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)

Basic fibroblast growth factor (bFGF) is a potent endothelial cell growth factor that does not normally circulate in healthy nonpregnant adults. bFGF has been reported in plasma from patients with certain tumors consistent with a postulated role in tumor angiogenesis. In the present study we used an endothelial cell bioassay to test for a bFGF-like substance in plasma and urine from patients with noninsulin-dependent diabetes mellitus. We found increased bFGF immunoreactivity that correlated with bFGF-like endothelial cell growth-promoting activity in plasma from a subset of diabetic patients with persistent microalbuminuria or overt proteinuria. Plasma (bFGF-like) growth-promoting activity was significantly correlated with glycosylated hemoglobin (P < 0.05), but not patient age, race, degree of proteinuria, or systolic blood pressure. In a group of microalbuminuric or proteinuric diabetic subjects well matched according to baseline clinical characteristics, plasma (bFGF-like) growth-promoting activity was significantly decreased (P < 0.0001) in the subgroup of patients who were being treated with an angiotensin-converting enzyme inhibitor simultaneous to blood drawing for plasma growth assay. In patients not treated with an angiotensin-converting enzyme inhibitor, multiple regression analysis showed that retinopathy was the only variable significantly associated with plasma growth-promoting activity. These results imply that plasma bFGF endothelial cell growth-promoting activity is increased and may contribute to pathophysiology in a heterogeneous subset of noninsulin-dependent diabetes mellitus patients with persistent microalbuminuria or overt proteinuria.
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PMID:Increased basic fibroblast growth factor-like substance in plasma from a subset of middle-aged or elderly male diabetic patients with microalbuminuria or proteinuria. 895 57

A patient with advanced rectal cancer was complicated by progressing proteinuria and hypoproteinemia. Low anterior resection was a procedure of choice. A surgical specimen obtained by intraoperative renal biopsy showed the findings of minimal change nephrotic syndrome. After surgery, nephropathy remitted promptly and completely. Her pre/postoperative serum level of vascular endothelial growth factor was 1,880/52.3 pg/ml, suggesting its elevation was associated with the nephropathy. Immunohistochemistry revealed strongly expressed tumor vascular endothelial cell growth factor. Minimal change nephrotic syndrome is a rare type of paraneoplastic nephropathy, and successful remission may require therapeutic resection of the underlying tumor, or administration of a vascular endothelial growth factor antagonist if the tumor is unresectable.
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PMID:Rectal cancer with paraneoplastic nephropathy: association of vascular endothelial growth factor. 1566 42

Although tighter blood pressure control is considered the main mechanism for preventing the progression of chronic renal failure, angiotensin-converting enzyme inhibitors and angiotensin receptors blockers seem to have an additional organ protective role. The effects of calcium antagonists in renal disease are not so clearly defined. Calcium antagonists have pleiotropic effects that might contribute to protect the kidney, such as attenuating mesangial entrapment of macromolecules, countervailing the mitogenic effect of platelet-derived growth factors and platelet-activating factors, and suppressing mesangial cell proliferation. They could also act as free radical scavengers and inhibit the renal effects of endothelin. Some evidence has been accumulated demonstrating that certain new dihydropyridinic calcium antagonists may affect postglomerular as well as preglomerular vessels, resulting in decreased filtration fraction and nephroprotective effect as renin-angiotensin axis-blocking drugs. Though there are few reports on the clinical renal effects of new calcium antagonists, they have rendered promising results. Manidipine does not increase proteinuria as do some classic calcium antagonists, and lercanidipine combined with renin-angiotensin axis-blocking drugs reduce proteinuria. Both drugs have been shown to decrease microalbuminuria when administered alone.
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PMID:Calcium antagonists and renal failure progression. 1835 Apr 43

Preeclampsia is a placental disease characterized by hypertension and proteinuria in pregnant women, and it is associated with a high maternal and neonatal morbidity. However, circulating biomarkers that are able to predict the prognosis of preeclampsia are lacking. Thirty-eight women were included in the current study. They consisted of 19 patients with preeclampsia (13 with severe preeclampsia and 6 with non-severe preeclampsia) and 19 gestational age-matched women with normal pregnancies as controls. We measured circulating factors that are associated with the coagulation pathway (including fibrinogen, fibronectin, factor VIII, antithrombin, protein S and protein C), endothelial activation (such as soluble endoglin and CD146), and the release of total and platelet-derived microparticles. These markers enabled us to discriminate the preeclampsia condition from a normal pregnancy but were not sufficient to distinguish severe from non-severe preeclampsia. We then used a microarray to study the transcriptional signature of blood samples. Preeclampsia patients exhibited a specific transcriptional program distinct from that of the control group of women. Interestingly, we also identified a severity-related transcriptional signature. Functional annotation of the upmodulated signature in severe preeclampsia highlighted two main functions related to "ribosome" and "complement". Finally, we identified 8 genes that were specifically upmodulated in severe preeclampsia compared with non-severe preeclampsia and the normotensive controls. Among these genes, we identified VSIG4 as a potential diagnostic marker of severe preeclampsia. The determination of this gene may improve the prognostic assessment of severe preeclampsia.
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PMID:Evaluation of current and new biomarkers in severe preeclampsia: a microarray approach reveals the VSIG4 gene as a potential blood biomarker. 2434 25