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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the last few decades, clinical and experimental data have established microalbuminuria/proteinuria as an independent risk factor for renal disease and for progression of renal disease in patients with diabetes and in those with essential hypertension. Reduction of proteinuria with the use of angiotensin-converting enzyme inhibitors has been shown in clinical trials to delay or stabilize the rate of progression of renal disease. This effect appears to be independent of any effect on blood pressure control. In conjunction with other therapeutic interventions such as dietary modification and control of serum lipids, it appears that for at least a subgroup of patients, it is possible to delay or prevent progression of kidney failure. More recently, evidence has accumulated that establishes microalbuminuria/proteinuria as an independent risk factor for cardiovascular morbidity and mortality even in those without other clinical evidence of kidney disease. There is frequently a clustering of risk factors in these individuals that includes insulin resistance, salt-sensitivity, hypertension, and dyslipidemia. The mechanism of this relationship of proteinuria and cardiovascular disease is unclear, but the presence of proteinuria as a marker for cardiovascular disease has important implications for the identification and treatment of individuals at risk.
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PMID:Proteinuria and cardiovascular disease. 1157 14

Clinical data have established microalbuminuria/proteinuria as an independent risk factor for the development and progression of renal disease in patients with either diabetes or essential hypertension. Decreased kidney function is associated with increased cardiovascular risk, even at modest reductions in estimated creatinine clearance (to approximately 60 mL/min/1.73 m(2)) or modest elevations in serum creatinine (>1.4 mg/dL). Treatment with angiotensin-converting enzyme inhibitors has been shown in clinical trials to delay or stabilize the rate of progression of renal disease. Reduction in cardiovascular events, such as stroke and myocardial infarction, also has been shown in these high-risk individuals. These effects are dependent and independent of blood pressure control, suggesting a nonhemodynamic effect in blockade of the renin-angiotensin system. In conjunction with other therapeutic interventions, such as dietary modification and control of serum lipids, it appears that for at least a subgroup of patients it is possible to delay or prevent progression of kidney failure. There frequently is a clustering of risk factors in these individuals, including insulin resistance, salt sensitivity, hypertension, and dyslipidemia. The mechanism of the relationship between albuminuria and cardiovascular disease is unclear but may be related to endothelial cell dysfunction. Nonetheless, the presence of microalbuminuria/proteinuria as a marker for cardiovascular disease has important implications for the identification and treatment of individuals at risk.
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PMID:Metabolic pathogenesis of cardiorenal disease. 1172 77

Microalbuminuria (MA) i.e. slightly elevated albumin excretion in the urine, is now considered to be an atherosclerotic risk factor. MA predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. It has been implicated as an independent risk factor for cardiovascular disease and premature cardiovascular mortality for patients with type 1 and type 2 diabetes mellitus, as well as for patients with essential hypertension. Although microalbuminuria is associated with a certain degree of sub-clinical artherosclerotic damage, it is not known how early in the atherosclerotic process microalbuminuria appears. Epidemiological studies have shown an association between MA and insulin resistance, obesity, salt sensitivity and dyslipidaemia in patients with essential hypertension and diabetes. Patients with microalbuminuria are also characterised by an increased prevalence of left ventricular hypertrophy and retinal microvascular lesions. Microalbuminuria, is associated with an excess of other cardiovascular risk factors. The mechanisms linking microalbuminuria and risk for cardiovascular disease are not fully understood, but in subjects at risk it may be related to increased transvascular leakiness of albumin in systemic as well as renal vessels. A recent concept is that microalbuminuria is a marker of extensive endothelial dysfunction or generalised vasculopathy, which may lead to heightened atherogenic states. One possible explanation is that endothelial dysfunction might promote increased penetration of atherogenic lipoprotein particles in the arterial wall, but glycaemic status, insulin resistance, procoagulant state and adhesion molecules have all been implicated in the pathogenesis. Current evidence suggests that tight blood pressure control may reduce the risk of microalbuminuria in diabetic patients with hypertension and that inhibitors of the rennin-angiotensin system (RAS) can prevent or delay the progression of microalbuminuria to overt nephropathy in normotensive persons. ACE inhibitors are currently recognised as first-line antihypertensive therapy in diabetic patients with proteinuria, and these agents afford unique benefits in modifying the progression and severity of cardiovascular disease (CVD) as well as of diabetic nephropathy. Whether albuminuria is a risk factor or just a marker for CV disease, it identifies the high-risk diabetic patient who should be targeted for early, aggressive intervention against proven risk factors. If persistent microalbuminuria is confirmed, strict blood pressure control with added RAS inhibition should be pursued in an attempt to stabilise or even reduce microalbuminuria, preserve kidney function and possibly improve cardiovascular risk.
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PMID:The link between microalbuminuria, endothelial dysfunction and cardiovascular disease in diabetes. 1238 63

Some patients with essential hypertension manifest greater than normal urinary albumin excretion (UAE). Salt-sensitive hypertensives also manifest greater UAE compared to salt-resistant individuals. Although the significance of these associations is not well established, several lines of evidence suggest that microalbuminuria and/or salt sensitivity may be associated with greater prevalence of cardiovascular risks and events. In this study, we have evaluated by ergometric exercise 42 subjects with microalbuminuria and 42 matched individuals with normal UAE. All these subjects also underwent a standardized protocol to determine blood pressure sensitivity to a high salt intake. Patients with microalbuminuria displayed greater levels of ambulatory blood pressure and a greater rise in systolic blood pressure during exercise compared to patients with normal UAE (33.1 +/- 1.56 vs 26.4 +/- 1.7 mmHg, P < 0.001). Seven hypertensive patients with microalbuminuria developed ST segment depression during exercise compared to only one subject with normal UAE. Salt-sensitive patients manifested greater UAE than salt-resistant subjects (58 and 14 mg, 24 h, P < 0.001) and greater prevalence of silent ischemia (6 vs 2) than salt-resistant individuals. In conclusion, these studies have shown that hypertensive individuals with microalbuminuria and/or salt sensitivity manifest an increased prevalence of silent ischemia.
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PMID:Silent ischemia is more prevalent among hypertensive patients with microalbuminuria and salt sensitivity. 1257 12

High-salt diet is known to induce or aggravate hypertension in animal models of hypertension and in humans. When Sprague-Dawley rats (n = 60) are fed a moderately high-fat diet (32% kcal fat, 0.8% NaCl) for 10 wk, about one-half develop obesity [obesity prone (OP)] and mild hypertension, whereas the other half [obesity resistant (OR)] maintain body weight equivalent to a low-fat control (C) and are normotensive. The aim of this study was to test the effect of high-NaCl diets (2 and 4% NaCl) on the development of hypertension and obesity, oxidative stress, and renal function. Both 2 and 4% NaCl induced an early increase in systolic blood pressure of OP but not OR or C rats. High-salt intake induced an increase in the size and reduction in number of adipocytes, concomitant to a twofold increase in circulating leptin in OP rats. Aortic superoxide generation indicated a 2.8-fold increase in the OP high-salt vs. normal-salt groups, whereas urine isoprostanes were not significantly increased. Also, hydroxynonenal protein adducts in the kidney were highly increased in OP rats on 2 and 4% NaCl, indicating oxidative stress in the renal tissue. Urine albumin was increased threefold in the OP on 2% NaCl and fourfold in the same group on 4% NaCl vs. 0.8% NaCl. Kidney histology indicated a higher degree of glomerulosclerosis in OP rats on high-salt diets. In summary, high-salt diet accelerated the development but did not increase the severity of hypertension; high salt increased oxidative stress in the vasculature and kidney and induced kidney glomerulosclerosis and microalbuminuria. Also, the OP rats on high salt displayed adipocyte hypertrophy and increased leptin production.
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PMID:Effect of salt on hypertension and oxidative stress in a rat model of diet-induced obesity. 1279 6

Discordant findings are reported on the left ventricular transforming growth factor-beta(1) (TGF-beta(1)) mRNA levels in various rat models. Left ventricular TGF-beta(1) mRNA levels did not differ between spontaneously hypertensive rats (SHR) and normal rats, between deoxycorticosterone (DOCA)-salt and sham-operated hypertensive rats, but were increased in stroke-prone spontaneously hypertensive rats (SHRSP) and in post-myocardial infarction (MI) rats. Renal cortical TGF-beta(1) mRNA levels were, however, higher in DOCA-salt hypertensive rats. Angiotensin II subtype 1 receptor antagonism (AT(1)R) and angiotensin converting enzyme inhibition (ACEI) decreased left ventricular and vascular smooth muscle TGF-beta(1) mRNA levels in SHR and renal TGF-beta(1) mRNA in DOCA-salt hypertensive rats and in SHRSP. In post-MI rats ventricular TGF-beta(1) mRNA decreased by AT(1)R antagonism. In essential hypertensive patients, TGF-beta(1) protein as well as TGF-beta(1) mRNA levels are hyperexpressed. The TGF-beta(1) overproduction in hypertension can be attributed to various factors such as elevated angiotensin II, increased systemic blood pressure (BP) per se, increased fluid shear stress and a differential expression of TGF-beta(1) linked to DNA polymorphism in the promoter. The Arg(25) polymorphism in the TGF-beta(1) gene is associated with higher BP. A higher plasma TGF-beta(1) concentration is found in hypertensive patients with microalbuminuria and left ventricle hypertrophy. In these patients, AT(1)R antagonism and ACEI reduced these plasma TGF-beta(1) levels significantly.
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PMID:Association between transforming growth factor-beta and hypertension. 1285 Mar 97

Blood pressure (BP) above optimal (< or =120/< or =80 mmHg) is established as a major cardiovascular disease (CVD) risk factor. Prevalence of adverse BP is high in most adult populations; until recently research has been sparse on reasons for this. Since the 1980s, epidemiologic studies confirmed that salt, alcohol intake, and body mass relate directly to BP; dietary potassium, inversely. Several other nutrients also probably influence BP. The DASH feeding trials demonstrated that with the multiple modifications in the DASH combination diet, SBP/DBP (SBP: systolic blood pressure, DBP: diastolic blood pressure) was sizably reduced, independent of calorie balance, alcohol intake, and BP reduction with decreased dietary salt. A key challenge for research is to elucidate specific nutrients accounting for this effect. The general aim of the study was to clarify influences of multiple nutrients on SBP/DBP of individuals over and above effects of Na, K, alcohol, and body mass. Specific aims were, in a cross-sectional epidemiologic study of 4680 men and women aged 40-59 years from 17 diverse population samples in China, Japan, UK, and USA, test 10 prior hypotheses on relations of macronutrients to SBP/DBP and on role of dietary factors in inverse associations of education with BP; test four related subgroup hypotheses; explore associations with SBP/DBP of multiple other nutrients, urinary metabolites, and foods. For these purposes, for all 4680 participants, with standardized high-quality methods, assess individual intake of 76 nutrients from four 24-h dietary recalls/person; measure in two timed 24-h urine collections/person 24-h excretion of Na, K, Ca, Mg, creatinine, amino acids; microalbuminuria; multiple nutrients and metabolites by nuclear magnetic resonance and high-pressure liquid chromatography. Based on eight SBP/DBP measurements/person, and data on multiple possible confounders, utilize mainly multiple linear regression and quantile analyses to test prior hypotheses and explore relations of multiple dietary and urinary variables to SBP/DBP of individuals. The 4680 INTERMAP participants are equally divided across four age/gender strata: diverse in ethnicity, education, occupation, physical activity; use of cigarettes, alcohol; diagnosed high BP, CVD, diabetes; CVD family history; women vary in parity, use of contraceptive medication and hormone replacement therapy.
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PMID:INTERMAP: background, aims, design, methods, and descriptive statistics (nondietary). 1367 50

The International Diabetes Federation (Europe) has updated these guidelines on hypertension management specifically in Type 2 diabetes in the light of recent results of the first prospective, randomized controlled studies to investigate clinical outcomes in people with diabetes and hypertension. The guidelines are knowledge based, i.e. based not only on evidence originating from clinical trials, but also from epidemiological and pathophysiological studies. A successful management strategy requires the following components: 1. Regular surveillance to detect developing hypertension and other cardiovascular (CV) risk factors. 2. Considering more frequent monitoring and review of CV risk factors if any single blood pressure (BP) measurement > 140/85 mmHg (or 130/75 if microalbuminuria); when appropriate, using ambulatory or home monitoring to establish the baseline BP. 3. Considering other CV risk factors, such as a raised albumin excretion rate, in setting the intervention threshold. 4. Individualizing the target BP in accordance with other CV risk factors. 5. Agreeing lifestyle and therapeutic interventions with the patient, with education and empowerment as required. 6. Implementing lifestyle modifications, including controlling calorie, salt and alcohol intake, increased physical activity, weight control and smoking cessation. 7. Therapeutic strategy: the primary goal of therapy is to reduce BP markedly. Combination therapy is often necessary, e.g. an angiotensin converting enzyme (ACE) inhibitor and a diuretic. Some classes are particularly useful for certain patients, notably longer-acting ACE inhibitors, angiotensin 2 receptor antagonists (A2RAs) and calcium antagonists in those at risk of diabetic nephropathy, loop diuretics and thiazides in those at risk of hyperkalaemia, beta-blockers and calcium antagonists (except short-acting dihydropyridines) in patients with angina, beta-blockers and ACE inhibitors after a myocardial infarction or in those with left ventricular dysfunction, and thiazide diuretics and long-acting dihydropyridine calcium antagonists for isolated systolic hypertension. A2RAs should be particularly considered when ACE inhibitors are not tolerated. alpha 1-Blockers should not be considered first line in the absence of outcome data. Cost of drugs will modify these strategies in developing countries. 8. Monitoring response to therapies and, if target levels are not achieved, either intensifying drug therapy if the CV risk justifies it, or reassessing the target. 9. Maintaining a quality assurance strategy. This strategy is summarized in a simple, practical management algorithm.
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PMID:Hypertension in people with Type 2 diabetes: knowledge-based diabetes-specific guidelines. 1463 98

Hypertension frequently coexists with diabetes mellitus, occurring twice as frequently in diabetic as in nondiabetic persons. It accounts for up to 75% of added cardiovascular disease (CVD) risk in people with diabetes, contributing significantly to the overall morbidity and mortality in this high-risk population. Patients with hypertension are two times more prone to have diabetes than are normotensive persons. Hypertension substantially increases the risk for coronary heart disease (CHD), stroke, retinopathy, and nephropathy. In patients with type 2 diabetes, hypertension usually clusters with the other components of the cardiometabolic syndrome, such as microalbuminuria, central obesity, insulin resistance, dyslipidemia, hypercoagulation, increased inflammation, and left ventricular hypertrophy (LVH). In type 1 diabetes, hypertension often occurs subsequent to the development of diabetic nephropathy. Hypertension in people with diabetes is characterized by volume expansion, increased salt sensitivity, isolated systolic blood pressure (BP) elevation, loss of the nocturnal dipping of BP and pulse, and increased propensity toward orthostatic hypotension and albuminuria. Among the treatment strategies tested in hypertensive diabetic persons, low-density lipoprotein (LDL)-cholesterol lowering to less than 100 mg/dL and aggressive BP control to less than 130/80 mm Hg have proven effective in CVD risk reduction. The combination of two or more drugs is usually necessary to achieve the target BP.
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PMID:Diabetes, hypertension, and cardiovascular derangements: pathophysiology and management. 1512 75

The relationship between dietary salt, blood pressure, and risk for cardiovascular disease has been debated for decades. Microalbuminuria is a biomarker for both cardiovascular and kidney disease. The presence of microalbuminuria correlates directly with the risk for myocardial infarction and stroke and indicates individuals at risk for the development of progressive kidney disease. Since patients with the metabolic syndrome, diabetes, or chronic kidney disease often are blood pressure salt sensitive, and it is well known that increasing dietary salt may offset both the antihypertensive and antiproteinuric effects of renin-angiotensin system blocking drugs, physicians must consider increased salt intake as a potential modifiable risk factor for progression of chronic kidney disease and possibly even cardiovascular disease.
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PMID:Dietary salt, blood pressure, and microalbuminuria. 1553 8


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