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PMID:Immunopathology of early and clinically silent lupus nephropathy. 32 2

Correlations between immunofluorescent protein deposits in the glomeruli, urinary sediment and proteinuria selectivity pattern have been attempted in different glomerulonephritis. The overall study showed following results: a) Glomerular and urinary casts deposits of immunoglobulins, C3 and fibrin/fibrinogen are related to moderately selective proteinuria; b) IgG and IgA are most often found in urinary sediment and c) Glomerular deposits of IgG and IgA are well correlated with the presence of these immunoglobulins in urinary casts. Analysis according to different histological types of nephritis: a) In "minimal changes" nephropathy, deposits are infrequent and well correlated with urinary sediment, when they are present; b) In lupus nephritis, constant and intense glomerular deposits of immunoglobulins, fibrin/fibrinogen are correlated with the same proteins found in urinary casts; c) Inconstant correlations are found in membranous nephritis and in IgA-IgG nephropathy.
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PMID:Study of the correlation between glomerular and urinary sediment deposits using immunofluorescent technique. 32 33

Two major categories of membranoproliferative glomerulonephritis (MPGN) designated type 1 and 2 MPGN are currently recognized, largely on the basis of characteristic morphologic and immunofluorescence features. In contrast to experience reported from outside the United States, type 2 MPGN has been observed rather infrequently in this country. In a retrospective clinicopathologic study, 24 kidney specimens obtained from 10 children and young adults including seven females and three males (mean age: 13 years) with type 2 MPGN were identified using light, immunofluorescence, and electron microscopy. The histopathologic findings were related to the clinical course of each patient. When initially seen all patients had hematuria and proteinuria, three were nephrotic, and five were mildly hypertensive. A single patient was mildly azotemic. Eight patients had experienced an upper respiratory ifnection preceding their illness, although only one patient had evidence of a streptococcal pharyngitis. During a period of follow-up averaging 10 years, eight patients were nephrotic at some time during their illness and seven were persistently so. Hypertension was a major problem in eight patients and renal function declined markedly within a year of its onset in five. Persistence of the nephrotic syndrome from early onset of the disease, especially when associated with hypertension, was an additional sign of poor prognosis. Four patients developed chronic renal failure and three received one or more renal allografts. Histologic evidence of recurrent disease was found in allografts from the three patients as early as 7 months after transplantation in the absence of clinical features indicative of recurrent glomerulonephritis. It is concluded that type 2 MPGN is a chronic progressive renal disease of unknown etiology and pathogenesis which chiefly afflicts children and young adults. Hypertension and the early and persistent presence of the nephrotic syndrome suggest a poor prognosis. The disease appears to be largely unresponsive to conventional forms of therapy. The disease recurs with great frequency in allografts, often in the absence of clinical evidence of recurrent glomerulonephritis.
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PMID:Membranoproliferative glomerulonephritis with dense intramembranous alterations. A clinicopathologic study. 32 95

In this paper, cell-mediated immunity (CMI) as evaluated by in vitro migration inhibition assays an in vivo delayed type skin reactions in experimental immune complex glomerulonephritis (ECGN) was studied as well as the effect of treatment with immunosuppressive drugs on these immune responses. In glomerulonephritic rats MIF production as well as delayed type skin reactions could be demonstrated directed against tubular brushborder antigen (Fx1A) containing immune complexes or to their constituents (FX1A or rabbit IgG). Treatment of the animals with immunosuppressive drugs during settled disease state (autologous phase) abolished these cellular immune reactions. However, neither the glomerular depositions of rat IgG associated with the autologous phase, nor the urinary excretion was influenced. When treatment of the animals was started simultaneously with the induction of the ECGN both cellular and humoral immune responses as well as proteinuria were affected. It was concluded that although in this glomerulonephritis model specific MIF response after specific stimulation in vitro as well as DTH reactions could be detected against immune complexes or their constituents, these immune reactions seem not to play important role in this ECGN in particular with respect to the proteinuria.
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PMID:Expermental glomerulonephritis in the rat induced by antibodies directed against tubular antigens. III. In vitro evaluation of cell-mediated immune responses against immune complexes influenced by immunosuppressive therapy. 32 7

Acute pulmonary silicoproteinosis, massive proteinuria and fatal renal failure developed in a 23 year old male sandblaster. Examination of the kidney by immunofluorescence revealed granular deposits of immunoglobulin M (IgM) and the third component of complement (C3) along the glomerular basement membrane. Light microscopy disclosed mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures. The silicon content of the kidney was 264 parts per million (ppm), but particles of silicon were not demonstrated by electron microscopy. No primary or systemic causes of renal diseases were elucidated. The renal dysfunction apparently resulted from acute renal silicon toxicity, a new complication of acute pulmonary silicoproteinosis.
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PMID:Massive proteinuria and acute renal failure in a patient with acute silicoproteinosis. 34 91


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