Current opinion in nephrology and hypertension
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During the past 12 months additional evidence has emerged from observational studies indicating that high blood pressure is an important independent predictor of incident renal damage, progression of existing renal disease, and morbidity and mortality in patients with renal failure. Several of these studies suggest that elevation of systolic blood pressure is a stronger predictor of risk than a corresponding increase in diastolic blood pressure. ⋯ Ongoing trials should help clarify optimal choice of antihypertensive medications and goals for reduction of blood pressure in prevention of renal disease. In the interim, two new guidelines for management of hypertension in patients with existing renal disease provide helpful guidance for the clinician.
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Curr. Opin. Nephrol. Hypertens. · Jul 1994
ReviewCurrent understanding of severe preeclampsia, pregnancy-associated hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, hemolysis, elevated liver enzymes, and low platelet syndrome, and postpartum acute renal failure: different clinical syndromes or just different names?
Endothelial cell injury, with subsequent vasospasm, platelet activation, unbalanced prostacyclin-thromboxane ratio, and decreased release of endothelium-derived relaxing factor, play a central role in the pathogenesis of several disorders such as preeclampsia, hemolysis, elevated liver enzymes, and low platelet syndrome, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, acute fatty liver of pregnancy, and acute renal failure. It is possible that all these diseases are part of a spectrum of the same illness. ⋯ Differential diagnosis is often difficult due to the overlap of these syndromes. The purpose of this review is to clarify the differences and similarities among these pregnancy-related complications.
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There is increasing evidence that the sodium pump plays a role in essential hypertension. Recent publications have focused on intrinsic alterations in pump activity, external modification of pump activity by circulating inhibitors, and endothelial mediation of endogenous inhibitor effects on the vascular response. Hence, this review focuses on these areas. Although there is intriguing evidence that alterations in sodium pump activity might contribute to the pathogenesis of hypertension, in at least some sodium-sensitive models and some patients with essential hypertension, the evidence remains circumstantial and areas of substantial controversy exist.