Prevention of the Development and Progression of Renal Disease

Hostetter, Thomas H.

doi:10.1097/01.asn.0000070150.60928.06

Cited by 55 publications

(24 citation statements)

References 23 publications

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“…Following this idea, CRF may lead to OSAS by alterations in chemoreflex responsiveness, pharyngeal narrowing due to fluid overload, and accumulation of uremic toxins. On the other hand, OSAS can also accelerate loss of kidney function since chronic intermittent hypoxia directly or indirectly via renin-angiotensin system (RAS) activation [22] leads to kidney damage by facilitating glomerular hyperfiltration and systemic hypertension, both of which can impair kidney function [23].…”

Section: Discussionmentioning

confidence: 99%

Analyses of melatonin, cytokines, and sleep in chronic renal failure

2015

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Section: Discussionmentioning

confidence: 99%

Analyses of melatonin, cytokines, and sleep in chronic renal failure

2015

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“…The progression of DN is commonly defined by an increase in albuminuria from normoalbuminuria to microalbuminuria and from microalbuminuria to macroalbuminuria. On average, 20-40% of patients with diabetes develop renal dysfunction (45), but type 2 diabetics with ESRD are rapidly increasing because of the continuing increase in the prevalence of T2D (2). Indeed, T2D patients represent the large majority of macroalbuminuric patients at risk of ESRD (2).…”

Section: A B C D E Fmentioning

confidence: 99%

Decreased expression of circulating microRNA-126 in patients with type 2 diabetic nephropathy: A potential blood-based biomarker

Al‐Κafaji

Al‐Mahroos

Al‐Muhtaresh

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Circulating microRNAs (miRNAs) have been proposed as promising biomarkers for multiple diseases. miR-126 is reported to be associated with type 2 diabetes mellitus (T2D), diabetic nephropathy (DN) and end stage renal disease. The aim of this study was to investigate the expression of circulating miR-126 and to assess its potential as a blood-based biomarker for DN in T2D patients. In 52 patients with T2D without history of DN (with noromoalbuminuria), 50 patients with T2D and DN (29 with microalbuminuria and 21 with macroalbuminuria), and 50 non-diabetic healthy controls, the expression of circulating miR-126 in peripheral whole blood was evaluated by quantitative polymerase chain reaction. The expression levels of circulating miR-126 were significantly decreased in T2D patients and further decreased in DN patients compared with those in the controls. Multivariate logistic regression analysis confirmed the independent association of lower miR-126 levels with T2D [adjusted odds ratio (OR), 0.797; 95% confidence interval (CI), 0.613-0.960] and DN (adjusted OR, 0.513; 95% CI, 0.371-0.708). miR-126 levels were associated with the degree of albuminuria and showed significantly low expression in DN patients with microalbuminuria (adjusted OR, 0.781; 95% CI; 0.698-0.952) and further lower expression in DN patients with macroalbuminuria (adjusted OR, 0.433; 95% CI, 0.299-0.701), respectively compared with T2D patients with normoalbuminuria. miR-126 levels negatively correlated with albuminuria positively with glomerular filtration rate (P<0.05), and in addition, negatively correlated with fasting glucose, glycated hemoglobin, triglyceride and LDL (P<0.05). Stepwise multiple regression analysis identified albuminuria as a significant predictor of miR-126 (P<0.001). miR-126 in peripheral blood yielded area under the receiver operating characteristic curves of 0.854 (95% CI, 0.779-0.929) and 0.959 (95% CI, 0.916-1.000) in the differentiation of DN patients from T2D patients and DN patients from non-diabetic controls respectively. These data suggest that decreased expression of circulating miR-126 is associated with the development of DN in T2D patients, and may be a promising blood-based biomarker for DN risk estimation.

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“…12 Price et al later reported that BMI accounted for Ϸ50% of the renal plasma flow (RPF) response to irbesartan in type 2 diabetic subjects. 13 Because activation of the RAS is associated with progression of kidney disease, 14 these observations raised the question of whether obesity is associated with activation of the intrarenal RAS. We hypothesized that a positive relationship existed between BMI and activation of the intrarenal RAS.…”

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confidence: 99%

Body Mass Index and Angiotensin-Dependent Control of the Renal Circulation in Healthy Humans

et al. 2005

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Abstract-Obesity is increasingly recognized as a risk factor for renal disease, but the mechanism is unclear. Renal plasma flow response to captopril, as an index of renin-angiotensin system activity, was measured by para-aminohippurate clearance technique in 100 healthy, normotensive subjects in balance on a high-salt diet. Of the 100 subjects, body mass index exceeded 25 in 56 and exceeded 30 in 22. The average vasodilator response to captopril was 27Ϯ7 mL/min per 1.73 m 2 (PϽ0.0001). After adjustment for other predictors of the renal plasma flow response to captopril using a multivariate linear regression model, there was a highly significant relationship between age-and plasma renin activity-adjusted body mass index and the renal plasma flow response to captopril; however, a quadratic model provided a substantially better fit (rϭ0.55; PϽ0.0001; Pϭ0.03 versus linear correlation). The strong association between increasing body mass index and angiotensin-dependent control of the renal circulation suggests that this may be a mechanism by which obesity contributes to renal disease. Weight loss should be considered in the overweight or obese patient for renal protection. Ն30) 1 and each year, an estimated 300 000 US adults die prematurely of obesity-related causes. 2 Obesity is an independent risk factor for the development of kidney disease. [3][4][5][6] There is little doubt that excess weight gain is a major cause of hypertension and type 2 diabetes, which, together, account for Ͼ70% of end-stage renal disease in the United States. 7 Moreover, evidence also suggests that even in nondiabetic obese patients, there is some degree of renal dysfunction that can lead to more serious injury to the kidneys because metabolic and hemodynamic disturbances worsen with prolonged obesity. 4,6,8,9 The mechanism by which obesity predisposes to kidney damage is unclear, but animal studies suggest an important role for the renin-angiotensin system (RAS). 9 -11 Because animal studies typically involve rapid weight gain from overfeeding, and obesity in humans represents a much more gradual weight gain over years, it has not been clear to what extent these observations in animal models apply to humans. Two observations from our laboratory brought this potential relationship to our attention. Hopkins et al observed that obesity was associated with a blunted renovascular response to angiotensin II (Ang II) infusion, a finding consistent with increased intrarenal Ang II production. 12 Price et al later reported that BMI accounted for Ϸ50% of the renal plasma flow (RPF) response to irbesartan in type 2 diabetic subjects. 13 Because activation of the RAS is associated with progression of kidney disease, 14 these observations raised the question of whether obesity is associated with activation of the intrarenal RAS. We hypothesized that a positive relationship existed between BMI and activation of the intrarenal RAS. We thus examined renal hemodynamic function at baseline and in response to the angiotensin-converting enzyme (ACE) inhibit...

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Prevention of the Development and Progression of Renal Disease

Abstract: Abstract. Prevention of the major causes of ESRD, hypertension, and diabetes, is possible. Careful glycemic control can prevent diabetes nephropathy.

Cited by 55 publications

References 23 publications

Analyses of melatonin, cytokines, and sleep in chronic renal failure

Analyses of melatonin, cytokines, and sleep in chronic renal failure

Decreased expression of circulating microRNA-126 in patients with type 2 diabetic nephropathy: A potential blood-based biomarker

Body Mass Index and Angiotensin-Dependent Control of the Renal Circulation in Healthy Humans

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