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)

Hantaviruses, the causative agents of HFRS, have become more widely recognized. Epidemiologic evidence indicates that these pathogens are distributed worldwide. People who come into close contact with infected rodents in urban, rural and laboratory environments are at particular risk. Transmission to man occurs mainly via the respiratory tract. The epidemiology of the hantaviruses is intimately linked to the ecology of their principal vertebrate hosts. Four distinct viruses are now recognized within the hantavirus genus and that number is likely to increase to six very soon; however, further investigations are necessary. Much more work is still needed before we fully understand the wide spectrum of clinical signs and symptoms of HFRS as well as the pathogenicity of the different viruses in the hantavirus genus of the Bunyaviridae family. HFRS is difficult to diagnose on clinical grounds alone and serological evidence is often needed. A fourfold rise in IgG antibody titer in a 1-week interval, and the presence of the IgM type of antibodies against hantaviruses are good evidence for an acute hantavirus infection. Physicians should be alert for HFRS each time they deal with patients with acute febrile flu-like illness, renal failure of unknown origin and sometimes hepatic dysfunction. Especially the mild form of HFRS is difficult to diagnose. Acute onset, headache, fever, increased serum creatinine, proteinuria and polyuria are signs and symptoms compatible with a mild form of HFRS. Differential diagnosis should be considered for the following diseases in the endemic areas of HFRS: acute renal failure, hemorrhagic scarlet fever, acute abdomen, leptospirosis, scrub typhus, murine typhus, spotted fevers, non-A, non-B hepatitis, Colorado tick fever, septicemia, dengue, heartstroke and DIC. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after onset of fever, resulted in a reduced mortality as well as shortened course of illness.
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PMID:Hemorrhagic fever with renal syndrome. 257 14

Heparin cofactor II (HC II) levels were measured by electro-immunoassay in healthy volunteers, and patients with liver disease, DIC, proteinuria or a history of venous thrombosis. Analysis of the data in 107 healthy volunteers revealed that plasma HC II increases with age (at least between 20 and 50 years). HC II was found to be decreased in most patients with liver disease (mean value: 43%) and only in some patients with DIC. Elevated levels were found in patients with proteinuria (mean value 145%). In 277 patients with a history of unexplained venous thrombosis three patients were identified with a HC II below the lower limit of the normal range (60%). Family studies demonstrated hereditary HC II deficiency in two cases. Among the 9 heterozygotes for HC II deficiency only one patient had a well documented history of unexplained thrombosis. Therefore the question was raised whether heterozygotes for HC II deficiency can also be found among healthy volunteers. When defining a group of individuals suspected of HC II deficiency as those who have a 90% probability that their plasma HC II is below the 95% tolerance limits of the normal distribution in the relevant age group, 2 suspected HC II deficiencies were identified among the healthy volunteers. In one case the hereditary nature of the defect could be established. It is concluded that hereditary HC II deficiency is as prevalent among healthy volunteers as in patients with thrombotic disease. Further it is unlikely that heterozygosity for HC II deficiency in itself is a risk factor for the development of venous thrombosis.
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PMID:Hereditary heparin cofactor II deficiency and the risk of development of thrombosis. 360 11

We report the case of a 39-year-old para-4 gravida-4 who received polychemotherapy 5-fluorouracil 600 mg/m2, cyclophosphamide 600 mg/m2 and epirubicin 50 mg/m2 for invasive breast cancer (pT2N2Mo) with extensive metastatic involvement of all 23 axillary lymph nodes removed at 29 gestational weeks. Soon after the second course of chemotherapy at 35 weeks, she developed two eclamptic tonic-clonic seizures which were treated by antihypertensive and anticonvulsive drugs and delivery of a healthy infant, 1650 g (< 10th percentile) by cesarean section. That this patient indeed suffered from eclampsia was supported by the findings of transient postpartum severe hypertension (peak 170/110 mmHg), proteinuria (peak 3.2 g/24 h), incomplete features of the HELLP syndrome (thrombocytopenia 81,000/mm3, haptoglobin < 10 mg/dl) and of DIC, and by the results of cerebral CT scanning showing two 1-cm ischemic lesions. Since the detrimental effect of antineoplastic agents on the rapidly proliferating trophoblast is well known and as abnormal placental function, such as in triploidy, trisomy or hydatiform mole, has been associated with an increased risk for preeclampsia/eclampsia, a possible causal relationship between polychemotherapy and the subsequent development of this rare disorder is suggested.
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PMID:Eclampsia after polychemotherapy for nodal-positive breast cancer during pregnancy. 884 12

Apparently healthy Wistar rats of body weight 250-300 g were chosen for the experiments. A group of 6 rats were assigned for each fraction. The dose of Russell's viper venom (RVV) fraction used for in vivo experiments was 0.75 microgram/g body weight. Of each batch of 6 rats 3 were sacrificed on the third day and the remaining 3 on the fifth day after the administration of test venom fractions. Daily urine output with proteinuria and serum creatinine were determined on the day they were sacrificed. Kidneys from the rats were also examined under light microscopy after hematoxylin and eosin staining. In the in vitro experiment, kidney slices (1 mm thickness) from normal rat was incubated with RVV fractions of 5 mg/ml concentration. The predominant renal lesions observed in both sets of animal experiments were tubular degeneration and necrosis. The changes were mostly confined to proximal tubules. Glomerular changes were mild. Similar tubulotoxic effects were produced by whole RVV as well as single fractions. Therefore, it is possible that RVV contains a common nephrotoxic (protein) component which is present in all fractions of the venom. The renal damage caused by RVV seemed to be due to both systemic effects (mainly DIC and renal ischemia) and direct tubulotoxic effects of the venom.
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PMID:Russell's viper venom fractions and nephrotoxicity. 956 25

It is believed that platelets play a key role in the production of pre-eclamptic toxaemia and toxaemia of pregnancy. Toxaemia of pregnancy is described as a condition of chronic DIC where there is thrombocytopenia as well as raised fibrin degradation products. Since fibrinogen receptors are involved in the final stage of the platelet aggregation reaction, we wanted to investigate the platelet receptors for fibrinogen in normal and abnormal pregnancy. Thirty-six normal pregnant women (12 in their 2nd trimester, 24 in their 3rd trimester), 24 pregnant pre-eclamptic toxaemia cases and 16 non-pregnant controls were included in the present study. All patients with pre-eclamptic toxaemia had oedema, proteinuria and hypertension. Flow cytometric study of platelets was undertaken utilizing fluorescein isothiocyanate (FITC)-labelled anti-human fibrinogen antibody in unstimulated and ADP-stimulated (final concentration 0.02 M) platelets. The intensity of platelet fluorescence was classified into three groups and expressed in arbitrary units. The results indicate that there are a higher number of stimulated platelets expressing fibrinogen receptors in the circulation of patients with pre-eclampsia. Thus, it is possible to hypothesize that platelets showing increased fibrinogen receptors aggregate and form microthrombi in smaller vessels in women with pre-eclamptic toxaemia.
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PMID:Functional and fibrinogen receptor studies in platelets in pre-eclamptic toxaemia of pregnancy. 1680 Oct 92