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)

Samples of renal tissue from 373 patients were examined for the presence of immunoglobulin E (IgE) by immunofluorescent techniques. Only trace to ++ amounts ( on a scale of ++++) were found in 20 patients: 4/9 with post-streptococcal acute glomerulonephritis (GN), 5/30 with GN associated with systemic lupus erythematosus, 3/20 with membranous GN, 1/4 with Goodpasture's syndrome, 2/18 with recurrent microhematuria and focal GN, 1/5 with hemolytic anemia and uremia, 3/73 with renal homografts, and 1/5 with dermatomyositis. No IgE was found in 18 patients with lipoid nephrosis, 8 of whom were being treated with prednisone, nor in 5 patients with focal glomerular sclerosis and the nephrotic syndrome. Serum IgE was measured in 9 of the 20 patients with glomerular deposits of this globulin. With one exception, levels of IgE were within the range generally considered to be normal. However, they were greater than the mean of this range in all but two and near the highest limits of normal in most. Neither the amounts of serum IgE nor the degree of proteinuria could be related to the intensity of stain for IgE in the glomeruli of these patients.
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PMID:Immunoglobulin E in renal disease. 5 86

This paper describes the characterization of proteinuria in Aotus monkeys infected with quartan malaria (Plasmodium brasilianum), using a micro-disc-electrophoresis system. In the post infection urine samples, increases in total proteinuria, albuminuria and gamma-globulinuria were noted a few weeks after peak parasitaemia. Two new proteins also appeared in the urine of malaria infected animals. These findings are discussed with reference to the belief that the Aotus-P. brasilianum system can be a model for human malaria in renal immunopathology.
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PMID:[Proteinuria in quartan malaria-infected Aotus monkeys]. 5 72

The authors examined, by means of disc electrophoresis, urine, obtained from football players before and after a match of the championship of the "A" republican football group. Proteinuria after effort was manifested by a considerable excretion of albumin, but there were also serum proteins: postalbumin, transferin, gamma-globulins and fractions found at the place of alpha2-macroglobulins till a complete resemblence of serum electrophoresis. Electrophoresis of lactate-dehydrogenase revealed the presence only of two quick fractions, mainly LDH-1, which increased after effort as well. The fractions of nonspecific esterases were of predominantly tissue origin but after effort of serum origin. The results were discussed in connection with various mechanisms, which could cause proteinuria after physical effort.
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PMID:[Disc electrophoresis of urinary proteins. Changes after exertion]. 5 60

Swiss albino mice infected with Plasmodium berghei berghi showed the serum-soluble malarial antigen and antibody on day 10 of infection onward. Immune complex nephritis in these mice developed on the seventh day after inoculation. The infected kidneys revealed the deposition of mouse gamma globulin, mouse beta1C globulin and malaria antigen along the capillary wall of the glomeruli. Proteinuria was detected on seventh day of infection. Serum-soluble malaria antigen in probably responsible for forming the soluble immune complex which causes glomerulonephritis in infected mice.
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PMID:Serum-soluble malarial antigens and immune complex nephritis in Plasmodium berghei berghei infected mice. 5 12

An experimental model has been developed in the dog in which a renal allograft was placed in the neck, leaving one of the dog's own kidney in situ. Five nonimmunosuppressed pairs of dogs have been studied by using the leucocyte migration test (LMT) as an in vitro measure of cell-mediated immunity. Antigen preparations from leucocytes, kidney, liver, and skeletal muscle from both the kidney donor and the recipient were used in the LMT in order to study responses against transplantation and organ-specific antigens. Inhibition of migration with donor-specific leucocyte and kidney antigens was detectable prior to clinical evidence of rejection, which was confirmed histologically. Concurrently, inhibition was also observed with autologous kidney antigen and histological damage was noted in the recipient's own nontransplanted kidney, accompanied by increasing proteinuria. Autologous serum withdrawn daily and added to the test culture medium abolished the inhibition of migration, thus suggesting the development of blocking factor.
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PMID:Allograft immunity to histocompatibility and organ-specific antigens. 5 81

The clinical manifestations of severe pre-eclampsia are normally separated from those of mild pre-eclampsia and normal pregnancy on arbitrary grounds. A clinical index, based on the increase in diastolic blood-pressure and the presence of proteinuria, was developed to reflect the spectrum of disease from mild to severe pre-eclampsia. This was related to a coagulation index based on the platelet-count, plasma-factor-VIII, and serum-fibrinolytic-degradation-products. The two indices were shown to be strongly correlated. All cases of perinatal death associated with pre-eclampsia had coagulation indices in the most severely abnormal range. These results suggest that intravascular coagulation is a highly characteristic feature of pre-eclampsia and that the coagulation index may be of value in monitoring the progress of the disease.
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PMID:Use of coagulation tests to predict the clinical progress of pre-eclampsia. 6 May 64

Assuming that urination is the principle route by which alpha-fetoprotein (A.F.P.) passes into the amniotic fluid from the normal fetus, and that A.F.P. is mainly degraded by a process of fetal swallowing and digestion, 4 possible mechanisms by which amniotic-fluid A.F.P. is increased by fetal abnormalities are postulated.(1) Amniotic-fluid A.F.P. is increased in open neural-tube defects by leakage of A.F.P. from fetal serum and cerebrospinal fluid.(2) In exomphalos exposure of blood-vessels in the extruding viscera permits transudation of A.F.P. into the amniotic fluid.(3) In nephrosis, fetal proteinuria increases amniotic-fluid A.F.P.(4) Impaired fetal swallowing or digestion would account for increased amniotic-fluid A.F.P. in congenital malformations of the orogastrointestinal tract.
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PMID:Mechanisms by which amniotic-fluid alpha-fetoprotein may be increased in fetal abnormalities. 6 May 74

A 34 years old white male patient suffering from a seropositive "probable" rheumatoid arthritis developed a severe hypocomplementemic mesangiocapillary glomerulnophritis. Rheumatoid factor-Latextest and Waaler-Rose-Titers and IgM have been found highly elevated in the serum. The third component of complement (C3) was markedly depressed, while the fourth component (C4) was within the normal range. The rapid progression of both diseases forced us to start an immunosuppressive drug therapy using azathioprine and steroids, 18 months after the beginning of the treatment the patient is well, has only slight proteinuria, normal levels of complement and no joint pain. The possible connections between rheumatoid arthritis and mesangiocapillary glomerulonephritis in this case as well as the therapeutic approaches are discussed.
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PMID:[Mesangiocapillary glomerulonephritis and rheumatoid arthritis. A case with diagnostic and therapeutic questions (author's transl)]. 6 Nov 63

The nephrotoxic activity of prepared antibodies against previously isolated glycoproteic fractions of the Rat glomerular basement membrane was studied using Masugi's model of Nephritis. This activity was determined by following the daily evolution of the proteinuria and the value of the seric complement. It seems linked to numerous factors.
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PMID:[Study of the nephrotoxicity of antibodies directed against the glomerular basement membrane glycoproteins of the Wistar rat]. 6 26

Indian childhood cirrhosis is a significant cause of morbidity and mortality in young children in India. One hundred patients with ICC, 66 boys and 34 girls, were studied. Pedigree analysis yielded a segregation ratio of 0-2196, suggestive of an autosomal recessive inheritance. Serum alpha1-antitrypsin level was normal. Serum alpha-foetoprotein (AFP) concentration was increased in all the patients, parents and in some siblings. Serum immunoglobulins G, A, M, and D were elevated. Haemolytic complement and C3 were low. Electrophoretically altered complement components were detected in 36% of patients. There was an inverse relationship between C3 concentration and immunoconglutinin titre. Circulatingimmune complexes were detected in the sera of six out of ten patients who had significant proteinuria. Hepatitis B surface antigen (HBsAg) was present in the serum, ascitic fluid, saliva, urine and faeces of ICC patients more frequently than in controls. HBsAb was detected less often. Lymphocyte response to HBsAg was impaired. The first-degree relatives had a higher incidence of HBsAg and HBsAb than healthy controls. It is suggested that ICC occurs in infants with an inherited hepatocyte vulnerability and that one of the precipitating causes of liver cell necrosis is infection with hepatitis virus(es). The consequent immunologic epiphenomena contribute to progressive hepatic damage ending in death.
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PMID:Indian childhood cirrhosis: genealogic data, alpha-foetoprotein, hepatitis antigen and circulating immune complexes. 6 6


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