Obesity-related glomerulopathy: An emerging epidemic

Kambham, Neeraja; Markowitz, Glen S.; Valeri, Anthony M.; Lin, Julie; D’Agati, Vivette D.

doi:10.1046/j.1523-1755.2001.0590041498.x

Cited by 1,127 publications

(979 citation statements)

References 42 publications

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“…However, the significant correlation between weight loss and serum creatinine and urinary protein excretion indicates that weight loss, at least, contributes greatly to the improvement. Several studies showed that obese patients could develop proteinuria and progressive loss of renal function, 17,18 and weight loss improved them. 8,19 The proposed mechanisms by which obesity increased renal risk include increasing GFR, 20 focal segmental glomerulosclerosis, 21 activation of the rennin-angiotensin system, 8 and adipocyte-derived cytokines.…”

Section: Discussionmentioning

confidence: 99%

Effect of weight loss using formula diet on renal function in obese patients with diabetic nephropathy

et al. 2005

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OBJECTIVE:To evaluate the effect and safety of treatment with low-calorie formula diet on renal function and proteinuria in obese patients with diabetic nephropathy. DESIGN: Prospective study on safety and efficacy of a 4-week low-calorie (11-19 kcal/kg/day) normal-protein (0.9-1.2 g/kg/ day) diet partly supplemented with formula diet. SUBJECTS: In all, 22 obese patients with diabetic nephropathy (BMI: 30.475.3 kg/m 2 , HbA1c: 7.171.4%, serum creatinine: 172.4757.5 mmol/l, urinary protein: 3.372.6 g/day). RESULTS: The mean body weight decreased by 6.273.0 kg. The mean systolic blood pressure, creatinine, blood urea nitrogen, urinary protein, and 8-hydroxydeoxyguanosine decreased significantly by 7.5712.7 mmHg, 41.6723.9 mmol/l, 1.5071.61 mmol/l, 1.871.7 g/day, and 3.173.6 ng/mg creatinine, respectively. No patient had increased serum creatinine and urinary protein. Mean creatinine clearance (40.6717.9 to 46.1714.6 ml/s/1.73 m 2 ) and serum albumin showed no significant changes. Dserum creatinine and Durinary protein correlated with Dbody weight (r ¼ 0.62 and 0.49, respectively) and Dvisceral fat area (r ¼ 0.58 and 0.58, respectively), but did not correlate with Dsystolic blood pressure, Dfasting blood glucose and Dsubcutaneous fat area. CONCLUSION: These results suggested that weight reduction using formula diet might improve renal function and proteinuria safely for a short term in obese patients with diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

Effect of weight loss using formula diet on renal function in obese patients with diabetic nephropathy

et al. 2005

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“…Increased numbers of interstitial cells and an increase in material rich in lipids and proteoglycans compresses the renal parenchyma toward the pole of the kidney resulting in the formation of round-shaped, enlarged kidneys in obese subjects. 29,30 Renal compression affects both vascular (mainly the vasa recta) and tubular (the Henle's loops) elements causing activation of the RAS and increased sodium reabsorption.…”

Section: Structural Changes In the Kidneymentioning

confidence: 99%

“…There is also evidence that SNS response to hypoxia may affect the renal circulation in patients with obstructive sleep apnea, an abnormality often seen in the obese population. 4,30 Hyperfiltration as a result of heightened blood flow to the kidney is always present in obesity, long before glomerulopathy occurs. It is, therefore, the primary cause of gradual sclerosis of the glomeruli wall because of physical stress and eventually of a vicious circle in which nephrons are injured, sodium retention worsens and arterial pressure reaches higher values to maintain sodium balance.…”

Section: Structural Changes In the Kidneymentioning

confidence: 99%

Mechanisms of obesity-induced hypertension

et al. 2010

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The relationship between obesity and hypertension is well established both in children and adults. The mechanisms through which obesity directly causes hypertension are still an area of research. Activation of the sympathetic nervous system has been considered to have an important function in the pathogenesis of obesity-related hypertension. The arterial-pressure control mechanism of diuresis and natriuresis, according to the principle of infinite feedback gain, seems to be shifted toward higher blood-pressure levels in obese individuals. During the early phases of obesity, primary sodium retention exists as a result of increase in renal tubular reabsorption. Extracellular-fluid volume is expanded and the kidney-fluid apparatus is resetted to a hypertensive level, consistent with a model of hypertension because of volume overload. Plasma renin activity, angiotensinogen, angiotensin II and aldosterone values display significant increase during obesity. Insulin resistance and inflammation may promote an altered profile of vascular function and consequently hypertension. Leptin and other neuropeptides are possible links between obesity and the development of hypertension. Obesity should be considered as a chronic medical condition, which is likely to require long-term treatment. Understanding of the mechanisms associated with obesity-related hypertension is essential for successful treatment strategies. Hypertension Research (2010) 33, 386-393; doi:10.1038/hr.2010.9Keywords: leptin; obesity; pressure natriuresis; rennin-angiotensin-aldosterone system; sympathetic nervous system INTRODUCTION Obesity is a common disorder that develops from the interaction between the genotype and the environment and involves social, behavioral, cultural, physiological, metabolic and genetic factors. A large number of studies have shown that obesity has an important negative impact on health in a population, leading to the recommendation for general practitioners to have an important function in the management of this condition and of its associated comorbidities such as hypertension, hyperlipidemia and hyperinsulinemia/insulin resistance. The relationship between obesity and hypertension is well established both in adults and children. 1,2 Obese individuals exhibit higher levels of office as well as ambulatory blood pressure (BP) from childhood to old age. Obese subjects display higher BP levels than non-obese individuals even in the normotensive range. The combination of obesity, hypertension and other cardiovascular risk factors significantly increases the probability of adverse cardiovascular outcomes, and raises considerations for aggressive treatment strategies. 3 The mechanisms through which obesity directly causes hypertension are still an area of research. Human and animal studies have elucidated the function of adipose tissue derivatives (adipokines and cytokines), neurohumoral pathways, metabolic functions and modulation of pressor/depressor mechanisms. Although obesity-related hypertension may be the result of a combinatio...

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“…These include ectopic lipid accumulation [42] and increased deposition of renal sinus fat [43,44], the development of glomerular hypertension and increased glomerular permeability caused by hyperfiltrationrelated glomerular filtration barrier injury [45], and ultimately the development of glomerulomegaly [46], and focal or segmental glomerulosclerosis [41] (Fig. 2).…”

Section: Mechanisms Of Action Underlying the Renal Effects Of Obesitymentioning

confidence: 99%