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)

Diabetic nephropathy (DN) is the most common cause of chronic renal failure (CRF), in Mexico prevalence of diabetes is higher than other countries. Genetic susceptibility, arterial hypertension, proteinuria and initial hyperfiltration are risk factors for CRF. Renal injury is mediated by protein glycation, proteinuria and hemodynamics alterations induced by arterial hypertension and impaired renal autoregulation. Angiotensin II is directly involved in renal injury through its hemodynamic effects, oxidative stress, induction of proinflammatory and profibrotic factors and cellular proliferative effect. Prospective, well controlled clinical trials in patients with type 1 and type 2 DM have shown that interrupting the renin angiotensin system with CEI or ARA effectively prevent progression of DN. Combination of both drugs may provide further nephroprotection. Antihypertensive therapy in patients with DN must include CEI or ARA and to reduce BP below 130/85 mmHg and if proteinuria is present, under 120/75.
Arch Cardiol Mex
PMID:[Arterial hypertension and diabetic nephropathy. Evidence based therapy]. 1296 48

The 2000 National Health Survey (ENSA 2000) was a probabilistic survey that included more than 45,000 subjects aged between 20 to 69 years old. It was directed to determine the prevalence of non-communicable chronic diseases such as hypertension, diabetes, obesity glucosa, and proteinuria. The survey was weighed with to the National Register of Population (INEGI). The prevalence for hypertension was 30.05%, for diabetes of 10.76%, for obesity 24.4%, abnormal capillary glucose 12.7% and for proteinuria of 9.2%. Using Conjunctive Consolidation Analysis the interrelationship among the non-communicable chronic diseases was demonstrated. The prevalence was directly related with age, and obesity was the most important modifier of the prevalence of non-communicable chronic disease. ENSA 2000 alerts on the urgent need of national strategies to restrain this important national public health problem.
Arch Cardiol Mex
PMID:[Arterial hypertension in Mexico and its association with other risk factors]. 1296 65

The safety and tolerability of rosuvastatin were assessed (as of August 2003) using data from 12,400 patients who received 5 to 40 mg of rosuvastatin in a multinational phase II/III program, which represented 12,212 patient-years of continuous exposure to rosuvastatin. An integrated database was used to examine adverse events and laboratory data. In placebo-controlled trials, adverse events, irrespective of causality assessment, occurred in 57.4% of patients who received 5 to 40 mg of rosuvastatin (n = 744) and 56.8% of patients who received placebo (n = 382). In fixed-dose trials with comparator statins, 5 to 40 mg of rosuvastatin showed an adverse event profile similar to those for 10 to 80 mg of atorvastatin, 10 to 80 mg of simvastatin, and 10 to 40 mg of pravastatin. Clinically significant elevations in alanine aminotransferase (>3 times the upper limit of normal) and creatine kinase (>10 times the upper limit of normal) were uncommon (<or=0.2%) in the groups that received rosuvastatin and comparator statins. Myopathy (creatine kinase >10 times the upper limit of normal with muscle symptoms) that was possibly related to treatment occurred in <or=0.03% of patients who took rosuvastatin at doses <or=40 mg. A positive finding of proteinuria with dipstick testing at rosuvastatin doses <or=40 mg was comparable to that seen with other statins, and the development of proteinuria was not predictive of acute or progressive renal disease. No deaths in the program were attributed to rosuvastatin, and no rhabdomyolysis occurred in patients who received 5 to 40 mg of rosuvastatin. Rosuvastatin was well tolerated by a broad range of patients who had dyslipidemia, and its safety profile was similar to those of the comparator statins investigated in this extensive clinical program.
Am J Cardiol 2004 Oct 01
PMID:Safety of rosuvastatin. 1546 70

In the United States, 50 million Americans are estimated to have hypertension. Over the past several decades, it has become clear that hypertension is both a cause and a consequence of kidney disease. In contrast to the striking decline in mortality rates from both stroke and coronary heart disease, the prevalence of hypertension as a cause of end-stage renal disease (ESRD) has increased such that it is now the second most common cause of ESRD in the United States. Hypertension and proteinuria occur in most patients with chronic kidney disease and are risk factors for faster progression of kidney disease. Antihypertensive agents reduce blood pressure and urine protein excretion and slow the progression of kidney disease. The level of blood pressure achieved and use of renin-angiotensin-aldosterone system-blocking agents is critical for delaying progression of renal disease in all ethnic groups.
Curr Cardiol Rep 2004 Nov
PMID:Antihypertensive drugs and the kidney. 1548 98

Large, placebo-controlled RCTs that involve only diabetic patients who have hypertension have not been performed. Subgroup analyses of hyper-tension control from several recent RCTs un-equivocally demonstrated greater benefit in diabetic populations (see Table 3) with ACE inhibitors, TDs, and CCBs. Treatment with fBs(atenolol) also was beneficial in diabetic patients who had hypertension in the actively-controlled UKPDS. The results of three RCTs support intensive BP control in diabetic patients (see Table 4). In these trials, diabetic patients gained more benefit than nondiabetic patients. Such an effect is consistent with the fact that diabetics are at higher risk for CV events. Although there are limited data from RCTs with head-to-head comparison of newer agents (eg,ACE inhibitors, ARBs, CCBs) to show that these drugs are better than diuretics and betaBs in reducing CV events by treating hypertension in the diabetic population, the available data support ACE inhibitors (and ARBs if ACE inhibitors are not tolerated) as an initial drug of choice in diabetic,hypertensive patients (see Table 5). Most diabetic patients require three or four drugs to control their BP to target range; as such, it is not necessary to justify the choice of any single class of drug. Tight BP control is cost-effective and is more rewarding than hyperglycemic control in diabetic,hypertensive patients. The optimal goal in diabetics should be to achieve BP that is less than 130/80 mm Hg. Appropriate action should be taken if BP is greater than 140/85 mm Hg. In subjects who have diabetes and renal insufficiency,the BP should be decreased to less than 125/75 mm Hg to delay the progression of renal failure. Limited data suggest that an ACE inhibitor or an ARB is the agent of choice, especially in patients who have proteinuria or renal insufficiency. betaBs can be the first-line agent in diabetics who have CAD. TDs and CCBs are the second line drugs.AAAs should be avoided. Most hypertensive patients require more than one agent to adequately control their BP. There is no evidence to support one combination regimen over the others, nevertheless, the combination of an ACE inhibitor with a TD or a fPB may be more beneficial and cost effective than other combinations in the diabetic population. Large outcome studies that compare different combination therapies in hypertensive,diabetic patients are needed.
Cardiol Clin 2005 May
PMID:Diabetes and hypertension, the deadly duet: importance, therapeutic strategy, and selection of drug therapy. 1569 43

Hypertension affects 24% of the adult US population. In the United States, 3% of the adult population has an elevated serum creatinine level, and 70% of these patients have hypertension. The prevalence of hypertension in chronic kidney disease (CKD) depends on the patient's age and the severity of renal failure, proteinuria, and underlying renal disease. As patients with CKD progress to end-stage renal disease (ESRD), 86% are diagnosed with hypertension. It has long been recognized that kidney function affects and is affected by hypertension. This article discusses the pathophysiology and management of hypertension in patients with CKD.
Cardiol Clin 2005 Aug
PMID:Hypertension in chronic kidney disease and dialysis: pathophysiology and management. 1608 75

This report reviews data on the development of proteinuria in patients with chronic kidney disease who are treated with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) for dyslipidemia. Although subgroup analyses of statin trials have shown cardiovascular benefits in subjects with chronic kidney disease, concern about statin-induced proteinuria remains high. Experimental studies have suggested that the proteinuria seen with statin treatment results from the inhibition of receptor-mediated endocytosis, the likely mechanism of protein uptake in proximal tubular cells. Transient proteinuria may signify little more than the effective inhibition of cholesterol synthesis at this site. The blockade of protein trafficking in tubular cells is thought to reduce inflammation, slow fibrosis, and diminish proteinuria in the long term. Post hoc analyses of large clinical trials in subjects without overt renal disease have generally supported this notion, showing that statins most benefit patients with the greatest baseline renal deficits. Statins have also been shown to preserve glomerular filtration rate and reduce proteinuria in subjects with nondiabetic renal disease. In conclusion, in the absence of prospective, randomized trials in renally impaired patients, the collective evidence indicates that statin therapy may slow the decrease in renal function that generally attends atherosclerotic disease. The incidence of proteinuria with potent statins is only 1% to 2% when these drugs are given in recommended doses. Several large trials are currently under way to examine the safety and efficacy of statins in renally compromised patients at high risk for cardiovascular disease.
Am J Cardiol 2006 Mar 01
PMID:Effects of statins on renal function. 1649 Apr 50

Safety has become a central issue in the management of dyslipidemia with statins. A review of New Drug Applications (NDAs) and the US Food and Drug Administration (FDA) Web site was conducted for all 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins, with a major focus on cerivastatin and rosuvastatin. The findings provide insight into the incidence of adverse events for this class of drugs and support the significant benefits of statins relative to associated risks. These data delineate the nature of statin associated liver, muscle, and renal adverse events. Although transaminase levels increase in a dose-related fashion with statins, a definitive correlation between statin therapy and hepatotoxicity is not supported by statin NDA data. Statin-induced myopathy is a relatively rare event (1 in 1,000) and rhabdomyolysis is even rarer (1 in 10,000). The cerivastatin NDA, along with its supplementary NDA, was the first to demonstrate a clear statin dose-response relation with myopathy and a threshold effect above which myotoxicity increases significantly. Proteinuria was identified as a consequence of statin therapy with data from the rosuvastatin NDA, and subsequent analysis suggests a class effect that is dose related but transient. Studies in cell culture suggest the mechanism is a pharmacologic effect on the proximal renal tubule. The available evidence suggests no clear renal toxicity with currently approved statins, because no declines in renal function or glomerular filtration rate have been documented over time. Overall, currently marketed statins have a very favorable benefit-to-risk relation with respect to liver, muscle, and renal issues.
Am J Cardiol 2006 Apr 17
PMID:Statin safety: lessons from new drug applications for marketed statins. 1658 28

A systematic review of cohort studies, randomized trials, voluntary notifications to national regulatory authorities, and published case reports was undertaken to assess the incidence and characteristics of adverse effects in patients treated with 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, or statins. For statins other than cerivastatin, the incidence of rhabdomyolysis in 2 cohort studies was 3.4 (1.6 to 6.5) per 100,000 person-years, an estimate supported by data from 20 randomized controlled trials. Case fatality was 10%. Incidence was about 10 times greater when gemfibrozil was used in combination with statins. Incidence was higher (4.2 per 100,000 person-years) with lovastatin, simvastatin, or atorvastatin (which are oxidized by cytochrome P450 3A4 [CYP3A4], which is inhibited by many drugs) than pravastatin or fluvastatin (which are not oxidized by CYP3A4). In persons taking simvastatin, lovastatin, or atorvastatin, 60% of cases involved drugs known to inhibit CYP3A4 (especially erythromycin and azole antifungals), and 19% involved fibrates, principally gemfibrozil. The incidence of myopathy in patients treated with statins, estimated from cohort studies supported by randomized trials, was 11 per 100,000 person-years. For liver disease, randomized trials reported fewer hepatobiliary disorders in patients allocated statins than in those allocated placebo. The notification rate of liver failure to regulatory authorities was about 1 per million person-years of statin use. Randomized trials show no excess of renal disease or proteinuria in statin-allocated participants, and the decline in glomerular filtration rate was smaller with statins than with placebo. Evidence from 4 cohort studies and case reports suggests that statins cause peripheral neuropathy, but the attributable risk is small (12 per 100,000 person-years). No change in cognitive function was found in randomized trials of statins in elderly patients.
Am J Cardiol 2006 Apr 17
PMID:Statin safety: a systematic review. 1658 29

To define the effect of short-term rosuvastatin treatment on the estimated glomerular filtration rate (eGFR), the database of controlled clinical trials in the Rosuvastatin Clinical Development Program was reviewed. Thirteen studies comprising 3,956 rosuvastatin-treated patients were selected based on a serum creatinine measurement at 6 or 8 weeks after initiation of rosuvastatin treatment, randomization to approved and marketed rosuvastatin doses (5 to 40 mg), and unchanged rosuvastatin dose from treatment initiation (baseline) through 6 to 8 weeks of treatment. eGFR was determined with the Modification of Diet in Renal Disease formula. eGFR significantly increased for each dose of rosuvastatin individually and for all doses combined compared with baseline (range +0.9 to +3.2 ml/min/1.73 m2). Further analysis of 5 blinded, placebo-controlled trials comprising 525 patients showed an increase in eGFR of +0.8 ml/min/1.73 m2 (95% confidence interval +0.1 to +1.5) for all rosuvastatin-treated patients, which was significantly different from baseline (p <0.04) and from a change of -1.5 ml/min/1.73 m2 in the placebo-treated patients (95% confidence interval -2.5 to -0.5, p <0.001). The increase in eGFR for rosuvastatin-treated patients was consistent across all major demographic and clinical subgroups of interest, including patients with baseline proteinuria, baseline eGFR <60 ml/min/1.73 m2, and in patients with hypertension and/or diabetes. In conclusion, these results are consistent with previous rosuvastatin studies that showed an upward trend in eGFR with long-term treatment (> or =96 weeks) and with the hypothesis that statins may have pleiotropic mechanisms of action that include beneficial renal effects.
Am J Cardiol 2006 Jun 01
PMID:Effect of short-term rosuvastatin treatment on estimated glomerular filtration rate. 1672 22


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