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      Obesity-Related Chronic Kidney Disease—The Role of Lipid Metabolism

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          Abstract

          Obesity is an independent risk factor for chronic kidney disease (CKD). The mechanisms linking obesity and CKD include systemic changes such as high blood pressure and hyperglycemia, and intrarenal effects relating to lipid accumulation. Normal lipid metabolism is integral to renal physiology and disturbances of renal lipid and energy metabolism are increasingly being linked with kidney disease. AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) are important regulators of fatty acid oxidation, which is frequently abnormal in the kidney with CKD. A high fat diet reduces renal AMPK activity, thereby contributing to reduced fatty acid oxidation and energy imbalance, and treatments to activate AMPK are beneficial in animal models of obesity-related CKD. Studies have found that the specific cell types affected by excessive lipid accumulation are proximal tubular cells, podocytes, and mesangial cells. Targeting disturbances of renal energy metabolism is a promising approach to addressing the current epidemic of obesity-related kidney disease.

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          Mechanisms of tubulointerstitial fibrosis.

          Michael Zeisberg, Eric G. Neilson (2010)
          The pathologic paradigm for renal progression is advancing tubulointerstitial fibrosis. Whereas mechanisms underlying fibrogenesis have grown in scope and understanding in recent decades, effective human treatment to directly halt or even reverse fibrosis remains elusive. Here, we examine key features mediating the molecular and cellular basis of tubulointerstitial fibrosis and highlight new insights that may lead to novel therapies. How to prevent chronic kidney disease from progressing to renal failure awaits even deeper biochemical understanding.
          Article 0 comments Cited 294 times – based on 0 reviews     Review now
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            Obesity-related glomerulopathy: an emerging epidemic.

            N Kambham, G S Markowitz, A Valeri … (2001)
            We report the first large renal biopsy-based clinicopathologic study on obesity-related glomerulopathy. Obesity was defined as body mass index (BMI)> 30 kg/m2. Obesity-related glomerulopathy (ORG) was defined morphologically as focal segmental glomerulosclerosis and glomerulomegaly (O-FSGS; N = 57) or glomerulomegaly alone (O-GM; N = 14). Review of 6818 native renal biopsies received from 1986 to 2000 revealed a progressive increase in biopsy incidence of ORG from 0.2% in 1986-1990 to 2.0% in 1996-2000 (P = 0.0001). Mean BMI in ORG was 41.7 (range 30.9 to 62.7). Indications for renal biopsy included proteinuria (N = 40) or proteinuria and renal insufficiency (N = 31). Seventy-one patients with ORG were compared to 50 patients with idiopathic FSGS (I-FSGS). Patients with ORG were older (mean 42.9 vs. 32.6 years, P < 0.001) and more often Caucasian (75% vs. 52%; P = 0.003). ORG patients had a lower incidence of nephrotic range proteinuria (48% vs. 66%; P = 0.007) and nephrotic syndrome (5.6% vs. 54%; P < 0.001), with higher serum albumin (3.9 vs. 2.9 g/dL; P < 0.001), lower serum cholesterol (229 vs. 335 mg/dL; P < 0.001), and less edema (35% vs. 68%; P = 0.003). On renal biopsy, patients with ORG had fewer lesions of segmental sclerosis (10 vs. 39%; P < 0.001), more glomerulomegaly (100% vs. 10%; P < 0.001), and less extensive foot process effacement (40 vs. 75%; P < 0.001). Glomerular diameter in ORG (mean 226 mu) was significantly larger than age- and sex-matched normal controls (mean 168 mu; P < 0.001). Follow-up was available in 56 ORG patients (mean 27 months) and 50 idiopathic FSGS controls (mean 38 months). A total of 75% of ORG patients received angiotensin-converting enzyme (ACE) inhibition or A2 blockade while 78% of the I-FSGS patients received immunosuppressive therapy. ORG patients had less frequent doubling of serum creatinine (14.3% vs. 50%; P < 0.001) and progression to ESRD (3.6% vs. 42%; P < 0.001). On multivariate analysis, presenting serum creatinine and severity of proteinuria were the only predictors of poor outcome in ORG. ORG is distinct from idiopathic FSGS, with a lower incidence of nephrotic syndrome, more indolent course, consistent presence of glomerulomegaly, and milder foot process fusion. The ten-fold increase in incidence over 15 years suggests a newly emerging epidemic. Heightened physician awareness of this entity is needed to ensure accurate diagnosis and appropriate therapy.
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              Risk factors for end-stage renal disease: 25-year follow-up.

              Chi-yuan Hsu, Carlos Iribarren, Charles E McCulloch … (2009)
              Few cohort studies have focused on risk factors for end-stage renal disease (ESRD). This investigation evaluated the prognostic value of several potential novel risk factors for ESRD after considering established risk factors. We studied 177 570 individuals from a large integrated health care delivery system in northern California who volunteered for health checkups between June 1, 1964, and August 31, 1973. Initiation of ESRD treatment was ascertained using US Renal Data System registry data through December 31, 2000. A total of 842 cases of ESRD were observed during 5 275 957 person-years of follow-up. This comprehensive evaluation confirmed the importance of established risk factors, including the following: male sex, older age, proteinuria, diabetes mellitus, lower educational attainment, and African American race, as well as higher blood pressure, body mass index, and serum creatinine level. The 2 most potent risk factors were proteinuria and excess weight. For proteinuria, the adjusted hazard ratios (HRs) were 7.90 (95% confidence interval [CI], 5.35-11.67) for 3 to 4+ on urine dipstick, 3.59 (2.82-4.57) for 1 to 2+ on urine dipstick, and 2.37 (1.79-3.14) for trace vs negative on urine dipstick. For excess weight, the HRs were 4.39 (95% CI, 3.38-5.70) for class 2 to class 3 obesity, 3.11 (2.51-3.84) for class 1 obesity, and 1.65 (1.39-1.97) for overweight vs normal weight. Furthermore, several independent novel risk factors for ESRD were identified, including lower hemoglobin level (1.33 [1.08-1.63] for lowest vs highest quartile), higher serum uric acid level (2.14 [1.65-2.77] for highest vs lowest quartile), self-reported history of nocturia (1.36 [1.17-1.58]), and family history of kidney disease (HR, 1.40 [95% CI, 1.02-1.90]). We confirmed the importance of established ESRD risk factors in this large cohort with broad sex and racial/ethnic representation. Lower hemoglobin level, higher serum uric acid level, self-reported history of nocturia, and family history of kidney disease are independent risk factors for ESRD.
              Article 0 comments Cited 173 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Peter Meikle: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): Metabolites
                Journal ID (iso-abbrev): Metabolites
                Journal ID (publisher-id): metabolites
                Title: Metabolites
                Publisher: MDPI
                ISSN (Electronic): 2218-1989
                Publication date (Electronic): 11 December 2015
                Publication date Collection: December 2015
                Volume: 5
                Issue: 4
                Pages: 720-732
                Affiliations
                [1 ]Department of Nephrology, Austin Health, Heidelberg, Melbourne 3084, Australia; E-Mails: Matthew.Davies@ 123456austin.org.au (M.D.); Suet-Wan.Choy@ 123456austin.org.au (S-W.C.); Natasha.Cook@ 123456austin.org.au (N.C.); David.Power@ 123456austin.org.au (D.P.)
                [2 ]Department of Medicine, Austin Health, University of Melbourne, Heidelberg 3084, Australia
                [3 ]Institute for Breathing and Sleep, Austin Health, Heidelberg, Melbourne 3084, Australia
                Author notes
                [* ]Author to whom correspondence should be addressed; E-Mail: Peter.Mount@ 123456austin.org.au ; Tel.: +61-3-9496-3059; Fax: +61-3-9496-5123.
                Article
                Publisher ID: metabolites-05-00720
                DOI: 10.3390/metabo5040720
                PMC ID: 4693192
                PubMed ID: 26690487
                SO-VID: 38637427-28a3-400f-84f6-8c705442a88c
                Copyright © © 2015 by the authors; licensee MDPI, Basel, Switzerland.
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 03 November 2015
                Date accepted : 08 December 2015
                Categories
                Subject: Review

                Keywords: obesity,chronic kidney disease,lipid metabolism,amp-activated protein kinase,acetyl-coa carboxylase,high fat diet,podocyte,mesangial cell,proximal tubule
                Data availability:
                Keywords: obesity, chronic kidney disease, lipid metabolism, amp-activated protein kinase, acetyl-coa carboxylase, high fat diet, podocyte, mesangial cell, proximal tubule

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