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)

The preeclampsia-eclampsia syndrome is a severe complication of the third trimester of pregnancy and represents the first cause of maternal death. It is mainly characterized by: weight increase, proteinuria and hypertension and can evolve with convulsions and maternal death. The etiology still remains unknown although a series of events have been identified, starting with endothelial damage and local vasoconstriction leading to hypertension. These events occur at first locally in the placental district and become generalized. This paper reports experimental and clinical data in order to demonstrate: 1) the presence of a substance that could evoke experimentally the damage present in this syndrome, 2) a mechanism that delivers such a substance to its primary action site, the placenta, and 3) the possibility to inhibit either the substance or the delivery mechanism in order to prevent this disease. Serotonin appears to play an important role in the chain of events leading to preeclampsia. Certain histological aspects, present in pregnant women with this type of hypertension, have been observed in experimental animals after the administration of serotonin. Platelet derived serotonin could be sufficient, in the case of endothelial damage, to determine vasospasm. In a condition of hypercoagulability, such as pregnancy, this situation can trigger a chain of mechanisms ending with renal damage. Low dose aspirin seems a valid therapeutic approach reducing thromboxane concentrations and therefore preventing vasospasm. In this way the pathogenetic sequence culminating in the preeclampsia-eclampsia syndrome is interrupted. Ketanserin inhibits the hypertensive potential of serotonin by selectively acting on S2 serotonin receptors and appears to be an effective treatment in this type of pregnancy induced hypertension.
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PMID:[Serotonin and hypertension in preeclampsia-eclampsia syndrome]. 210 37

The pathogenesis of hypertension associated with diabetes mellitus (DM) involves an interplay of hereditary and acquired mechanisms. A familial trait for essential hypertension appears to be a risk factor for the development of both hypertension and nephropathy in type I DM and coexists commonly with impaired insulin sensitivity, relative hyperinsulinemia, and dyslipidemia, which can already be detected before the appearance of hypertension, obesity, or upper abdominal redistribution of body fat. The latter finding helps explain the frequent development of hypertension as well as dyslipidemia and/or type II DM in given individuals. Obesity is an important factor promoting these complications. Type I or II DM but not uncomplicated essential hypertension is characteristically accompanied by excess body Na+. This abnormality complements a tendency toward vascular hyperreactivity and a presumably morphologic and functional vasculopathy, thereby promoting the pathogenesis of hypertension in diabetic patients. For the treatment of hypertension in diabetic patients, nonpharmacologic measures are indispensable. If drugs are needed, angiotensin-converting enzyme (ACE) inhibitors and some but not all calcium antagonists are the preferred agents. Monotherapy or a combination of these drug types allows effective blood pressure control in most diabetic patients without further metabolic impairment; ACE inhibitors even tend to improve glucose control. Ketanserin may be a potential alternative, and if a diuretic is also needed, the metabolically neutral indapamide is a reasonable choice. If these agents do not allow satisfactory blood pressure highly selective beta 1-blockers or alpha 1-blockers may be introduced as a second choice. In diabetic patients with nephropathy, effective antihypertensive therapy can reduce proteinuria and slow the progression of the nephropathy; ACE inhibitors may improve diabetic proteinuria even at unchanged systemic blood pressure levels. Unless diuretics are needed for reasons other than hypertension, the treatment of diabetic patients with thiazides or loop diuretics in conventional dosage should probably be avoided until clarification of their influence on prognosis. Nevertheless, whether and to what extent other agents and nonpharmacologic measures can modify the prognosis in diabetic patients is also unclear, and the approach to antihypertensive therapy is therefore still largely empiric.
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PMID:Pathogenesis and treatment of hypertension associated with diabetes mellitus. 848 Jun 21