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)

To determine the prevalence of unrecognized silent myocardial ischemia, 925 noninsulin-dependent diabetic outpatients (333 women and 592 men), aged 40 to 65 years, asymptomatic, free from known coronary artery disease (CAD), advanced diabetic retinopathy, and nephropathy, severe hypertension, and poor prognosis disease, underwent exercise electrocardiogram (ECG), followed, if abnormal, by an exercise thallium scintigraphy. The exercise ECG tests were abnormal in 112 patients (12.1%, 31 women, 81 men), of whom 59 (6.4%, 12 women, 47 men) had perfusion defects at thallium scintigraphy. Adopting the more restrictive criteria (positive response to both tests) the prevalence of silent CAD resulted in 6.4%. Multivariate analysis showed that in the whole population and in the men, the associated independent risk factors were age, total cholesterol, proteinuria, and ST-T abnormalities at ECG at rest. This last factor had the highest odds ratio (9.27, confidence interval [CI] 4.44 to 19.38) and was the only one identified also in women. The relevance of ST-T abnormalities at ECG at rest as a predicting factor for silent CAD outlines the importance of a periodical ECG at rest in noninsulin-dependent diabetic patients and suggests an indication of performance of further investigations in presence of these abnormalities.
Am J Cardiol 1997 Jan 15
PMID:Prevalence of unrecognized silent myocardial ischemia and its association with atherosclerotic risk factors in noninsulin-dependent diabetes mellitus. Milan Study on Atherosclerosis and Diabetes (MiSAD) Group. 919 11

Amyloid cardiomyopathy may exist when echocardiography does not suggest infiltration. Clinicians should be alert for the presence of a monoclonal protein, nephrotic range proteinuria, or peripheral neuropathy in a patient with heart failure.
Am J Cardiol 1997 Jul 01
PMID:Endomyocardial biopsy-proven light chain amyloidosis (AL) without echocardiographic features of infiltrative cardiomyopathy. 920 31

Pregnant women with hypertension can be divided into two groups: normotensive women who develop the uniquely pregnancy-related syndrome of preeclampsia, which is characterized by hypertension, proteinuria, and edema; and women with chronic hypertension who become pregnant and are at increased risk for developing superimposed preeclampsia. Preeclampsia is a syndrome of generalized endothelial dysfunction initiated by abnormal placentation and consequent placental under-perfusion, release of cytokines and other toxins, and vasoconstriction and platelet activation. Preeclampsia is the major cause of both maternal and fetal morbidity and mortality and may be complicated by eclampsia (seizures) and hepatic and renal failure. The process is completely reversible by delivery of the fetus and placenta, but intrauterine growth retardation and premature delivery pose major threats to the fetus and may require care in tertiary care center. Treatment of preexisting or pregnancy-induced hypertension does not prevent or reverse the process, but is justified to prevent maternal cardiovascular complications, especially during labor and delivery.
Cardiol Clin 1998 Feb
PMID:Hypertension and pregnancy-related hypertension. 950 83

This report describes the simultaneous manifestation of ischemic heart disease and nephrotic syndrome in a 37-year-old woman presenting with acute anterior myocardial infarction. Symptoms of nephrotic syndrome, such as facial and peripheral edema accompanied by proteinuria and hyperlipidemia, and onset of severe retrosternal pain developed within 24 h. Coronary angiography revealed a complete thrombotic occlusion of the proximal portion of the left anterior descending artery with no evidence of arteriosclerotic lesions. Histologic examination of renal biopsy, including electron microscopy, revealed evidence of minimal change glomerulonephritis. Ultrastructural studies demonstrated widespread effacement of epithelial foot processes. Elevated levels of circulating fibrinogen appeared to be an important factor for the hypercoagulable state in this patient, suggesting a causative relationship between coronary thrombosis and nephrotic syndrome.
Clin Cardiol 1998 Jul
PMID:Simultaneous manifestation of acute myocardial infarction and nephrotic syndrome. 966 62

It is now well-established that inhibition of the angiotensin-converting enzyme (ACE) can retard the progression of chronic renal failure in a variety of experimental and clinical settings. The recent introduction of highly specific angiotensin receptor type 1 (AT1) antagonists has raised the issue whether these compounds produce comparable beneficial effects on the natural progression of chronic renal injury. Currently, a large body of experimental and clinical evidence indicates that both ACE inhibition and AT1 blockade lead to similar changes in renal hemodynamics and proteinuria. Animal studies have also shown that AT1 blockade effectively attenuates the development and progression of renal injury caused by a variety of mechanisms ranging from unilateral ureteric obstruction to renal ablation or immune-mediated acute glomerular injury. These findings make it likely that AT1 blockade may ultimately prove to be a promising new therapy for slowing the progression of renal injury in patients with kidney disease.
Basic Res Cardiol 1998
PMID:Angiotensin II receptor blockade and renal protection. 983 73

Diabetic nephropathy has become the single most important cause of endstage renal failure in most countries of the Western world. Against this background, the role of the renin-angiotensin system (RAS) and its blockade command considerable interest. In diabetic patients and in diabetic animals, the circulating components of the RAS are suppressed. Although the evidence is not completely uniform, there are indirect arguments (renal hemodynamic response to RAS blockade, AT1 receptor expression), however, which would be consistent with increased intrarenal action of angiotensin (ANG) II. There is solid evidence that ACE inhibitors effectively interfere with progression of micro-albuminuria both in IDDM and NIDDM. They also prevent progression of advanced renal failure in IDDM, while there is only preliminary evidence in this respect for NIDDM. ACE inhibitors are superior to conventional antihypertensive agents (with the possible exception of some calcium channel blockers), but such superiority is seen only when the levels of blood pressure are relatively high. In diabetic animals, treatment with ANG II receptor blockers interferes with the development of glomerular lesions. In acute and subacute studies on diabetic patients, ANG II receptor blockers reduced albuminuria (or proteinuria) more than beta-blockers. Head-on comparison of equipotent doses ACE inhibitors and ANG II receptor blockers in non-diabetic patients produced equal reductions in proteinuria. The long-term effects of ANG II receptor blockers on progression of advanced diabetic nephropathy is the object of two large international studies. The results will not be available before the year 2000.
Basic Res Cardiol 1998
PMID:Diabetes--renal function--what are the special problems? 983 74

Angiotensin II antagonists block the actions of angiotensin II by occupying the AT1 receptors. With this blockade there is no bradykinin increase, the angiotensin II synthetized by the cardiac chymase is also blocked, and the AT2 receptor is stimulated (antiproliferative effect). In animal experiments, losartan reverses left ventricular hypertrophy, inhibits myocardial fibrosis and diabetic glomerulosclerosis and significantly protects from vascular cerebral diseases. In humans, the efficacy of the angiotensin II antagonists and that of other antihypertensives is similar and is potentiated by the addition of a thiazide. They are very well tolerated and no important adverse reactions are reported. Losartan decreases insulin resistance, has a very favourable hemodynamic and neurohormonal profile in patients with cardiac insuficiency, reverses proteinuria and has a uricosuric effect. Angiotensin II antagonists are a step forward towards the ideal antihypertensive drugs.
Rev Port Cardiol 1999 Apr
PMID:[Therapy of arterial hypertension with angiotensin receptor blockers]. 1037 49

Proteinuria is common after streptokinase treatment. An immunological mechanism in the renal glomerulus has been suggested to explain this side effect. However, thrombopenia and acute renal failure streptokinase induced are uncommon. We present a case of thrombopenia and acute renal failure after streptokinase administration for myocardial infarction that improved with steroid therapy. We discuss the probable pathophysiology of these adverse effects of streptokinase and the potential usefulness of steroids in its prevention and treatment.
Rev Esp Cardiol 1999 Oct
PMID:[Thrombopenia and acute renal insufficiency after treatment with streptokinase. Role of steroids]. 1056 65

The treatment of hypertension and heart failure has evolved in recent years. It may no longer be sufficient to lower blood pressure per se or correct hemodynamics alone in these conditions to achieve optimal long-term outcomes; rather, the effects of drugs on the cellular events and structural alterations that occur in the vasculature, heart, and kidney must be considered. Drugs that target angiotensin II, which include the angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs), may protect target organs from damage and thereby improve outcomes. Nevertheless, it remains to be demonstrated whether these agents are more effective in reducing cardiovascular morbidity and mortality in hypertensive patients than conventional treatment with diuretics and beta blockers. In certain subgroups of hypertensive patients, including those with heart failure, type 1 diabetes with proteinuria, or after myocardial infarction with systolic dysfunction, there is compelling evidence for use of ACE inhibitors. The results from animal models and initial clinical studies suggest that ARBs are also highly effective in these patients. Several large-scale clinical studies, comparing the effect of ARBs and other drug classes on morbidity and mortality outcomes, have been initiated to better define the long-term benefit of ARBs in the treatment of hypertension and heart failure.
Am J Cardiol 1999 Nov 18
PMID:Long-term benefits of angiotensin II blockade: is the consensus changing? 1058 90

We sought to evaluate safety, tolerability, pharmacokinetics, and pharmacodynamics of basic fibroblast growth factor (bFGF), administered as a single intracoronary injection, to subjects with stable angina pectoris secondary to coronary artery disease. bFGF, an angiogenic growth factor, has been shown to enhance collateral development in animal models of progressive coronary occlusion. To our knowledge, this study represents the initial introduction of parenteral bFGF into humans. This was a phase 1, randomized, dose-escalation trial of bFGF in 25 subjects with coronary artery disease and stable angina. Subjects were randomized 2:1 to a single dose of bFGF or placebo, injected into the left main coronary artery. bFGF doses ranged from 3 to 100 microg/kg, increasing in half-log increments. bFGF was generally well tolerated at doses of 3 to 30 microg/kg. Plasma clearance was 20 +/- 2 ml/kg/min, with an elimination half-life of 85 +/- 11 minutes. bFGF caused acute hypotension ( approximately 10%) that did not appear to be dose-related through the dose range studied. Of the 9 subjects who received 30 to 100 microg/kg bFGF, 2 had sustained hypotension, mild to moderate in severity, lasting 1 to 3 days, and 3 subjects developed bradycardia hours to days after bFGF administration. bFGF dilated epicardial coronary arteries (7.4 +/- 2.5% mean diameter increase, p <0.02). Transient mild thrombocytopenia and proteinuria were observed in some subjects in the 30-microg/kg cohort. No subject had signs suggesting systemic angiogenesis. Thus, intracoronary bFGF, at doses of 3 to 30 microg/kg, was generally well tolerated in subjects with stable angina.
Am J Cardiol 2000 Jun 15
PMID:Effects of a single intracoronary injection of basic fibroblast growth factor in stable angina pectoris. 1085 85


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