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      Avaliação da microalbuminúria em indivíduos não diabéticos Translated title: Evaluation of microalbuminuria in non-diabetic individuals

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          Abstract

          OBJETIVO: Avaliar a presença de microalbuminúria em indivíduos não diabéticos, associando-a à presença de fatores de risco cardiovasculares como hipertensão arterial, tabagismo, dislipidemia e obesidade. A taxa de excreção urinária de albumina (EUA) foi avaliada em relação aos índices de secreção e resistência insulínica (RI). PACIENTES E MÉTODOS: 105 indivíduos com idade de 33,4 ± 1,4 anos (57,1% mulheres) foram submetidos ao TOTG com 75 g de dextrose, sendo avaliadas as curvas de glicose e insulina: valores basais e em 2h, valores de pico e áreas sob a curva (ASC). Para a avaliação da secreção e RI, utilizamos os índices: insulinogênico, delta, HOMA, QUICKI, relação glicose/insulina e relação entre os índices insulinogênico e HOMA. As amostras para avaliação da albuminúria foram colhidas overnight. Os indivíduos foram divididos em dois grupos: 1) tolerância normal à glicose e 2) alteração do metabolismo glicídico. RESULTADOS: Houve diferença entre os 2 grupos para idade, IMC, PA, cintura, RCQ, colesterol, triglicerídeos (TG), glicemias (GJ e G2h), ASCg, índices HOMA e QUICKI, e relação entre os índices insulinogênico e HOMA. A EUA foi de 4,28 ± 2,73 µg/mL, apresentando correlação com PAD, GJ, G2h, ASCg, VPG, HOMA, I2h, VPI e ASCi. Após regressão em stepwise, apenas ASCg foi preditora de EUA. Na comparação da amostra estratificada em quartis de EUA, o 1º e o 4º quartis foram estatisticamente diferentes para IMC, PAS, PAD, cintura, quadril, G2h, TG, LDL, ASCg, ASCi, VPG e índices HOMA e QUICKI. CONCLUSÃO: Embora não houvesse nenhum indivíduo com microalbuminúria, encontramos diferença entre a EUA em indivíduos com diferentes graus de tolerância à glicose e diferenças entre as variáveis clínicas e laboratoriais entre o 1º e o 4º quartis de EUA. Nossos achados sugerem que em indivíduos não diabéticos o aumento da EUA está relacionado a algumas características da síndrome metabólica, o que pode conferir uma maior suscetibilidade aterogênica.

          Translated abstract

          AIM: To evaluate the presence of microalbuminuria in non-diabetic subjects, associating it to the presence of cardiovascular risk factors like hypertension, smoking, dislipidemia and obesity. The urinary albumin excretion rate (UAE) was also evaluated regarding to insulin secretion and resistance indices. DESIGN AND METHODS: 105 subjects aged 33.4 ± 1.4 years (57.1% women), received 75 g dextrose for an OGTT, and the following variables were evaluated for glucose and insulin curves: basal and 2 hours values, peak values (PV) and area under the curves (AUC). To evaluate insulin secretion and resistance, we used the insulinogenic, delta, HOMA, QUICKI, glucose to insulin ratio and the relation between insulinogenic and HOMA indices. A urine sample was collected overnight for albuminuria. Individuals were allocated in two groups: 1) normal, and 2) altered glucose metabolism. RESULTS: The two groups differed in age, BMI, BP, abdominal circumference (AC), WHR, cholesterol, triglycerides (TG), glycemias (basal and 2h), AUCg, HOMA and QUICKI indices and the relation between insulinogenic and HOMA. Mean UAE was 4.28 ± 2.73 µg/mL, correlating to DBP, glycemias, AUCg, GPV, HOMA, 2h insulin, IPV e AUCi. By stepwise multiple-regression analysis, only AUCg was predictive of UAE. By comparing interquartile intervals of UAE, we found statistical significance between the 1st and 4th quartile for: BMI, SBP, DBP, AC, waist, 2h glucose, TG, LDL, AUCg, AUCi, GPV and HOMA and QUICKI indices. CONCLUSION: Although in the absence of microalbuminuric individuals, we found differences among UAE in individuals across a range of glucose tolerance and differences between clinical and laboratorial variables in the interquartile analysis. Our findings suggest that in non-diabetic individuals, UAE is associated to some characteristics of the metabolic syndrome, probably predisposing to greater atherogenic susceptibility.

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          Banting lecture 1988. Role of insulin resistance in human disease.

          G M Reaven (1988)
          Resistance to insulin-stimulated glucose uptake is present in the majority of patients with impaired glucose tolerance (IGT) or non-insulin-dependent diabetes mellitus (NIDDM) and in approximately 25% of nonobese individuals with normal oral glucose tolerance. In these conditions, deterioration of glucose tolerance can only be prevented if the beta-cell is able to increase its insulin secretory response and maintain a state of chronic hyperinsulinemia. When this goal cannot be achieved, gross decompensation of glucose homeostasis occurs. The relationship between insulin resistance, plasma insulin level, and glucose intolerance is mediated to a significant degree by changes in ambient plasma free-fatty acid (FFA) concentration. Patients with NIDDM are also resistant to insulin suppression of plasma FFA concentration, but plasma FFA concentrations can be reduced by relatively small increments in insulin concentration. Consequently, elevations of circulating plasma FFA concentration can be prevented if large amounts of insulin can be secreted. If hyperinsulinemia cannot be maintained, plasma FFA concentration will not be suppressed normally, and the resulting increase in plasma FFA concentration will lead to increased hepatic glucose production. Because these events take place in individuals who are quite resistant to insulin-stimulated glucose uptake, it is apparent that even small increases in hepatic glucose production are likely to lead to significant fasting hyperglycemia under these conditions. Although hyperinsulinemia may prevent frank decompensation of glucose homeostasis in insulin-resistant individuals, this compensatory response of the endocrine pancreas is not without its price. Patients with hypertension, treated or untreated, are insulin resistant, hyperglycemic, and hyperinsulinemic. In addition, a direct relationship between plasma insulin concentration and blood pressure has been noted. Hypertension can also be produced in normal rats when they are fed a fructose-enriched diet, an intervention that also leads to the development of insulin resistance and hyperinsulinemia. The development of hypertension in normal rats by an experimental manipulation known to induce insulin resistance and hyperinsulinemia provides further support for the view that the relationship between the three variables may be a causal one.(ABSTRACT TRUNCATED AT 400 WORDS)
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            Microalbuminuria and cardiovascular risk.

            Microalbuminuria is a marker for generalized vascular dysfunction. Its prevalence in United States and European general population surveys ranges from 6% to 10%. Increased risk for cardiovascular morbidity and mortality begins with albumin excretion rates that are well within normal limits. Although microalbuminuria interacts with the traditional cardiovascular risk factors, it has an independent relationship to renal and cardiovascular outcomes. For example, microalbuminuria doubles the risk for a cardiovascular event in patients with type 2 diabetes mellitus even after adjusting for the usual risk factors. Elevated rates of urinary albumin excretion predict target organ damage, notably renal disease, but are also related to left ventricular dysfunction, stroke, and myocardial infarction. Screening for microalbuminuria, which is recommended by several expert committees and associations, has become a readily accessible procedure. Screening can give clinicians prognostic information concerning cardiovascular risk and assist in guiding therapy. The goal of treatment is to prevent progression of, and even to reverse, microalbuminuria. Abundant evidence demonstrates that antihypertensive therapy is an important key to the control of urinary albumin excretion, and blockade of the renin-angiotensin system (with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers) is the treatment of choice. These drugs have successfully halted or delayed the progression to nephropathy and have reversed elevated rates of albumin excretion to normal values, even when blood pressure reduction has been minimal.
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              IV Diretrizes Brasileiras de Hipertensão Arterial

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                abem
                Arquivos Brasileiros de Endocrinologia & Metabologia
                Arq Bras Endocrinol Metab
                Sociedade Brasileira de Endocrinologia e Metabologia (São Paulo )
                1677-9487
                June 2006
                : 50
                : 3
                : 472-480
                Affiliations
                [1 ] Universidade do Estado do Rio de Janeiro Brazil
                Article
                S0004-27302006000300010
                10.1590/S0004-27302006000300010
                c1f80401-d71b-41d8-b945-4371f2bedf8d

                http://creativecommons.org/licenses/by/4.0/

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                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0004-2730&lng=en
                Categories
                ENDOCRINOLOGY & METABOLISM

                Endocrinology & Diabetes
                Microalbuminuria,Insulin resistance,Insulin secretion,OGTT,Microalbuminúria,Resistência insulínica,Secreção insulínica,TOTG

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