Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020639 (hypoproteinemia)
 1,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ICR-derived glomerulonephritis (ICGN) mouse is a novel inbred mouse strain with a hereditary nephrotic syndrome, considered to be a good model of human idiopathic nephrotic syndrome and develops proteinuria, hypoproteinemia and anemia. In the present study, we compared the cell kinetics in the kidneys of ICGN mice with age-matched ICR mice as normal controls. The proliferating cells were visualized by 5-bromo-2'-deoxyuridine labeling, and apoptotic cells were determined by terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nick end-labeling. Many proliferating epithelial cells of renal tubules, glomerular mesangial cells and tublointerstitial fibroblast-like cells were observed in the kidneys of ICGN mice, but no proliferating cells were seen in the kidneys of ICR mice. Apoptotic cells had round nuclei, and were observed only in the tubulointerstitium in the kidneys of ICGN mice but not in that of controls. The proliferation of renal tubular epithelial cells may represent a compensatory response, and that of mesangial and fibroblast-like cells may play a pathogenic role in nephrotic syndrome. Apoptosis in tubulointerstitial cells with round nuclei may have been erythropoietin-producing cells, and probably caused anemia.
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PMID:Localization of proliferative and apoptotic cells in the kidneys of ICR-derived glomerulonephritis (ICGN) mice. 1150 6

The ICR-derived glomerulonephritis (ICGN) mouse, a new inbred mouse strain with a hereditary nephrotic syndrome, is considered to be a good model of human idiopathic nephrotic syndrome and notably exhibits proteinuria and hypoproteinemia from the neonatal stage. In chronic renal disorder (CRD), anemia is a major subsequent symptom (renal anemia). The precise cause of renal anemia remains unclear, primarily owing to the lack of appropriate spontaneous animal models for CRD. To establish adequate animal models for anemia with CRD, we examined the hematological-biochemical properties and histopathological characteristics. With the deterioration of renal function, ICGN mice developed a normochromic and normocytic anemia, and exhibited normochromic and microcytic at the terminal stage. The expression of erythropoietin (EPO) mRNA both in the kidneys and liver and the EPO leak into the urine were observed in ICGN mice, indicating a disrupted metabolism of EPO in ICGN mice. In addition, a lack of iron induced by the hemolysis in the spleen and the leak of transferrin into urine as proteinuria aggravated the anemic condition. In conclusion, the ICGN mouse is a good model for anemia with CRD.
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PMID:Anemia with chronic renal disorder and disrupted metabolism of erythropoietin in ICR-derived glomerulonephritis (ICGN) mice. 1513 73

The nephrotic syndrome is characterized by the loss of many proteins, via the urinary system. It exceeds the bodies compensatory abilities and results in abnormalities in blood clotting system, particularly due to antithrombin deficiency. It significantly increases the risk of thromboembolic complications. A loss of erythropoietin and transferrin leads to anemia. Polycythemia is a rarely reported phenomenon. The case describes a 20-years old patient with massive nephrotic syndrome and polycythemia, complicated by a pulmonary embolism. The patient had a steroid-dependent submicroscopic glomerulonephritis with a severe episode of nephrotic syndrome associated with centralization of circulation, proteinuria 40.9 g/day, deep hypoproteinemia (albumin=1.2 g/dl), hyperlipidemia, hypercoagulable state (antithrombin activity 29%), polycythemia (Hb=21.1 g/dl, HTC=60%). Kidney function parameters were normal. We started the immunosupression (glycocorticosteroids i.v., continuated p.o. and cyclosporine A) and intensive symptomatic treatment. To reverse hypovolemia and polycythemia, 20% albumin solutions, intravenous infusions and diuretics were used. There was no effect. Due to intensive polycythemia the erythroapheresis procedure was performed. It resulted in normalization of the red blood cell count (Hb=13.4 g/dl, HCT=37%) and the improvement of blood circulation. To prevent the patient from thromboembolism, the prophylactic dose of low molecular weight heparin (LMWH) was administered (dalteparin 5000 IU subcutaneously, once a day). Despite the prophylaxis, an episode of dyspnea with tachycardia occured. It was connected with elevated Ddimer and troponin levels and a right ventricle overload in echocardiographic imaging. The pulmonary embolism was suspected. Perfusion lung scintigraphy confirmed this diagnosis. We supposed that the heparin was ineffective due to an antithrombin deficiency. Therefore, apart from a therapeutic dose of LMWH, intravenous antithrombin concentrate was given to the patient (1500 IU twice). The dyspnea resolving was observed. The D-dimer and troponin level reversion to normal was noticed. Heparin injections, connected with antithrombin infusion, was an effective treatment of the pulmonary embolism. Due to the lack of antithrombin in nephrotic syndrome, using only heparin may be insufficient. The erythroapheresis is an effective treatment of polycythemia.
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PMID:[Above-standard proceeding in nephrotic syndrome - case report]. 2708 3