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)

We report herein the case of a 14-year-old female who has acute tubulo-interstitial nephritis (AIN) associated with bilateral diffuse uveitis. She was admitted for the evaluation of "proteinuria", following general fatigue and weight loss about 2 weeks ago. Her laboratory data showed mild anemia, hyper gamma-globulinemia, mild proteinuria, and the reduced glomerular filtration rate with the increased urinary excretion of beta 2-microglobulin. The histological examination obtained by renal biopsy showed mild edema and diffuse infiltration of mononuclear cells in interstitium without any glomerular or vascular abnormalities, which were compatible with AIN. As for the etiology of AIN, clinical investigations could not reveal any specific causes, such as bacterial and viral infections, drugs and systemic diseases. About 4 months after the onset of nephritis, she also became to suffer from bilateral diffuse uveitis. Therefore, the diagnosis of the acute tubulo-interstitial nephritis and uveitis syndrome (TINU syndrome) (Vanhaesebrouck et al., 1985) could be confirmed. In her clinical course, it was noteworthy that uveitis relapsed frequently in spite of systemic administration of prednisolone, and it took two years until uveitis cured, whereas the AIN subsided spontaneously prior to the specific treatment. In this case, characteristic findings of granulomatous uveitis was closely similar to those of sarcoidosis, which has been rarely reported in TINU syndrome. In this respect, the involvement of immune processes, especially cell-mediated, was suggested as the possible pathogenesis in this case.
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PMID:[A case of acute tubulo-interstitial nephritis and uveitis syndrome]. 219 32

This article describes a case of Goodpasture's syndrome controlled by double filtration plasmapheresis (DFPP) combined with steroid and immunosuppressant therapy. A 48-year-old male, clerk, complaining of fever, dry cough and macroscopic hematuria, was admitted to our hospital. Microscopic hematuria was first pointed out at age 40 on an annual check up. His laboratory data on admission revealed severe anemia, azothemia, macroscopic hematuria and proteinuria. His chest radiograph and CT revealed diffuse nodular densities in bilateral lung fields. Specimens obtained by transbronchial lung biopsy and open renal biopsy revealed linear deposition of IgG by direct immunofluorescent antibody methods. Circulating antiglomerular basement membrane antibody level determined with radioimmunoassay was 1.8% on admission, but one week later it elevated to 5.6% with progression of dyspnea, hypoxemia, and renal failure. Steroid pulse therapy and a total of 6 double filtration plasmaphereses were performed in the first month. Subsequently hypoxemia and dyspnea disappeared, and the chest radiograph of the 40th hospital day showed no abnormal shadows. Two months later recurrence of pulmonary hemorrhage was noticed. Immunosuppressant administration (Cyclophosphamide 100 mg/day) and a total of 10 DFPP procedures were performed with success. By DFPP, circulating anti-GBM antibody fell rapidly to within normal ranges, and anti-GBM antibody level elevated in removed plasma. We think DFPP is effective to remove circulating anti-GBM antibody in Goodpasture's syndrome.
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PMID:[Double filtration plasmapheresis in case of Goodpasture's syndrome]. 221 5

Experimental and spontaneous infections with Corynebacterium suis in sows were investigated. In early stages animals show no clinical disorders or only for a short time. However, there are already marked changes in urinary samples (hematuria, proteinuria, leukocyturia, gross alterations). Using an endoscope mucosal irritations can be seen mainly on the floor of the bladders. In chronic cases alterations in urine are more pronounced. If a pyelonephritis is present in addition to the cystitis, general signs of illness are evident including anorexia, emaciation, anemia, subnormal body temperature and abortions. Bladders demonstrate an erosive and ulcerative, hemorrhagic cystitis on the whole mucosal surface. Uremia appears only in late stages of the disease.
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PMID:[Corynebacterium suis infection in swine. 1. Clinical diagnosis with special consideration of urine studies and cystoscopy]. 221 5

A rare case of idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia (IPL) associated with chronic renal failure was described in this report. A 73-year-old male was admitted and diagnosed as IPL. IPL is proposed by Mori et al. in 1980. Clinical entity of IPL is (1) Polyclonal hyperimmunoglobulinemia (2) Systemic Lymphadenopathy characterized by remarkable mature plasmacytosis without atypism and by no destruction of the structures. (3) All disease with polyclonal hyperimmunoglobulinemia can be excluded. In this patient, physical findings showed enlarged lymph nodes (1-2 cm) in bilateral nuchal, submandibular, axillary and inguinal lesions. Laboratory examinations showed polyclonal hyperimmunoglobulinemia (especially IgG, IgA), anemia and renal dysfunction. Microscopic observation of hematoxylin-eosin staining in the axillary lymph node showed increased mature plasma cells without evidence of malignant growth. Immunoperoxidase staining showed intracytoplasmatic polyclonal immunoglobulins. IPL is known as invading other organs besides lymph node, for example skin, lung or kidney. This patient showed renal dysfunction (Cr clearance 11 ml/min, severe proteinuria). Nine cases of IPL and multicentric plasma cell type Giant Lymphnode Hyperplasia (GLH) concurrent with renal dysfunction were reported. Only in two of them chronic renal failure were reported. Twice a week hemodialysis improved his condition and laboratory findings.
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PMID:[A case of idiopathic plasmacytic lymphadenopathy with polyclonal hyperimmunoglobulinemia associated with chronic renal failure]. 228 6

Chronic renal failure developed in 5 patients who were taking germanium dioxide (GeO2)-containing compounds. Renal functional deterioration was slow but progressive and dialysis treatment was necessitated temporarily in 2 patients. After the discontinuation of GeO2, the impaired renal function tended to improve but remained abnormal for an observation period of 10-40 months. The lack of proteinuria and hematuria was characterized as the clinical manifestations. Renal biopsy specimens revealed the tubular epithelial cell degeneration containing hematoxylin-positive fine granules on light microscopy, and electron-dense inclusions in the swollen mitochondria on electron microscopy. These findings localized mainly in distal segment of the tubules. In the rats given GeO2 orally for 10 weeks, similar histological lesions were evident, as manifested by marked weight loss, anemia, azotemia, and negative proteinuria. In the rats given carboxyethylgermanium sesquioxide, these changes were not observed and Ge concentration of kidney was significantly lower than in the rats given GeO2. The present study indicates that chronic GeO2 intake causes progressive renal dysfunction characterized by the degeneration of distal tubules.
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PMID:Germanium dioxide-induced nephropathy: a new type of renal disease. 229 45

A case of IgD myeloma that began with high paraproteinaemia, BJ proteinuria of type and 40% marrow plasmacellular infiltration is reported. These onset data suggested a large tumoral mass and hence a poor prognosis. On the other hand, after subjecting the patient to 4 polychemotherapy cycles (alkeran and prednisone) CM disappeared from serum and urine and bone lesion progression stopped. It is also stressed that this from presents clinical (frequent extra-osseous growth, presence of amyloidosis), laboratory (severe anaemia, renal insufficiency, BJ proteinuria) and particular prognostic features.
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PMID:[IgD myeloma. Presentation of a case and review of the literature]. 231 11

Recombinant human erythropoietin (r-HuEPO) therapy for anemia in chronic renal failure patients could have unfavorable renal effects since reversal of anemia can raise blood pressure and accelerate experimental glomerular injury. Thus, the effects of r-HuEPO on renal and systemic hemodynamics and the progression of renal disease were studied in predialysis chronic renal failure patients. The clearances of inulin and p-aminohippurate, fractional excretions of albumin and immunoglobulin G, cardiac output, plasma renin activity and aldosterone concentration were assessed at baseline, after short-term r-HuEPO (n = 4) or placebo (n = 4) therapy, and after long-term r-HuEPO for all patients (n = 8). In addition, the slope of l/serum creatinine with time was determined before and during continued r-HuEPO therapy. In contrast to placebo therapy, hematocrit increased with r-HuEPO from 32 to 37% after 7.6 +/- 2.7 weeks (mean +/- SD). Antihypertensive drug therapy was increased in 2 patients in each group. Renal function, cardiac output, plasma renin activity and aldosterone did not change significantly in either group. After 18 +/- 9 weeks of therapy for all patients, hematocrit increased from 31 to 39%. Antihypertensive drug therapy was increased in 5 patients and decreased in 1. Renal function decreased while proteinuria tended to increase. Cardiac output, plasma renin activity and aldosterone did not change. During 37 +/- 22 weeks of r-HuEPO therapy, the slope of l/serum creatinine did not worsen in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal function during erythropoietin therapy for anemia in predialysis chronic renal failure patients. 234 56

A 73-year-old male was admitted to our hospital in October 1987 because of severe anemia, anorexia, and loss of weight. The hemoglobin level was 5.7 g/dl, the white blood cell count 2,500/microliters with 5% myeloblasts positive for peroxidase, and the platelet count 8.6 x 10(4)/microliters. The LDH was 656 mU/ml, the total protein in the serum 7.4 g/dl, IgG 419 mg/dl, IgA 104 mg/dl, IgM 10 mg/dl, and urine Bence Jones (BJ) protein 8.8 g/day. The X-ray survey of the bones showed multiple osteolytic lesions. A bone marrow aspirate was hypercellular with 91.4% plasma cells, and was cultured a whole day for chromosome study. It revealed an abnormal karyotype of 46, XY, -15, t(6; 14) (p21.1; q32.3), +der(15)t(1; 15) (q23; q24). Immunoelectrophoresis demonstrated lambda type BJ protein. He was treated with melphalan and prednisolone. Proteinuria and marrow plasma cells decreased in amount. In December a white cell count was 6,030/microliters with 80% myeloblasts. A bone marrow aspirate revealed an increase of 82.6% myeloblasts or promyelocytes. The patient was refractory to chemotherapy and died of sepsis in April 1988. An unrelated abnormal karyotype; 48, XY, +8, +13 appeared concomitant with an increase of the leukemic cells, but no cells showed the t(6; 14). We cytogenetically discussed the simultaneous presence of multiple myeloma with acute myelogenous leukemia.
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PMID:[Acute myelogenous leukemia (M2) simultaneously associated with multiple myeloma with special reference to chromosome abnormality of t(6; 14) (p21.1; q32.3)]. 236 41

Acute non-suppurative tubulointerstitial nephritis was recorded within a five-month interval in 1988 in one girl and two boys aged 15, 16 and 12 years. The common feature was non-selective proteinuria, slight glycosuria, anaemia, a sedimentation rate of more than 100 mm/2 hrs hyperatotaemia not calling for dialyzation treatment (268, 354 and 266 mumol/l plasma creatinine resp.), a markedly impaired concentrating capacity (540, 593 and 520 mOsm/kg urine resp.). In all patients circulating serum immunocomplexes were elevated (PEG-IKEM). One patient developed acute uveitis at the onset of the disease, the remainder after 5 and 6 months resp. and in all there was a tendency of a protracted course and relapses resp. In two patients uveitis was diagnosed by an aimed examination by means of a slit lamp at a time when there were not yet any clear signs of affection of the eyes. All patients were subjected to percutaneous renal biopsy which revealed an interstitium with uneven lymphoplasmacytic cellulization with infrequent eosinophil and neutrophil polynuclear cells. Electron microscopy revealed sections of varying size with fibrotization of the tubular basal membrane; the glomerular changes were not typical. All patients had prednisone treatment and their renal functions were gradually restored. Despite extensive serological examinations, the aetiology was not cleared, however before the onset of the disease the patients had penicillin, cotrimoxazol and erythromycin resp.
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PMID:[Acute interstitial nephritis with uveitis in children and adolescents]. 239 34

Toxic side effects of germanium dioxide contained in drugs that promote health, include nephropathy, anemia and peripheral neuropathy. Although the neuropathy, which we are interested in, is believed to occur in the patients taking excessive amounts of germanium dioxide, the pathogenesis of such neuropathy is not well understood. Therefore, we studied whether germanium dioxide causes the degeneration of the peripheral nerve in rats and monkeys. Our results showed that in rats, germanium dioxide administered orally and intraperitoneally, 100 mg/kg per day, 3 days a week for 8 weeks and 400 mg/kg per day, once a week for 8 weeks, respectively, did not produce a degeneration of myelinated fibers in teased fiber preparations and Epon-embedded sections of the peripheral nerve. In two monkeys also, germanium dioxide, administered orally, 30 to 40 mg/kg per day, 5 days a week for 8 months, did not produce a degeneration of myelinated fibers of the sural nerve on biopsy, although our results revealed proteinuria and elevated blood urea nitrogen. Further studies are warranted to elucidate the pathogenesis of germanium dioxide induced neuropathy.
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PMID:[Evaluation of germanium dioxide neurotoxicity in rats and monkeys]. 251 Feb 28


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