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)

Preeclampsia has been recognized clinically since the time of Hippocrates: however its etiology and pathophysiology remain enigmatic. This pregnancy-specific syndrome typically presents in late pregnancy as hypertension, edema, and proteinuria. Investigations over the past 15 years have revealed that preeclampsia is associated with abnormal placentation, reduced placental perfusion, endothelial cell dysfunction, and systemic vasospasm. Since it occurs more commonly in primigravidae and in women with underlying collagen-vascular diseases, an immunological component has long been suspected. Increased prevalence in high-order and molar pregnancies and those associated with increased placental mass suggests that trophoblastic volume and fetal antigen load are correlated with the syndrome. Epidemiological reports indicate that the prevalence of preeclampsia is decreased in women who received heterologous blood transfusions, practiced oral sex, or when a long period of cohabitation preceded an established pregnancy. Conversely, the use of condoms as a primary mode of contraception is associated with a higher risk of preeclampsia. These studies suggest that prior exposure to foreign or paternal antigens imparts a protection against the likelihood of developing preeclampsia. Clinical evidence of cellular and humoral immune dysfunction is associated with the syndrome. Fibrin and complement deposition and "foam" cells in atherosis lesions resemble the histopathology of renal allograft rejection. Relative T-cell, natural killer cell, and neutrophil activation have been reported in preeclampsia and circulating cytokines and antiphospholipid antibodies are more prevalent in preeclampsia than in normal pregnant women. These abnormalities are consistent with the systemic endothelial cell dysfunction that has been postulated as a pathophysiological feature of preeclampsia. While such associations do not prove causality, they suggest testable hypotheses for continued basic and clinical investigation of this major complication of human pregnancy.
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PMID:Review: immunobiology of preeclampsia. 913 57

The urokinase receptor (uPAR) is a multifunctional molecule involved in pericellular, fibrinolytic, and proteolytic activities, as well as in cell adhesion and chemotaxis and may play a role in the pathogenesis of tissue remodeling occurring during glomerulonephritis. We analyzed sequentially the expression of uPAR by immunohistochemistry and in situ hybridization in an accelerated model of nephrotoxic nephritis in rats. A strong induction of uPAR mRNA expression was observed in glomeruli as soon as 1 h after nephrotoxic serum injection. The intensity of glomerular uPAR mRNA and antigen expression increased and peaked at 24 h. At that time, numerous glomerular fibrin deposits, monocyte/marcrophage infiltration, and heavy proteinuria were observed. Fibrin deposition was detected at 6 h, peaked at 24 h, and progressively declined over the next 3 weeks, while uPAR antigen expression remained elevated until the end of the study (3 weeks). By double labeling, we showed that the expression of uPAR was mediated by both intrinsic glomerular cells and infiltrating macrophages. Severe podocytic lesions developed within 3 days after antiserum injection, and glomerulosclerosis rapidly progressed within 2-3 weeks. These results show that glomerular uPAR expression is induced in nephrotoxic nephritis and suggest that uPAR may promote local proteolysis and also tissue remodeling, leading to the late development of glomerulosclerosis.
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PMID:Induction of urokinase receptor expression in nephrotoxic nephritis. 1170 99

Renal thrombotic microangiopathy (TMA) is an uncommon vascular complication of severe hypertension. Until now, its clinical-pathological characteristics and renal survival have been unclear. Twenty-one patients with biopsy-proven renal TMA and with severe or malignant hypertension were retrospectively studied. All the patients exhibited severe hypertension, with systolic blood pressure at 200-280 mmHg and diastolic pressure at 110-180 mmHg. No patients had hemorrhagic manifestations. Elevated lactate dehydrogenase and thrombocytopenia were found in 6 and 5 patients, respectively. Significant proteinuria (>3 g/day) was present in 2 patients and microscopic hematuria in 18 patients. All patients presented with renal insufficiency (creatinine 3.1+/-2.1 mg/dL). The level of von Willebrand factor:antigen (vWF:Ag) in patients was not significantly higher than that in the healthy subjects, while the ADAMTS13 (a disintegrin and metalloprotease, with thrombospondin-1-like domains) activity was not significantly lower than that in the healthy subjects. Renal histology showed a TMA involving preglomerular arterioles and/or interlobular arteries characterized by fibrin deposits and vascular wall sclerosis. Fibrin glomerular microthrombi were not observed in these patients. Four patients required hemodialysis upon admission for severe acute renal failure. On follow-up, 3 patients had recovered normal renal function and 14 had mild renal insufficiency (creatinine 1.8+/-0.3 mg/dL), while 4 patients still required persistent hemodialysis. In conclusion, compared with patients having hemolytic uremic syndrome/thrombocytopenic purpura, our patients showed a low incidence of thrombocytopenia and better renal outcome.
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PMID:Renal thrombotic microangiopathies induced by severe hypertension. 1849 67


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