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)

Individuals with elevated blood pressure are at increased risk for cardiovascular events and death. Almost 50% of essential hypertension is salt-sensitive, this characteristic increases and becomes more prevalent with age. Salt sensitivity has been linked to an increased risk for the development of left ventricular hypertrophy, proteinuria, and a blunted nocturnal decline in blood pressure ("non-dipping"). Salt sensitivity implies an alteration in the relation between arterial pressure and sodium excretion or "pressure natriuresis". The development of salt-sensitive hypertension is proposed to occur in three phases. In the first phase, the kidney is structurally normal, and sodium is excreted normally. However, the kidney may be exposed to various stimuli that result in renal vasoconstriction. In the second phase, subtle renal injury develops, impairing sodium excretion and leading to an increase in blood pressure. In the third phase, the kidneys equilibrate at a higher blood pressure, allowing them to resume normal sodium handling. Other mechanisms, such as primary tubulointerstitial disease, genetic alterations in sodium regulation and excretion, or a congenital reduction in nephron number that limits sodium filtration are important in the development of salt-sensitive hypertension.
Arch Cardiol Mex
PMID:[Salt-sensitive hypertension]. 1701 93

Kidney disease may be the cause or a consequence of hypertension. Hypertension affects 25% of the adult population in the United States. Similarly, chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been steadily increasing in incidence because of the increasing age of the US population and rise in the incidence of risk factors, including hypertension. Substantial evidence supports the notion that elevated blood pressure is the most significant risk factor for the development of CKD. Microalbuminuria has been shown to be the early marker of hypertensive renal disease. Furthermore, therapy to reduce microalbuminuria was associated with delay in the progression of renal disease. Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. Hypertension is a major risk factor for cardiovascular events in patients with CKD and ESRD and those who have undergone renal transplantation. Studies have documented that elevated serum creatinine and CKD are risk factors for a cardiovascular event. Tight blood pressure control has been shown to reduce microalbuminuria and proteinuria and to delay progression of renal disease. Tailoring the choice of antihypertensive medication to the clinical setting to achieve a blood pressure goal is critical in reducing complications from this deadly connection.
Curr Cardiol Rep 2006 Nov
PMID:Hypertension and kidney disease: a deadly connection. 1705 92

The use of fibrates in the management of lipoprotein disorders has a history dating back to the mid-1960s. This group of drugs has now been tested in several large long-term trials with cardiovascular end points. Overall, there is good evidence for the reduction of cardiovascular disease in primary prevention studies and in those of subjects with manifest disease. More recent trials have suffered from high interference due to 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) introduction, particularly in their placebo control groups. However, there is very good evidence for overall safety from a combined study of >20,000 patients in these controlled clinical trials lasting approximately 5 years. Abdominal pain has been observed more frequently in the statin vs placebo group. Myopathy, liver enzyme elevations, and cholecystitis have been potential adverse reactions of interest. However, these have occurred at a very low rate and are rarely found to be statistically more frequent in the active-treatment group compared with the subjects taking placebo. The recent Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study found a slightly higher incidence of pancreatitis, deep venous thrombosis, and pulmonary embolism. Small creatinine and homocysteine elevations are observed in many patients taking fibrates, and the effect of this on long-term outcomes is under study. The FIELD study also described a significant reduction in the rates of progression of proteinuria and vascular retinopathy with fibrate therapy. To date, there has been no study exclusive to patients with elevated triglycerides, raising the question of the potential benefit of these drugs in patients with the lipid abnormalities most effectively treated with fibrates.
Am J Cardiol 2007 Mar 19
PMID:Expert commentary: the safety of fibrates in lipid-lowering therapy. 1736 73

In a large randomized trial of statin therapy in patients of South-Asian origin with hypercholesterolemia, 740 patients in the United States and Canada received 6 weeks of treatment with rosuvastatin 10 or 20 mg or atorvastatin 10 or 20 mg. A total of 485 patients (66%) were categorized as being at high risk of coronary heart disease and had a National Cholesterol Education Program Adult Treatment Panel III treatment goal of low-density lipoprotein (LDL) cholesterol <100 mg/dl (<2.6 mmol/L). LDL cholesterol decreased by 45% with rosuvastatin 10 mg versus 40% with atorvastatin 10 mg (p = 0.0023) and by 50% with rosuvastatin 20 mg versus 47% with atorvastatin 20 mg (p = NS). National Cholesterol Education Program Adult Treatment Panel III LDL cholesterol goal achievement rates in high-risk patients (all patients) were 76% (79%) and 88% (89%) with rosuvastatin 10 and 20 mg, respectively, compared with 70% (76%) and 81% (85%) with atorvastatin 10 and 20 mg, respectively. Rosuvastatin and atorvastatin were well tolerated. There were no clinically relevant differences between statins in adverse events or incidence of creatine kinase >10 times the upper limit of normal, alanine aminotransferase >3 times the upper limit of normal on 2 consecutive occasions, or proteinuria or hematuria over the relatively short duration of treatment. In conclusion, statin therapy was well tolerated and effective in decreasing LDL cholesterol in patients of South-Asian origin, with the 10- and 20-mg doses of rosuvastatin and atorvastatin allowing most patients to reach recommended LDL cholesterol goals.
Am J Cardiol 2007 Jun 01
PMID:Comparison of rosuvastatin versus atorvastatin in South-Asian patients at risk of coronary heart disease (from the IRIS Trial). 1753 77

Hypertension is highly prevalent in patients with chronic kidney disease (CKD). As either the cause or the consequence of CKD, hypertension is an important independent factor determining the rate of loss of renal function. Hypertension is also a significant independent risk factor for cardiovascular events in patients with CKD, the leading cause of their morbidity and mortality. Based on evidence from observational cohort studies and randomized clinical trials, the Canadian Hypertension Education Program (CHEP) recommends a target blood pressure (BP) of lower than 130/80 mmHg in hypertensive patients with nondiabetic CKD. The CHEP also endorses the use of renin-angiotensin system blockers for the BP-lowering regimen in nondiabetic patients with CKD and significant proteinuria. It is recognized that the majority of nondiabetic patients with CKD will require two or more BP-lowering drugs to attain target BP. Furthermore, extracellular fluid volume expansion is a major contributor to hypertension in patients with CKD, and diuretics should be part of the BP-lowering regimen in the majority of patients. Patients with CKD are recognized to be at high risk for cardiovascular events, and studies testing new emerging treatments of hypertension to reduce the burden of CKD on renal and cardiovascular outcomes are underway. In this regard, the CHEP will continue to review and update all its recommendations annually.
Can J Cardiol 2007 May 15
PMID:Treatment of hypertension in patients with nondiabetic chronic kidney disease. 1753 70

Transient and massive glomerular proteinuria, previously reported as one of the nephrotoxic reactions after ionic radiocontrast medium (RCM) exposure, is rarely observed in patients since the introduction of non-ionic RCM. However, whether the very low-range microalbuminuria might be encountered after non-ionic RCM exposure remains unknown. In this study we sought to investigate the effects of non-ionic RCM (Ultravist 370) exposure on the presence of microalbuminuria, defined as urine albumin-to-creatinine ratio (UACR) >30 mg/g, by a turbidmetric method in total of 64 patients (17 female, mean age 58+/-12 years) undergoing coronary angiography. The results showed that after non-ionic RCM (mean volume 103+/-57 ml) exposure, no significant differences were found in urinary albumin concentration or UACR; however, urinary creatinine was significantly reduced from 116+/-62 to 69+/-43 mg/dl (p<0.001). Changes in the presence of microalbuminuria before and after procedure were also not significant (p=0.891, McNemar test). In conclusion, non-ionic RCM exposure during CAG had negligible effect on the excretion of urinary albumin even within the detection range of microalbuminuria.
Int J Cardiol 2008 Jun 23
PMID:Evaluation of microalbuminuria after non-ionic radiocontrast medium exposure in patients undergoing coronary angiography. 1803 35

In the rat renin induces an intense but transient proteinuria, associated with the excretion of fibrinogen but not accompanied by any evidence of damage to the glomerulus. The inactivation of renin with respect to its pressor effect leads to a loss of its capacity to induce proteinuria. Angiotonin, when given in large amounts, induces proteinuria in the rat. It is concluded that this form of proteinuria is dependent on the pressor action of renin.
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PMID:Renin proteinuria in the rat; the relation between the proteinuria and the pressor effect of renin. 1810 67

Contrast-induced nephropathy (CIN) remains one of the most common hospital-acquired acute renal deterioration in patients undergoing angiographic procedure. Transient and massive non-selective proteinuria of glomerular origin was previously reported in patients with stable renal function shortly after ionic radiocontrast medium (RCM) exposure. Since non-ionic RCM is mostly used nowadays for coronary angiographic procedures, the effects of non-ionic RCM exposure on microalbuminuria might be worthy to be clarified. By measuring urine albumin-creatinine-ratio, we found that exposure to non-ionic, low osmolar RCM has almost negligible effect on either the presence or the levels of microalbuminuria in patients who underwent coronary angiography using ordinary dose. The findings of neutral effect of non-ionic RCM on microalbuminuria in our study might offer another rationale in an effort to prevent CIN. Further large-scaled clinical trials in delineating the effects on microalbuminuria after non-ionic RCM exposure were warranted, particularly in those with pre-existing renal insufficiency, to clarify the clinical implications of our study results.
Int J Cardiol 2009 Feb 06
PMID:Negligible effect of non-ionic radiocontrast medium exposure on microalbuminuria in patients undergoing coronary angiography. 1803 35

Proteinuria was associated with cardiovascular events and mortality in community-based cohorts. The association of proteinuria with mortality and cardiovascular events in patients undergoing percutaneous coronary intervention (PCI) was unknown. The association of urinary dipstick proteinuria with mortality and cardiovascular events (composite of death, myocardial infarction, or nonhemorrhagic stroke) in 5,835 subjects of the EXCITE trial was evaluated. Dipstick urinalysis was performed before PCI, and proteinuria was defined as trace or greater. Subjects were followed up for 210 days/7 months after enrollment for the occurrence of events. Multivariate Cox regression analysis evaluated the independent association of proteinuria with each outcome. Mean age was 59 years, 21% were women, 18% had diabetes mellitus, and mean estimated glomerular filtration rate was 90 ml/min/1.73 m(2). Proteinuria was present in 750 patients (13%). During follow-up, 22 subjects (2.9%) with proteinuria and 54 subjects (1.1%) without proteinuria died (adjusted hazard ratio 2.83, 95% confidence interval [CI] 1.65 to 4.84, p <0.001). The severity of proteinuria attenuated the strength of the association with mortality after PCI (low-grade proteinuria, hazard ratio 2.67, 95% CI 1.50 to 4.75; high-grade proteinuria, hazard ratio 3.76, 95% CI 1.24 to 11.37). No significant association was present for cardiovascular events during the relatively short follow-up, but high-grade proteinuria tended toward increased risk of cardiovascular events (hazard ratio 1.45, 95% CI 0.81 to 2.61).In conclusion, proteinuria was strongly and independently associated with mortality in patients undergoing PCI. These data suggest that such a relatively simple and clinically easy to use tool as urinary dipstick may be useful to identify and treat patients at high risk of mortality at the time of PCI.
Am J Cardiol 2008 Nov 01
PMID:Usefulness of proteinuria as a prognostic marker of mortality and cardiovascular events among patients undergoing percutaneous coronary intervention (data from the Evaluation of Oral Xemilofiban in Controlling Thrombotic Events [EXCITE] trial). 1894 Feb 82

Antihypertensive therapy remains the most effective strategy for slowing the progression of chronic kidney disease (CKD). However, in proteinuric nephropathies, calcium channel blockers (CCBs) are less effective than other antihypertensives unless normotension is achieved. This is because the glomerular capillaries, rather than larger vessels, are the primary site of hypertensive injury in proteinuric nephropathies. CCBs impair renal autoregulation, which protects glomerular capillaries against the transmission of systemic pressures. CCBs' renoprotective inferiority in the comparator group likely accounts for the greater renoprotection observed with renin-angiotensin system blockade rather than blood pressure (BP)-independent renoprotective superiority. Nevertheless, CKD patients are at greater absolute risk for cardiovascular events rather than end-stage renal disease. Therefore, if the needed BP reductions cannot be achieved with other agents, it may be appropriate to use CCBs because of their antihypertensive effectiveness, provided care is taken to ensure normotension and to closely monitor proteinuria and renal disease progression.
Curr Cardiol Rep 2008 Nov
PMID:Potential risks of calcium channel blockers in chronic kidney disease. 1895 May 53


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