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)

Reflux nephropathy (RN), the main complication of the vesico-ureteral reflux (VUR), relatively frequent in adults, is often the consequence of recurrent urinary infections in the child, hood or during pregnancy. Unilateral RN has generally a benign course but the bilateral one, with important nephron destruction, leads to focal and segmental glomerulosclerosis, manifested by high levels of proteinuria. A certain degree of cicatrization and renal failure are followed by progressive impairment of the remaining renal function, even if VUR is cured. An early diagnosis, treatment of the acute bacterial infection, adequate ingestion of liquids, regulation of the intestinal transit and complete bladder voiding by miction, associated with hypotensive and antiinfectious drug therapy lead to VUR disappearance in 80% of the cases, avoiding renal failure. Surgery is indicated only in the patients with severe reflux and with congenital or obstructive anomalies, as well as in the case of recurrent infection resistant to antibiotherapy.
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PMID:Reflux nephropathy in adults. 129 13

Renal involvement has been well documented in patients with hepatosplenic schistosomiasis and in patients with prolonged Salmonella bacteremia (PSB). Whether there is a specific renal lesion related to PSB or the chronic bacterial infection aggravates a pre-existing schistosomal glomerulopathy has been a matter of controversy. To analyze the clinical manifestations and histopathological findings of the renal involvement, 8 patients with hepatosplenic schistosomiasis and PSB (group I) were compared with 8 patients with schistosomal glomerulopathy (group II) matched by sex and glomerular disease. The mean age in group I was 17.7 years. All patients presented with hematuria, in 4 cases associated with non-nephrotic proteinuria. In group II the mean age was 23 years; nephrotic syndrome was the clinical presentation in 7 of the 8 patients in the group. All patients in group I experienced remission of the clinical and laboratory abnormalities as the salmonella infection was cured; in group II the patients had persistent, steroid-resistant, nephrotic syndrome. On histological examination, no difference was noted between the two groups, except for pronounced glomerular hypercellularity and interstitial mononuclear cell infiltration in group I. These observations strongly suggest that PSB exacerbates a pre-existing sub-clinical schistosomal glomerulopathy by the addition of active lesions directly related to the prolonged bacteremia.
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PMID:Renal involvement in prolonged Salmonella bacteremia: the role of schistosomal glomerulopathy. 134 69

Patients with systemic lupus erythematosus experience clinical exacerbation during superimposed bacterial infection. Previous studies in mice indicated that heightened immune phenomena during exposure to bacterial lipopolysaccharide (LPS) appear to be related, in part, to polyclonal B cell activation, to abnormal disposal of immune complexes (IC), and to increased localization of IC in tissues. To investigate whether such effects were reversible, we administered bacterial LPS to C57BL/6 mice for 5 weeks. Control mice received vehicle alone. We then discontinued LPS, and 6 weeks later LPS and control mice were challenged with a subsaturating dose of radiolabeled IC; the removal of IC from the circulation, their localization in the liver, spleen, and kidney were determined. In comparison to values in control mice, in mice previously exposed to LPS, serologic features of polyclonal B cell activation persisted; liver uptake of pathogenic IC (greater than Ag2Ab2) was normal, but removal of small size IC (less than or equal to Ag2Ab2) from the circulation was delayed; localization of IC in the kidneys was enhanced, and pathologic proteinuria developed. The effects of repeated exposure to bacterial LPS are partially reversible, but they last long after LPS is discontinued and may contribute to altered disposal of IC, enhanced organ localization of IC, and organ dysfunction.
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PMID:Defective disposal of immune complexes and polyclonal B cell activation persist long after exposure to bacterial lipopolysaccharide in mice. 281 Dec 99

Urinary trypsin inhibitory capacity is mainly due to the excretion of a glycoprotein which is immunologically related to the inter alpha-trypsin inhibitor and may be a proteolytic degradation product of that substance. It was tested in 133 subjects divided into 7 groups: 24 healthy controls (group A), 21 patients with bacterial infection (group B), 37 with bacterial infection under antibiotic therapy (group C), 25 with connective tissue disease (group D), 8 with infected connective tissue disease (group E), 14 with cancer (group F) and 4 with infected cancer (group G). Urinary trypsin inhibitory capacity level was very low in controls (3.32 +/- 0.8 U/g urinary creatinine), but it was dramatically increased when infection was present (149.67 +/- 23.6 U/g urinary creatinine). This test appeared to be more effective than serum C-protein measurement simultaneous carried out in the same patients. Urinary trypsin inhibitory capacity is not related to the degree of proteinuria in the urine sample, but it is increased in patients with chronic renal failure excluded from this study. Thus, its measurement is a sensitive, easy and useful test for detecting and monitoring infections. The return to its physiological value is a very good argument in favour of therapeutic effectiveness.
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PMID:[Clinical value of the determination of urinary antitrypsin activity]. 296 52

A single observer reviewed 842 of the 917 known diabetic patients registered with 40 GPs in the Poole area. A midstream urine specimen was tested for proteinuria using Albustix (Ames) and cultured to detect bacterial infection. After the first 3 months of the survey, the aliquot of this specimen was frozen for later determination of the random albumin/creatinine ratio (R-Alb/Creat). Patients were requested to submit a timed overnight urine collection for estimation of urinary albumin excretion rate (AER). Of the 842 patients reviewed, 493 (59%) submitted timed overnight urine collections; 43 were excluded because of urinary infection and/or proteinuria. One hundred and thirty-three (30%) of 450 diabetic patients were found to have microalbuminuria, although only 31 (7%) had an AER greater than 30 micrograms/min. Six hundred and seven urine samples were collected for R-Alb/Creat but 68 were excluded because of infection and/or proteinuria; in 10 further samples urinary creatinine was not measured. Two hundred and four (38%) of 532 diabetic patients were found to have an elevated R-Alb/Creat. There was a significant correlation between AER and R-Alb/Creat (r = 0.32, p less than 0.001) but a considerable number of patients showed either a normal AER and high R-Alb/Creat or the reverse. The value of R-Alb/Creat or an overnight urinary albumin concentration, or an overnight urinary albumin/creatinine ratio (ON-Alb/Creat) as screening tests to predict AER greater than 30 micrograms/min was assessed. An ON-Alb/Creat greater than 2.0 mg/mmol was the optimal screening test (sensitivity 96% and specificity 99.7%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Microalbuminuria in diabetes: a population study of the prevalence and an assessment of three screening tests. 296 83

Thirty-six patients received allogeneic (34) or syngeneic (two) bone marrow transplants as treatment for severe aplastic anaemia or acute leukaemia. Nineteen of the allogeneic recipients received methotrexate (MTX) and 15 received cyclosporin A (CyA) as the predominant immunosuppressive agent to minimize graft-versus-host disease (GVHD) post transplant. In the first 100 d post transplant renal dysfunction was much less frequent in the MTX recipients than in the CyA recipients who exhibited three distinct syndromes of nephrotoxicity: most commonly. CyA recipients developed asymptomatic azotaemia, proteinuria, urinary casts, impaired urinary concentrating ability and hypertension. Secondly, two CyA recipients developed acute reversible renal failure precipitated by systemic bacterial infection which required dialysis and in which the kidney was the sole target organ; thirdly, two recipients of HLA-genotypically non-identical grafts developed a rapidly progressive fatal syndrome with multiple organ involvement including lung, brain and kidney which clinically and histologically resembled thrombotic thrombocytopenic purpura.
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PMID:Cyclosporin A associated nephrotoxicity in the first 100 days after allogeneic bone marrow transplantation: three distinct syndromes. 634 55

Baboons with long term, indwelling, intravascular catheters developed clinical signs of renal and hepatic impairment. These included proteinuria and hypoalbuminemia without edema, and albumin to globulin ratios were reversed. Serum IgM, IgG, rheumatoid factor, and liver enzyme concentrations were above normal. Immunofluorescent staining of renal glomerular capillary loops was positive for IgG, IgM, B1c, and C4. Major microscopic lesions were membranoproliferative glomerulonephritis, chronic active hepatitis, degenerative arthritis, and chronic sialoadenitis. Electron microscopy of renal glomeruli demonstrated dense deposits in a variety of locations, mesangial cell interpositioning, and foot process fusion. These alterations, found in conjunction with the isolation of Staphylococcus aureus from the blood of affected baboons as well as the intravascular catheters, suggested that chronic bacterial infection was important in the pathogenesis of this disease.
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PMID:Immune complex glomerulonephritis in baboons (Papio cynocephalus) with indwelling intravascular catheters. 645 37

The clinical, laboratory and pathologic findings were studied in 62 consecutively autopsied patients with multiple myeloma between 1954 and 1975. All patients were 40 years of age or older. Bone pain was the initial symptom in 2/3 of patients. Anemia (81%), thrombocytopenia (29%), azotemia (41%), hypercalcemia (46%) and hyperuricemia (52%), were common laboratory findings at diagnosis. Ninety-seven percent had a monoclonal protein in serum or urine. Extensive plasma cell replacement of marrow was invariably seen at autopsy although in 15% of patients no abnormality was found on skeletal survey. Extraskeletal spread (67%) was due to direct extension to paraosseous tissue resulting from cortical destruction and to distant organ involvement mainly of splenic red pulp and hepatic sinusoids. The patients were susceptible to bacterial infection, mainly gram-negative, of the lung (56%), urinary tract (35%), and blood (24%). Fungal infection was less frequent and usually consisted of superficial candidal overgrowth of gastrointestinal tract ulcerations (18%). Amyloidosis (10%) was perivascular and associated with light chain proteinuria. Renal failure as a cause of death (21%) was secondary only to infection (52%). Severity of histologic findings in the kidney at autopsy had little correlation to initial BUN concentration. The median survival was 11.5 months with alkylating agent therapy (responders, 29 months; non-responders, 6 months), and 6 months with urethan. Initial azotemia (greater than 80 mg/dl) and hypercalcemia (greater than 12 mg/dl) were important prognostic indicators (median survival, less than 1 month and 3 months, respectively). A good response to alkylating agent therapy, initial BUN less than 40 mg/dl and serum calcium less than 12 mg/dl were favorable to prognostic indicators.
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PMID:Multiple myeloma: a clinicopathologic study of 62 consecutively autopsied cases. 743 54

A 25-year-old man was admitted with complaints of fever and macrohematuria. Laboratory tests showed a substantial increase in serum creatine phosphokinase and creatinine in association with myoglobinuria and proteinuria. Blood culture grew Streptococcus salivarius and Streptococcus oralis. Findings of renal biopsy were compatible with IgA nephropathy. The glomeruli had a mild mesangial proliferation without crescentic lesions. Changes of the interstitium and tubules were not evident. The clinical course and laboratory results strongly suggested a possible link between Streptococcus salivarius/oralis infection, and rhabdomyolysis. Rhabdomyolysis is rarely seen as a complication of bacterial infection, and the present case emphasizes the importance of suspecting bacteremia due to Streptococcus salivarius/oralis in the presence of rhabdomyolysis.
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PMID:Rhabdomyolysis associated with bacteremia due to Streptococcus viridans. 856 22

Staphylococcal neutral phosphatase (NPtase) is a highly cationic bacterial surface bound protein. It has significant affinity for human and rat immunoglobulins in vitro and an electrostatic interaction may be involved. Radioisotopic studies showed that NPtase had a high affinity for the polyanionic structures of the rat renal glomerulus. When the left kidneys of germ-free or naive (non-immune) Wistar rats were perfused with 80 micrograms of I125 NPtase, 21 micrograms of NPtase were found in the left kidneys and 11 micrograms in the isolated glomeruli 15 minutes after perfusion. Deposits of autologous immunoglobulin and C3 were seen in the glomeruli of rats immediately after perfusion with NPtase (15 min) and persisted throughout the 14-day observation period. Histologically, neutrophil influx into the glomerulus was seen at 15 minutes and increased until three hours; subepithelial electron-dense deposits were found after three days and were still visible on day 14. Proteinuria started within the first 24 hours despite the absence of an immune response at this time and was still present on day 14. Similar results were observed in immune deficient athymic nude rats in the early phase. Perfusion of heparin after NPtase inhibited the deposition of IgG and C3 and prevented proteinuria in naive but not in actively immunized rats. This result provides further evidence that specific antibodies to NPtase were not involved in the immune complex-like deposits seen in the early phase. NPtase is a novel molecule, as it reveals both high affinity for the GBM and binding of circulating immunoglobulins, by a non-antigen-antibody mechanism, to form IC-like deposits on the GBM. These deposits are capable of activating the complement system, thus triggering a series of events leading to glomerulonephritis. These results delineate an additional pathway for the pathogenesis of ICGN related to bacterial infection.
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PMID:Induction of glomerulonephritis in rats with staphylococcal phosphatase: new aspects in post-infectious ICGN. 880


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