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 records of 1,000 asymptomatic male air force personnel were examined retrospectively for the results of 15 yearly examinations (1968 through 1983) of urinary sediment, beginning with subjects aged 18 to 33 years. The cumulative incidence of four to six or more WBCs per high-power field on one or more examinations was 31.8% after an average of 12.2 examinations per person over the 15-year period. In 107 subjects the WBCs were found on two or more occasions within five consecutive examinations. In 106 subjects, 140 urine cultures were sterile. In 28 cases the urine was also sterile after culture for Mycobacterium tuberculosis. Intravenous pyelograms, obtained in eight cases, were normal. Renal biopsy in one case with recurrent hematuria and trace proteinuria showed focal glomerulonephritis. All subjects are currently active and free of urinary symptoms an average of 7.6 years after detection of leukocyturia.
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PMID:The importance of leukocyturia in young adults. 397 Jun 52

To determine the nature and frequency of renal disorders in AIDS we reviewed the records of thirty-two patients hospitalized over a twenty-two month period. Group I, including all patients with AIDS who demonstrated proteinuria and/or renal insufficiency, numbered thirteen patients, in ten of whom renal tissue was available. Renal abnormalities included proteinuria in twelve patients, which exceeded two grams per day in seven. The glomerular histologic lesions included focal glomerulosclerosis, diffuse mesangial hypercellularity, diffuse proliferative glomerulonephritis, and membranoproliferative glomerulonephritis. The nonglomerular histologic lesions included acute tubular necrosis, nephrocalcinosis, focal interstitial nephritis, and one case each of intrarenal cryptococcal infection and renal cell carcinoma. Nine of these thirteen patients developed renal insufficiency, and four of them required dialysis. Their mortality by the end of the study period was eleven of thirteen patients (85 percent), significantly worse in the short term than AIDS patients without renal problems. The patients in Group I were compared to the nineteen AIDS patients without renal abnormalities in Group II. The Group I patients had a higher incidence of oral and esophageal candidiasis, other fungal infections, and infections with Mycobacterium avium-intracellulare. They also had a higher incidence of exposure to aminoglycoside antibiotics and amphotericin B, and experienced more clinical shock than their Group II counterparts. It is concluded that patients with AIDS may demonstrate renal abnormalities on the basis of immune, hemodynamic, infectious, and neoplastic derangements.
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PMID:Renal disease in patients with AIDS: a clinicopathologic study. 673 86

It was recently proposed that the diabetes genes of non-obese diabetic (NOD) mice are linked to the Bcg gene that is associated with resistance to infection by mycobacteria; however, it has not been established whether NOD mice are resistant or susceptible to the infection, although there are previous investigations on response of NOD mice to other intracellular parasites (e.g. Kaye et al., Eur. J. Immunol. 22: 357-364). We have investigated here this question, as well as the consequences of mycobacterial infection on the natural history of murine diabetes. Female NOD mice were intraperitoneally infected with 10(8) viable bacilli of Mycobacterium avium at 2 months of age, i.e. before the mice show diabetes; they were studied up to the sixth month of age (when more than half of untreated female NOD mice show glycosuria). To determine whether NOD mice were susceptible or resistant to M. avium infection, we have compared the kinetics of bacterial growths in liver and spleen of the mice with those determined in M. avium-susceptible (BALB/c) and resistant (C3H) strains of mice. NOD mice were able to control the M. avium infection, following a pattern similar to that observed in infected C3H mice. The mycobacterial infection prevented the expression of diabetes in all of the infected NOD mice and it also decreased the incidence of proteinuria in the treated mice. The infected NOD mice showed a marked enhancement in antibodies against the 65,000 mycobacteria antigen (heat-shock protein (hsp) 65) up to the second month of infection and these elevated titres slowly decreased in the following months; anti-hsp 65 antibodies were not detected in age-matched controls. This is the first demonstration that NOD mice are naturally resistant to mycobacterial infection, and we reinforce evidence on the role of immune response triggered by mycobacteria and its hsp 65 antigen in prevention of diabetes in NOD mice.
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PMID:Diabetes-prone NOD mice are resistant to Mycobacterium avium and the infection prevents autoimmune disease. 891 Nov 35

A 31-year-old man who presented with smear- and culture-negative pulmonary tuberculosis had associated macroscopic hematuria, elevation of serum creatinine and immunoglobulin A (IgA) levels, overt proteinuria, and peripheral edema. Renal biopsy revealed focal mesangial proliferation with IgA deposits, and a diagnosis of IgA nephropathy was made. The patient received treatment with isoniazide and rifampin. After 4 months, pulmonary lesions were almost completely healed, and a significant improvement of creatinine clearance with normalization of serum creatinine and IgA levels and disappearance of proteinuria were observed. Treatment with isoniazide and rifampin was discontinued after 6 months, without reappearance of either pulmonary or renal symptoms. Two years after the diagnosis of IgA nephropathy, the patient is in good general condition. Serum creatinine and IgA levels are normal, proteinuria is absent, and there is neither macrohematuria nor microhematuria. These findings suggest that IgA nephropathy may be a consequence of tuberculosis, possibly due to an abnormal IgA-mediated immune response against Mycobacterium tuberculosis with formation of nephrotoxic immune complexes.
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PMID:Immunoglobulin A nephropathy complicating pulmonary tuberculosis. 1055 77

Renal granulomatoses represent 0.5%-0.9% of nephropathies examined by renal biopsies. Granulomas can be isolated to the kidney or associated with other tissue involvement. We describe 40 consecutive patients with renal granulomatoses, associated with pauci-immune crescentic glomerulonephritis in 2 patients and with vasculitis in another, seen in northeastern Paris hospitals between January 1991 and February 2004. The criterion for inclusion was the presence of 1 or more epithelioid granulomas in the renal interstitium. Our population of 25 men and 15 women had a median age of 53 years. All patients suffered from renal insufficiency with median creatininemia of 236.8 micromol/L (range, 124-805 micromol/L), associated with hypertension (25%), median proteinuria of 0.6 g/24 h (range, 0.08-3.00 g/24 h), microscopic hematuria (15%) and leukocyturia (22.5%). Histologic examination of extrarenal specimens detected granulomas in 82.4% of the bronchial biopsies taken, and in 100% of the 2 skin biopsies, the 2 lymph-node biopsies, and the liver and colon biopsies. The following etiologies were retained: sarcoidosis for 20 (50%) patients, drug-induced for 7 (17.5%), tuberculosis for 3 (7.5%), Wegener granulomatosis for 2 (5%), and leprosy, Mycobacterium avium infection, and Crohn disease for 1 (2.5%) patient each. No etiology could be identified for 5 (12.5%) patients. Treatment must be adapted to the etiology of each case. The renal outcome after treatment was generally favorable, with the estimated median creatinine clearance increasing from 26 mL/min (range, 5.4-80.0 mL/min) to 46.5 mL/min (range, 0-118 mL/min) after a median follow-up of 35.5 months (range, 3-158 mo). Nonetheless, 32 patients had persistent renal insufficiency; 1 required hemodialysis and another underwent renal transplantation. Sarcoidosis and medications are the most common causes of renal granulomatosis. Idiopathic and drug-induced forms do not relapse after treatment discontinuation, and remission persists at long-term follow-up.
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PMID:Renal granulomatoses: a retrospective study of 40 cases and review of the literature. 1750 56

A 54-year old man was admitted to our hospital because of high fever, productive cough and purpura in both legs in June 2005. Urinalysis showed microscopic hematuria and proteinuria. Chest radiograph showed consolidation of right upper field. Because acid-fast bacilli and polymerase chain reaction test for Mycobacterium tuberculosis were positive in bronchial lavage fluid, we made a diagnosis of pulmonary tuberculosis, and prescribed antituberculosis therapy with isoniazid, rifampicin, ethambutol and pyrazinamide. In addition, anaphylactoid purpura was diagnosed by skin biopsy. In July 2005, renal function was deteriorated and nephrosis appeared. We treated with corticosteroid in addition to antituberculosis therapy. His symptoms and renal dysfunction improved. We report a rare case of an anaphylactoid purpura following occurence of pulmonary tuberculosis.
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PMID:[A case of anaphylactoid purpura associated with nephrosis followed by pulmonary tuberculosis]. 1878 34

Tuberculosis-related chronic granulomatous tubulointerstitial nephritis (GTN) and chronic renal dysfunction as a consequence of GTN is a rarely seen clinical condition, with a few case reports in the literature. In this report, a case with end stage renal failure as an unexpected late extrapulmonary sequela of tuberculosis has been presented. A 60 years old female patient was admitted to hospital with the complaints of fever, malaise and nausea. Her history revealed that she had pulmonary tuberculosis 30 years ago and received antituberculosis therapy for nine months. The laboratory results on admission were as follows: blood urea nitrogen 90 mg/dl, serum creatinine 9 mg/dl, sodium 116 mEq/L, potassium 6.6 mEq/L, albumine 2.9 g/dl, hemoglobin, 8.4 g/dl, white blood cell count 10.800/mm3, C-reactive protein 187 mg/L and erythrocyte sedimentation rate 110 mm/hour. Urinalysis showed 8.1 g/L protein, 10-12 leukocytes, 1-2 erythrocytes, while 24-hours urinalysis yielded proteinuria with 8 ml/minutes creatinine clearance value. Urine and blood cultures of the patient revealed neither bacteria or mycobacteria. PPD skin test was negative. Acid-resistant bacilli (ARB) were not detected in sequential urine samples obtained on three consecutive days. Since sputum samples could not be obtained, diagnostic procedures for sputum were not performed. Abdomen ultrasonography yielded bilateral edema and grade II echogenity in kidneys. Computed tomography of the chest showed bilateral pulmonary nodules, chronic sequela lesions, pleural scarring and calcifications, as well as minimal interstitial infiltrate. Transthoracic lung biopsy showed chronic inflammation and fibrosis, while amyloid was negative. Renal biopsy showed GTN with central caseified necrosis and granulomas, multinuclear giant cells, tubular atrophy and interstitial fibrosis. Amyloid was negative and ARB were not detected in renal biopsy sample. Definitive diagnosis was achieved by the demonstration of Mycobacterium tuberculosis nucleic acid in kidney biopsy by polymerase chain reaction (PCR). Antituberculosis therapy was not initiated since there were no signs of active tuberculosis. The patient became clinically stable following dialysis and was discharged, however, she has been undergoing hemodialysis three times a week. The aim of this case presentation was to emphasize that renal tuberculosis should be considered in the differential diagnosis of patients with end stage renal failure, especially in countries like Turkey where tuberculosis incidence is high.
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PMID:[Chronic renal failure: unexpected late sequela of pulmonary tuberculosis after 30 years]. 2164 81

A 72-year-old man with ESRD on hemodialysis was referred to the hospital because of hemoptysis. A chest radiograph showed diffuse infiltration in the right lung field. Laboratory data showed hematuria and proteinuria. A kidney biopsy revealed diffuse crescentic glomerulonephritis with linear staining of IgG along the glomerular basement membrane (GBM). However, circulating IgG anti-GBM antibodies were not detected. Because the findings of renal biopsy suggested Goodpasture's disease, the patient was treated with plasmapheresis and pulse steroid therapy, which resulted in a rapid resolution of his pulmonary symptoms and chest radiograph abnormalities. However, sputum culture on admission yielded Mycobacterium tuberculosis 3 weeks later. Therefore, immuosuppressive agents were discontinued and antituberculous agents were administered. There was no relapse of pulmonary hemorrhage during the next 1-year period of follow-up, but the patient did not regain renal function and remained on hemodialysis.
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PMID:Pulmonary hemorrhage complicating Goodpasture's disease in the course of pulmonary tuberculosis. 2282 44

A 66-year-old man with uremia and on hemodialysis was referred to our hospital because of hemoptysis. A chest radiograph showed diffuse infiltration in the right lung field. Laboratory data were remarkable for renal failure accompanied by hematuria and proteinuria. A kidney biopsy revealed diffuse crescentic glomerulonephritis with linear staining of IgG along the glomerular basement membrane (GBM). Circulating IgG anti-GBM antibody was not detected. Because the findings of renal biopsy suggested anti-GBM disease, the patient was treated with plasmapheresis and pulse steroid therapy, which resulted in a rapid resolution of his pulmonary symptoms and chest radiograph abnormalities. However, sputum culture submitted on admission yielded Mycobacterium tuberculosis 3 weeks later. Therefore, immunosuppressive agents were discontinued and antituberculous agents were administrated. No relapse of pulmonary hemorrhage occurred during the next 1-year period of follow-up, but the patient did not regain renal function and remained on hemodialysis.
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PMID:Anti-glomerular basement membrane glomerulonephritis with subsequent pulmonary hemorrhage in the course of pulmonary tuberculosis. 2295 Aug 33

The reports of glomerular lesions of kidney due to tuberculosis are sparse. A 48-year-old gentleman, presented with swelling of feet of 3 months duration. As he had renal impairment, proteinuria and normal-sized kidneys, he was subjected to renal biopsy. The light microscopy and immunofluorescence revealed the diagnosis was membrano-proliferative glomerulonephritis. During hospital stay, the patient complained fever and stiffness at thoracic spine. The MRI of thoraco-lumbo-sacral spine revealed paravertebral abscess at D11-D12. The pus aspirated was positive for Mycobacterium tuberculosis. He was started on anti-tuberculous medication. After 8 weeks of therapy, the serum creatinine was 1.5 mg/dL and 24 h urine protein 250 mg.
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PMID:Membranoproliferative glomerulonephritis and Pott's disease. 2585 15


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