Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Experimental pathogenicity was for the first time demonstrated in a strain of C. lusitaniae of clinical origin by the use of concentrated inocula (5.10(7) Y-shaped cells) and the administration of 4 mg of methylprednisolone acetate i.m. injected 4 days before and 3 days after the inoculation. Counts on malt-agar (fig. 1) in kidney and brain showed a decrease during the first 12 hours, followed by a definite increment in cell number between the first and second day. Clinical tests showed a strong proteinuria, high levels of blood urea and creatinine, and a low GOT increase. Glycemia, GPT, and total serum protein values were normal. Histological examinations of kidney showed a delayed penetration with discrete clumps of Y-shaped cells, inflammatory focuses, and compromised tubules and glomerula (Fig. 2). After 2 weeks of study accumulations of cells followed by degenerative phenomena were seen in the various structures examined. Reparation processes were seldom observed (Fig. 3-4).
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PMID:[Experimental pathogenicity of Candida lusitaniae in mice]. 729 97

Although the occasional occurrence of glomerulonephritis associated with hepatitis C virus (HCV) infection has been reported recently in the literature, the type described has been mainly membranoproliferative glomerulonephritis (MPGN); membranous glomerulonephritis (MGN) is very rare. In this paper, two cases of MGN associated with HCV infection are reported. Case 1 was a 56-year-old male who had positive HCV Ab and HCV RNA. The diagnosis of chronic active hepatitis was verified by liver biopsy. Laboratory data showed proteinuria (5g per day), hematuria and hypocomplementemia by hemolytic assay. Renal biopsy led to the diagnosis of MGN in stage II. The patient was treated with interferon alpha for 6 months, resulting in improvement of hypocomplementemia, transient reduction of GOT and GPT during the course of treatment. The GOT and GPT were aggravated again after the completion of therapy. No improvement was seen in proteinuria and hematuria, and HCV Ab remained positive. Case 2 was a 69-year-old male who had positive HCV Ab and HCV RNA, and had normal liver function. Subsequently, his GOT value was slightly elevated. Proteinuria (2g per day) was demonstrated. The diagnosis of MGN in stage II was made on the basis of renal biopsy. The clinical characteristics of these two cases suggest that MGN is a type of glomerulonephritis associated with HCV infection.
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PMID:[Two cases of membranous glomerulonephritis associated with hepatitis C virus infection]. 781 54

Halogenated anilines and aminophenols are nephrotoxicants and hepatotoxicants in mammals. The purpose of this study was to determine the in vivo and in vitro nephrotoxic and hepatotoxic potential of 4-amino-2,6-dichlorophenol, a putative metabolite of 3,5-dichloroaniline. In the in vivo experiments, male Fischer 344 rats (four/group) were administered a single intraperitoneal (i.p.) injection of 4-amino-2,6-dichlorophenol (0.25, 0.38 or 0.50 mmol/kg) or vehicle (dimethylsulfoxide (DMSO), 1.0 ml/kg) and renal and hepatic function monitored for 48 h. Only minor changes in function or morphology were observed in the 0.25 mmol/kg treatment group. However, in the 0.38 mmol/kg treatment group evidence of both nephrotoxicity and hepatotoxicity were evident. Nephrotoxicity was characterized by increased proteinuria, glucosuria, hematuria, elevated blood urea nitrogen (BUN) concentration and kidney weight, decreased p-aminohippurate (PAH) accumulation and proximal tubular necrosis in the corticomedullary region of the kidney. Hepatotoxicity was characterized by elevated plasma alanine aminotransferase (ALT/GPT) activity and liver weight. Animals administered the 0.5 mmol/kg dose died within 24 h. In the in vitro experiments, the effect of 4-amino-2,6-dichlorophenol on organic ion accumulation, gluconeogenesis and lactate dehydrogenase (LDH) leakage was quantitated in liver and/or renal cortical slices. Organic anion accumulation was inhibited in renal cortical slices by 4-amino-2,6-dichlorophenol bath concentrations of 5 x 10(-6) M or higher, while organic cation uptake was decreased at 4-amino-2,6-dichlorophenol bath concentrations of 1 x 10(-5) M or greater. Renal and hepatic pyruvate-stimulated gluconeogenesis were inhibited and renal LDH leakage increased at 4-amino-2,6-dichlorophenol bath concentrations of 5 x 10(-5) M or greater. Increased LDH leakage from liver slices was not observed. These results demonstrate that 4-amino-2,6-dichlorophenol is a nephrotoxicant and hepatotoxicant in vivo and in vitro and that the kidney is more susceptible to 4-amino-2,6-dichlorophenol toxicity than the liver.
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PMID:In vivo and in vitro 4-amino-2,6-dichlorophenol nephrotoxicity and hepatotoxicity in the Fischer 344 rat. 802 37

A 42-year-old female was admitted to a hospital, because of acute hepatitis A. Laboratory data were GOT 8210mU/ml. GPT 4650mU/ml, LDH 11860mU/ml, total bilirubin 4.7mg/dl, BUN 19.5mg/dl and creatinine 1.9mg/dl. Urinalysis showed proteinuria 3+ and occult blood 1+. Soon after admission, she suffered from anuric acute renal failure and was transferred to our hospital for hemodialysis. Her urine-volume was under 20 ml per day. Urinalysis showed proteinuria 4+, occult blood 1+ and casts. Laboratory data showed BUN 58.2mg/dl and creatinine 8.5mg/dl. She was treated by hemodialysis for 35 days, before recovering from renal failure. However, her renal function did not recover perfectly and her 24-hour creatinine clearance remained at 50ml/min after 6 months. Renal biopsy was performed on the 17th day after admission. Examination by light microscopy revealed the findings of acute tubular necrosis and examination by immunofluorescence antibody method was negative. Urinalysis of 8 patients with acute hepatitis A showed that all patients had proteinuria at the onset. Patients with acute hepatitis A have symptoms of appetite-loss, nausea, vomiting and/or diarrhea. These symptoms cause hypovolemia, and hepatic dysfunction causes discontrol of vasoactive hormones, which gives rise to disturbance of renal circulation. Subsequently, acute tubular necrosis and acute renal failure occur.
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PMID:[A case of acute hepatitis A associated with acute renal failure from the onset]. 823 Aug 22

A total of 34,000 adults in Fukui City who had participated in annual health examinations at least once between 1986 and 1988, were followed for a period of 5 years. The results were as follows; (1) The mortality rate during a 5 year period was significantly lower for participants in health examinations than in nonparticipants of the same age group. (2) Mortality was significantly related to obesity, systolic and diastolic blood pressure, glucosuria, proteinuria, occult blood in urine, GOT and cholesterol in man, in women obesity, systolic and diastolic blood pressure, glucosuria, proteinuria, GOT, GPT and cholesterol were related to mortality. (3) An increase in hazard ratio with increasing degree of thinness was suggested particularly in males. (4) Hazard ratios increased with decreasing cholesterol in both men and women combined. (5) Except for hypertension which increased risk for circulatory disease, none of the above data appeared to be related to specific causes of death.
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PMID:[Relationship between participation in annual health examinations and mortality rate over a 5-year period]. 867 9

A 33-year-old man presented malar rash in April, 1992. The rash had gradually developed and he was admitted to our hospital in February, 1994. Laboratory findings showed proteinuria of 0.5-0.8 g/ day, thrombocytopenia (4.8 x 10(4)/mm3), false positive serologic test for syphilis, anti-nuclear antibody with a speckled type at a titer of 1 : 80. Activated partial thromboplastin time was prolonged (41.3 s), and anti-beta 2-GPI antibody was strongly positive (56.6 U/ml on enzyme linked immunosorbent assay). The diagnosis of systemic lupus erythematosus with antiphospholipid syndrome was made and prednisolone 60 mg/day improved his manifestations. He could be discharged in July, 1994. Nine months after the discharge he developed dyspnea, and he was admitted to our hospital again. On admission the blood pressure was 212/170 mmHg, Levine III/VI systolic murmur was noted at the apex of heart. Significant laboratory findings showed as follows: WBC 15, 110/mm3 (Neu 73%, Lym 18%), RBC 380 x 10(4)/mm3, Hb 10.2 g/dl, Plt 20.0 x 10(4)/mm3, GOT 23 IU/l, GPT 21.
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PMID:[Acute cardiac failure due to dilated cardiomyopathy in systemic lupus erythematosus with antiphospholipid antibody]. 912 25

We report a 50-year-old male patient with hepatitis C virus (HCV)-associated membranous glomerulonephritis (MN), for which he had been treated with corticosteroid therapy for one and a half years. This patient received blood infusion at 38 years of age. He visited our hospital because of liver dysfunction at 42 years. One year later, proteinuria and microhematuria were pointed out (43 years). Renal biopsy revealed MN with focal fibrocellular crescents. HBsAg, cryoglobulin, rheumatoid factor were all negative. Prednisolone was administered at the dose of 30 mg/day for 4 weeks and tapered subsequently. The steroid treatment was effective (urinary protein excretion: 4.2-->0.3 g/day, serum albumin: 2.4-->4.0 g/dl, 3 months later), and transaminase slightly elevated (GPT 50-->60-80 IU/l). One and a half years later he proved to be positive for HCV antibody, and corticosteroid administration was terminated. Subsequently proteinuria increased, and reached 3.0 g/day 6 years later. However, serological markers and ultrasonographic study for chronic hepatitis revealed mild changes of the liver. These findings suggest that corticosteroid therapy is not contraindicated against HCV-associated MN, and may possibly be used as the treatment for this condition.
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PMID:[A case of hepatitis C virus associated membranous glomerulonephritis ameliorated by corticosteroid therapy]. 965 13

A 67-year-old woman was admitted to our hospital with a fever. She had been experiencing arthralgia for about one month. On admission, she had a fever of 38.5 degrees C, was anemic and was experiencing tenderness in the joints of both hands, elbows and feet. Laboratory data revealed proteinuria, urinary cylinders, pancytopenia (WBC 900/mm3, Hb 9.5 g/dl, Plt 7.8 x 10(4)/mm3), liver dysfunction (GOT 414 IU/l, GPT 140 IU/l), and hyper-gamma globulinemia. Antibiotics and granulocyte-colony stimulating factor were administered intravenously. Bone marrow aspiration was unsuccessful, but a bone marrow biopsy revealed bone marrow fibrosis. Immunological examinations were positive for antinuclear antibodies, anti-deoxyribonucleic acid (DNA) antibodies, anti-double stranded anti- DNA antibodies, as well as a decreased level of serum complement and an increased level of serum immune complexes. Tests for viral antigens and antibodies known to cause hepatitis were negative. Based on these findings, a diagnosis of SLE accompanied by liver dysfunction and bone marrow fibrosis was made. Steroid pulse therapy was initiated, but her liver function deteriorated on the first day of steroid therapy, and she died three days later. SLE accompanied by myelofibrosis is extremely rare, and only 17 and cases have been reported to date. Among these reports, the present case is the second oldest subject and the first SLE patient to suffer from both myelofibrosis and severe liver dysfunction.
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PMID:[A case of elderly-onset systemic lupus erythematosus (SLE) complicated with severe liver dysfunction and pancytopenia due to myelofibrosis]. 1068

We report a case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive, rapidly progressive glomerulonephritis(RPGN). A 60-year-old woman was admitted to our hospital for evaluation of RPGN. Laboratory evaluation revealed microhematuria, proteinuria(800 mg/day), anemia, renal failure(blood urea nitrogen 27 mg/dl, serum creatinine 2.2 mg/dl), cryoglobulinemia, hypocomplementemia, positive MPO-ANCA(232 EU), and hepatitis C virus infection(GOT 58 IU/l, GPT 38IU/l, HCV-RNA(PCR) 1,200 kcopy/ml, serotype 1). After admission, the patient's renal function and anemia deteriorated rapidly, then prednisolone(30 mg/day) was started. After treatment her renal function gradually improved, then a renal and liver biopsy was performed. The renal biopsy revealed six sclerosing fibrous crescentic glomeruli in twelve glomeruli. Immunofluorescent examination revealed granular deposits of IgG, C3, and fibrinogen along the glomerular basement membrane and mesangial matrix. The pathogenesis of RPGN in this case may relate to the deposition of immune complexes in the glomeruli because immunofluorescent examination was revealed to be the immune-complex type, but not pauci immune type nephritis. Liver histology revealed chronic active hepatitis with mild piecemeal necrosis and did not reveal vasculitis. Although her renal function was improved after treatment with prednisolone, she suffered from pulmonary manifestations(dry cough etc.) on the 120th hospital day. Suddenly she died because of pulmonary hemorrhage on the 180th hospital day. These findings suggest that various HCV-induced immunological abnormalities, such as positive MPO-ANCA, cryoglobulinemia and hypocomplementemia, play an important role in the pathogenesis of this RPGN, although we could not demonstrate deposition within glomeruli of immune complexes containing HCV. The effect of interferon therapy on such immunological abnormalities remains to be documented. Since interferon is known to have immunomodulatory effects, we selected corticosteroid therapy. Future studies need to focus on the optimal treatment strategy for hepatitis C virus-associated glomerulonephritis.
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PMID:[A case of hepatitis C virus-associated glomerulonephropathy presenting with MPO-ANCA-positive rapidly progressive glomerulonephritis]. 1089 95

We report a patient, a 23-year-old man, who was a hepatitis B virus(HBV) carrier complicated with nephrotic syndrome. He was admitted to our hospital because of generalized edema and massive ascites. Laboratory data on admission were as follows: proteinuria 9,850 mg/day, Cr 2.7 mg/dl, BUN 73 mg/dl, albumin 1.9 g/dl, cholesterol 501 mg/dl, GOT 23 IU/l, GPT 19 IU/l, HBsAg(+), and HBeAg(222.7). Since his nephrotic symptoms were seriously complicated with renal failure, we selected steroid therapy for nephrosis preference. His renal function was improved and the urinary protein decreased immediately, but his liver function deteriorated. The renal biopsy revealed focal mesangial proliferative glomerulonephritis. Immunofluorescent examination revealed slight deposits of IgG, IgM, and C3 along the glomerular basement membrane and mesangial matrix. He was not compliant and often stopped taking the steroid therapy, thereby causing nephrosis to recur each time. After all, nephrotic symptoms have been well-controlled with cyclosporin and steroid. In spite of the seroconversion of HB virus by formation of HBe antibody, mutant HBV infection continued. The fact that liver biopsy revealed severe lymphoid infiltration at the portal area suggested chronic active hepatitis. His clinicopathologic course suggests that HBV-associated nephropathy does not always remit as there are some cases in whom hepatitis remains in an active state even after seroconversion, due to its mutant status. In these cases, the long-term prognosis of HBV nephropathy has not been defined. Further study is necessary to establish the optimal treatment for HB nephropathy in adults.
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PMID:[A case of hepatitis B virus carrier complicated with nephrotic syndrome]. 1099 20


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