Microalbuminuria in hypertension is not a determinant of insulin resistance

Toft, Ingrid; Bønaa, Kaare Harald; Eikrem, Jorunn H; Bendiksen, Åse Lund; Iversen, Hege; Jenssen, Trond

doi:10.1046/j.1523-1755.2002.00286.x

Cited by 17 publications

(12 citation statements)

References 48 publications

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“…34 A similar explanation, supported by the lower hs-CRP levels and the preserved insulin sensitivity in our group of subjects with MA and a lean body size, might apply to insulin sensitivity. 35,36 However, IR, at least as assessed through the HOMA model, did not clearly differ by CRP levels in our microalbuminuric subgroups. Therefore, the hypothesis is plausible, although to be verified in more numerous groups, including females rather than an all-male hypertensive cohort such as ours, and possibly through more precise methods for the evaluation of insulin sensitivity.…”

Section: Discussionmentioning

confidence: 54%

Low-Grade Inflammation and Microalbuminuria in Hypertension

Pedrinelli

Dell’Omo

Bello

et al. 2004

ATVB

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Background-Albuminuria and C-reactive protein (CRP), a marker of systemic low-grade inflammation, are frequently elevated in essential hypertension and predict cardiovascular prognosis independent of conventional risk factors. However, in spite of their potentially important links, the interrelationships between the 2 parameters have not been explored in depth in hypertensive patients. Methods and Results-Albuminuria (the mean of 3 overnight urine collections), high-sensitive CRP (hs-CRP), 24-hour blood pressure (BP), weight, lipids, poststimulative (75 g PO) plasma glucose, insulin, and insulin sensitivity by the homeostasis model assessment model were evaluated in 220 never treated, nondiabetic, uncomplicated essential hypertensive men. Albuminuria Ն15 g/min was defined as microalbuminuria and hs-CRP values above and below median (2.3 mg/L) as high and low, respectively. Concentric left ventricular hypertrophy was diagnosed by echocardiography, and a full-blown metabolic syndrome was identified in presence of hypertension and at least 3 of following: obesity, subclinical hyperglycemia, low high-density lipoprotein (HDL) and high triglycerides. Microalbuminuria was present in 54 patients, 29 with high hs-CRP characterized by higher 24-hour systolic BP, postload glucose, body mass index, lower HDL cholesterol, more frequent metabolic syndrome, concentric LVH, and active smoking than those with either isolated microalbuminuria (nϭ27) or normoalbuminuria. Conclusions-Microalbuminuria accompanied by evidence of subclinical inflammation is a strong correlate of metabolic abnormalities in essential hypertension and identifies a patient subset at very high cardiovascular risk. In contrast, isolated microalbuminuria may represent a distinct pathophysiological condition characterized by a more benign profile and possibly a better prognosis.

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Section: Discussionmentioning

confidence: 54%

Low-Grade Inflammation and Microalbuminuria in Hypertension

Pedrinelli

Dell’Omo

Bello

et al. 2004

ATVB

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“…29 In diabetes and hypertension, insulin resistance has also been related to microalbuminuria, 30 -32 although not in all studies. 33,34 Moreover, CRP and microalbuminuria both predict incident cases of type 2 diabetes, which underlines their role in insulin resistance. 35,36 Because we did not measure insulin sensitivity or insulin concentrations, we cannot exclude that our findings relate more directly to insulin resistance than to CRP.…”

Section: Discussionmentioning

confidence: 96%

C-Reactive Protein Modifies the Relationship Between Blood Pressure and Microalbuminuria

et al. 2004

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Abstract-C-reactive protein (CRP) and microalbuminuria reflect intimately related components of the atherosclerotic disease process. Epidemiological studies found only modest associations between CRP and microalbuminuria. Blood pressure, one of the components of the metabolic syndrome in the general population, is the main determinant of microalbuminuria in diabetes and hypertension. We questioned whether CRP modifies the relationship of blood pressure and other cardiovascular risk factors with microalbuminuria in a cross-sectional study in 8592 inhabitants from Groningen, The Netherlands. The crude data showed an increase in the prevalence of microalbuminuria with increasing CRP quartiles (4.8, 9.6, 14. Key Words: cardiovascular diseases Ⅲ blood pressure Ⅲ risk factors Ⅲ kidney Ⅲ albuminuria C -reactive protein (CRP), a sensitive marker of (sub)clinical inflammation, is thought to represent the state of chronic low-grade inflammation of the arterial vessel wall at atherosclerotic sites. 1 CRP consistently predicts cardiovascular (CV) outcome. [2][3][4] Microalbuminuria is also an established risk marker for future cardiovascular events in various populations. 5,6 The appearance of low levels of albumin in the urine is thought to be the consequence of generalized endothelial damage along the vascular tree, including the glomerulus. 7 Blood pressure has been shown to be the main determinant of microalbuminuria in diabetes and hypertension. 8 Many other CV risk factors, which cluster within the metabolic syndrome, have been shown to relate to microalbuminuria in the population. 9,10 Because CRP and microalbuminuria reflect closely related components of the same disease processes, one might anticipate a strong relationship between them. However, studies that investigated this relationship in large populations only found weak associations. 11,12 Interdependence between CRP and other cardiovascular risk factors with the risk of microalbuminuria may have been overlooked.We questioned whether elevated serum CRP levels modify the relation of blood pressure and other CV risk factors with microalbuminuria. Methods Study DesignThis study is part of the PREVEND study (Prevention of REnal and Vascular ENdstage Disease) in Groningen, The Netherlands. PREVEND investigates the natural course of microalbuminuria in relation to renal and cardiovascular morbidity and mortality in the general population. All inhabitants aged 28 to 75 years (nϭ85 421) were asked to send in a morning urine sample and to complete a brief questionnaire on demographics and renal and cardiovascular morbidity. A total of 40 856 subjects responded. Pregnant women and subjects using insulin were excluded. All subjects with an albumin concentration of Ͼ10 mg/L in their morning urine sample plus a random sample of the population with a morning urine albumin excretion Ͻ10 mg/L were invited to our outpatient clinic. A detailed overview of this protocol is described elsewhere. 13 All subjects completed an extensive questionnaire on demographics, renal and cardio...

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“…Insulin (endogenous and lispro) during HEC was measured with radioimmunoassay methods (HI-14K; Millipore, Billerica, MA) at the Hormone Laboratory, Oslo University Hospital (Aker, Norway). HEC was performed after a 12-h fast, as previously described (10). After the drawing of fasting blood samples, a primed /min, and continued for 120 min.…”

Section: Measurements and Calculationsmentioning

confidence: 99%

Renal Denervation for Resistant Hypertension Fails to Improve Insulin Resistance as Assessed by Hyperinsulinemic-Euglycemic Step Clamp

et al. 2016

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We assessed whether insulin sensitivity improved after renal denervation (RDN) for resistant hypertension. Twentythree patients underwent a two-step hyperinsulinemiceuglycemic clamp (HEC) with glucose tracer and labeled glucose infusion and oral glucose tolerance test (OGTT) before and 6 months after RDN. Eighteen patients had metabolic syndrome at baseline. Blood pressure declined significantly after RDN, whereas mean (SD) fasting plasma glucose concentration (5.9 6 0.7 mmol/L), median (minimum-maximum) insulin concentration (254 pmol/L [88-797 pmol/L]), and median C-peptide concentration (2.4 nmol/L [0.9-5.7 nmol/L]) remained unchanged. Endogenous glucose release during HEC was less suppressed after RDN, suggesting a slight decrease in hepatic insulin sensitivity. During high-dose insulin infusion, whole-body glucose disposal was low and remained unchanged after RDN, indicating persistent peripheral insulin resistance (IR). Area under the curve for 0-120 min for glucose and insulin during OGTT, Quantitative Insulin Sensitivity Check Index, Simple Index Assessing Insulin Sensitivity Oral Glucose Tolerance, and HOMA-IR were high, and did not improve after RDN. Despite a significant decrease in blood pressure, neither peripheral nor hepatic insulin sensitivity improved 6 months after RDN treatment in this group of insulin-resistant patients without diabetes and with resistant hypertension, as measured with gold standard methods.More than 50% of patients with essential hypertension are considered to have insulin resistance (IR) (1). The link between these two disorders is partly unknown, but it has been hypothesized that increased sympathetic nerve activity (SNA) plays an important role (2). Sympathetic activation results in peripheral vasoconstriction through the release of norepinephrine, which acts upon vascular muscle adrenoreceptors. A subsequent reduction in skeletal muscle blood flow leads to reduced whole-body glucose utilization (3). Consequently, increased SNA may reduce insulin sensitivity (IS) through direct effects on the regulation of glucose uptake by skeletal muscle (4,5).Targeting both sympathetic tone and IR might be of relevance to reduce the cardiovascular risk associated with hypertension. Renal denervation (RDN) has been shown to lower SNA by the ablation of both afferent and efferent nerves (6). The first study showing improved IS after RDN used only surrogate indexes of whole-body IR (7). To investigate the possible effects of RDN on IR in more detail, we applied a two-step hyperinsulinemiceuglycemic clamp (HEC) with glucose tracer infusion and labeled glucose infusate to separately assess glucose turnover, as well as hepatic and peripheral IS before and after RDN. Patients were also subjected to an oral glucose tolerance test (OGTT).

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Microalbuminuria in hypertension is not a determinant of insulin resistance

Abstract: In hypertension, MA is not a determinant of insulin resistance, provided confounding factors such as degree of adiposity are carefully controlled.

Cited by 17 publications

References 48 publications

Low-Grade Inflammation and Microalbuminuria in Hypertension

Low-Grade Inflammation and Microalbuminuria in Hypertension

C-Reactive Protein Modifies the Relationship Between Blood Pressure and Microalbuminuria

Renal Denervation for Resistant Hypertension Fails to Improve Insulin Resistance as Assessed by Hyperinsulinemic-Euglycemic Step Clamp

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