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 renal lesions of a 5-year-old girl with progressive systemic sclerosis are described. The nephropathy was clinically characterised by moderate proteinuria, microscopic hematuria and transient hypertension. Light microscopy showed membranoproliferative glomerulonephritis of segmental character. On electron microscopy intramesangial, subendothelial and extramembranous glomerular deposits were observed. By immunofluorescence miscrosocpy deposit of IgG, Clq, C4, C3, C5, C8 and C9 in a predominantly subendothelial location were found in all glomeruli. Vascular lesions were of minor degree. Histological and immunohistological findings are compatible with an immune complex disease.
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PMID:Membranoproliferative glomerulonephritis in systemic sclerosis of childhood. 15 Jun 97

Hypothyroidism, microscopic hematuria, and proteinuria developed in an 11-year-old girl. A renal biopsy specimen showed increased mesangial cells and matrix with focal glomerular basement membrane thickening. Three years later, a pronounced increase in proteinuria was detected. Elevated levels of antibody to thyroid microsomal antigen and thyroglobulin were found in the serum. A renal biopsy specimen showed a pronounced increase in mesangial cells and matrix with generalized glomerular basement membrane thickening. Electron microscopic studies demonstrated granular deposits in the capillary walls and mesangium. Immunofluorescent studies revealed granular deposits of IgG, IgM, and C3, primarily on the glomerular basement membrane. By indirect immunofluorescence, granular glomerular basement membrane and mesangial staining were detected with antibody specific for thyroglobulin and thyroid microsomal antigen. These observations suggest development of immune complex glomerulonephritis mediated by thyroid antigens.
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PMID:Immune complex glomerulonephritis mediated by thyroid antigens. 15 97

Twelve inbred rat strains were tested for their susceptibility to autologous immune complex glomerulonephritis (AIC) after a single injection of a primary tubular epithelial fraction emulsified in Freund's complete adjuvant. Six strains (Lewis, AS, BDV, L.BDV, AS2, L.AS2) showed high responsiveness in terms of proteinuria and immunohistological changes, which could be observed after 3 months. Strains BN, AVN and DA were completely resistant, even after 6 months of observation. An additional adjuvant (pertussis vaccine) did not break non-responsiveness in one of these strains (BN). Strains which share the Lewis strain genetic background (L.BN, L.AVN and L.WP) seemed to be at least weakly susceptible to AIC. A close association between susceptibility and the major histocompatibility haplotypes is demonstrated in segregation studies involving Lewis, L.BN and BN rats. A threshold model of AIC susceptibility, based on the action of major histocompatibility-linked genes and background genes, is suggested.
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PMID:Genetic control of susceptibility to autologous immune complex glomerulonephritis in inbred rat strains. 15 75

Decreased synthesis (hypomorphism) of the fast variant of the third component of complement was detected in three generations of a family in which the propositus has an immune complex-type glomerulonephritis, arthritis, and a false positive test for syphilis. An affected sibling has bursitis, hematuria, and proteinuria. Decreased serum C3 protein was detected in three of four and decreased C3H50 in four of four family members with this hypomorphic variant (C3f). This is the first association between C3f and immune complex-type disease.
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PMID:Hypomorphic variant of C3, arthritis, and chronic glomerulonephritis. 15 8

Functional, histological and immune-histological examination were performed in altogether 64 Wistar-rats, in order to control the effect of a therapy with 2 mg/kg per body weight indomethazine lasting 2 months at the model of an experimental immune complex nephritis. In 44 rats after presensibilisation an immune complex nephritis was performed by intraperitoneal injections with human serum albumin which were repeated three times a week. 24 glomerulonephritis animals and other 20 animals without glomerulonephritis were daily administered indomethazin through a tube probe, the remaining 20 animals with glomerulonephritis served as untreated control groups. The excretion function of the kidney was tested before the beginning of the experiment, 2 weeks after the beginning of the therapy and the regular serum injections, respectively, and before the end of the experiment by determination of the biological half-life period of 131J-hippuran. In every case one day before this the proteinuria during 24 hours was determined. At the end of the experiment the kidneys were examined histologically and immune-histologically. The results showed that indomethazin does not lead to a clear influence on the proteinuria in the immune complex nephritis of the rat. The excretion of 131J-hippuran was significantly restricted, whereas the histological and immune-histological preparations in the animals with foreign serum injections showed clear changes of the glomeruli in the sense of an early stage of the immune complex nephritis, however, they did not show any essential influence by indomethazin. That is, indomethazin had altogether no favourable effect on the immune complex nephritis of the rat.
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PMID:[Treatment of experimental immune complex nephritis with indomethacin]. 15 98

Experimental glomerulonephritis was produced in 16 rabbits by intravenous injections of ovalbumin in high doses (0.1 g/day during the first week, 0.2 g x 6/day during the second). The animals were killed on day 14. At that time all animals had 2--4+ proteinuria and a serum C3 level reduced to about 50% of the control level; 11 animals had a significantly raised blood urea level. In all rabbits the antigen had induced severe proliferative glomerulonephritis. Electron microscopy showed that many of the cells accounting for the hypercellularity were monocytes. Surprisingly, electron dense deposits were few and small, mainly on the subendothelial and subepithelial aspects of the glomerular basement membrane. In all the animals ultrastructural immunoperoxidase technique revealed deposits containing ovalbumin, rabbit IgG and C3. With immunofluorescence sparse deposits were occasionally seen. It is concluded that a severe experimental glomerulonephritis can be produced in a state of antigen excess, with the deposition of immune complexes being minimal. Immuno-electron microscopy is essential, however, in detecting even the smallest animals of deposited immune reactants.
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PMID:Glomerulonephritis induced by high doses of ovalbumin. Studies by electron microscopy, immunofluorescence and immuno-electron microscopy. 15 29

This investigation was initiated to study and correlate the clinical and ultrastructural aspects of glomerulonephritis induced in the laboratory mouse by the intraperitoneal injection of a sublethal dose of murine cytomegalovirus. An attempt was made to ascertain the pathogenesis of the glomerular changes and the resultant viremia. Murine cytomegalovirus infection caused an acute transient glomerulonephritis in young female mice of the HA/ICR strain. Mice that survived a sublethal inoculation of homogenized infected gland developed transient proteinuria and excreted tubular casts. The murine cytomegalovirus infection resulted in a glomerular lesion that was selective for the mesangial cell. After entering the mesangial cell by phagocytosis the virus replicated in the nucleus and was excreted into the channel of the mesangial matrix, with extension toward the periphery of the capillary loop and adjacent to the urinary space. Virus particles were rarely found in the glomerulus after the 5th day of infection and chronic renal disease was not observed.
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PMID:Murine cytomegalovirus glomerulonephritis: clinical and ultrastructural observations. 18 Aug 54

Histologic and immunopathologic studies were performed at autopsy on the kidneys of a patient in whom hematuria and proteinuria developed in association with cytomegalovirus (CMV) pneumonitis. Light microscopic examination of the kidneys revealed focal mesangial proliferative glomerulonephritis. Immunofluorescent microscopy revealed a granular deposition of IgG, IgA, C3, and C4, mainly in the mesangium. CMV antigens were also demonstrated in a similar immunofluorescent pattern. Glomerulus-bound immunoglobulins were eluted and demonstrated to contain antibodies to CMV antigens. These findings suggest that in some patients who have CMV infection immune-complex glomerulonephritis is induced by glomerular deposition of CMV antigen-antibody complexes.
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PMID:Immune-complex glomerulonephritis associated with cytomegalovirus infection. 22 31

In 26 cases of myelofibrosis, the authors investigated for possible renal impairment that can be appraised from the usual clinical, laboratory, and roentgenographic signs. No anomalies were demonstrated in 12 of these cases. In 14 (or 53%) of the patients, some anomaly was discovered : essentially proteinuria with minor alteration of renal function, but also, two cases of poorly functioning left kidney evidenced on intravenous urograms, one case of acute anuric renal failure connected with hyperuricemia, one case of hypokalemic tubulo-interstitial nephritis, and one case of glomerulonephritis with, nephrotic syndrome. This study, when compared to the literature, indicates that besides nephropathy specific to myelofibrosis and attributed to myeloid metaplasia in the kidney, serious consideration must be given to lesions due to (1) compression of the left kidney by the enlarged spleen, (2) urate precipitation in the urinary passages, and (3) a possible glomerular disorder whose mechanism remains undefined.
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PMID:[Renal lesions in myelofibrosis (author's transl)]. 22 98

The purpose of the present paper was to study clinical, morphological and immunological aspects of late rejection of renal allotransplants. We have, therefore, analyzed the occurrence and nature of renal transplant disease and graft failure among 125 recipients surviving for 1 to more than 8 years after transplantation. In this population transplant disease as defined by the appearance of heavy proteinuria and/or steadily declining graft function occurred in 22 patients. At the closure date of the study on December 31, 1972 complete graft failure had occurred in 12 of these 22 patients and 4 of these have died. In addition two patients died in the presence of normal graft function, due to chronic hepatitis and metastatic cancer respectively. As based on clinical findings, pathophysiological features and renal lesions the patients with late transplant disease were classified into two groups and described accordingly. Group A, termed glomerular transplant disease, included a majority of 16 patients, constituting a rather homogenous idsease entity in relation to course of disease, clinical findings and renal lesions as studied by light-, immunofluorescence- and electron microscopy. All these patients presented with heavy proteinuria, which was non-selective in all but two, resulting eventually in complete loss of graft function in eight cases. All these patients developed hypoalbuminemia and hypercholesterolemia, and one half manifested a classical nephrotic syndrome. Arterial hypertension occurred in all patients except two. Glomerular structure as studied by light microscopy revealed a number of lesions of a rather polymorphous pattern in all patients in group A. Endomesangial proliferation, hyperplasia and segmental proliferation of epithelial cells and thickening of capillary walls were prominent features, although the degree of severity, extension and type of lesion occurred in such varying proportions that classification into any well characterized category of glomerulonephritis was not possible. All cases in group A revealed immune deposits, most frequently containing IgG, IgM, complement and fibrinogen. IgA, IgD and IgE were also demonstrated in a lesser proportion of cases in this group. The immunofluorescent pattern was a mixed granular and linear, and in no case strictly linear or granular alone. The ultrastructural investigation contains a detailed analysis of the
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PMID:Late failure or human renal transplants. An analysis of transplant disease and graft failure among 125 recipients surviving for one to eight years. 23 63


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