- Email: [email protected]
Comment on: determinants associated with the correction of glomerular hyperfiltration one year after bariatric surgery
1766
G. Favre et al. / Surgery for Obesity and Related Diseases 13 (2017) 1760–1767
[7] Tomaszewski M, Charchar FJ, Maric C, et al. Glomerular hyperfiltration: a new marker of metabolic risk. Kidney Int 2007;71 (8):816–21. [8] Bosma RJ, Kwakernaak AJ, van der Heide JJ, de Jong PE, Navis GJ. Body mass index and glomerular hyperfiltration in renal transplant recipients: cross-sectional analysis and long-term impact. Am J Transplant 2007;7(3):645–52. [9] Ruggenenti P, Porrini EL, Gaspari F, et al. Glomerular hyperfiltration and renal disease progression in type 2 diabetes. Diabetes Care 2012;35(10):2061–8. [10] Kwakernaak AJ, Toering TJ, Navis G. Body mass index and body fat distribution as renal risk factors: a focus on the role of renal haemodynamics. Nephrol Dial Transplant 2013;28(Suppl 4):iv42–9. [11] Iannelli A, Martini F, Rodolphe A, et al. Body composition, anthropometrics, energy expenditure, systemic inflammation, in premenopausal women 1 year after laparoscopic Roux-en-Y gastric bypass. Surg Endosc 2014;28(2):500–7. [12] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes - 5-year outcomes. N Engl J Med 2017;376(7):641–51. [13] Ozmen S, Kaplan MA, Kaya H, et al. Role of lean body mass for estimation of glomerular filtration rate in patients with chronic kidney disease with various body mass indices. Scand J Urol Nephrol 2009;43(2):171–6. [14] Jesudason DR, Clifton P. Interpreting different measures of glomerular filtration rate in obesity and weight loss: pitfalls for the clinician. Int J Obes (Lond) 2012;36(11):1421–7. [15] Navaneethan SD, Yehnert H, Moustarah F, Schreiber MJ, Schauer PR, Beddhu S. Weight loss interventions in chronic kidney disease: a systematic review and meta-analysis. Clin J Am Soc Nephrol 2009;4 (10):1565–74. [16] Chagnac A, Weinstein T, Herman M, Hirsh J, Gafter U, Ori Y. The effects of weight loss on renal function in patients with severe obesity. J Am Soc Nephrol 2003;14(6):1480–6. [17] Iannelli A, Anty R, Schneck AS, Tran A, Gugenheim J. Inflammation, insulin resistance, lipid disturbances, anthropometrics, and metabolic syndrome in morbidly obese patients: a case control study comparing laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy. Surgery 2011;149(3):364–70. [18] Engeli S, Bohnke J, Gorzelniak K, et al. Weight loss and the reninangiotensin-aldosterone system. Hypertension 2005;45(3):356–62. [19] Lieske JC, Collazo-Clavell ML, Sarr MG, Rule AD, Bergstralh EJ, Kumar R. Gastric bypass surgery and measured and estimated GFR in women. Am J Kidney Dis 2014;64(4):663–5. [20] Brochner-Mortensen J, Rickers H, Balslev I. Renal function and body composition before and after intestinal bypass operation in obese patients. Scand J Clin Lab Invest 1980;40(8):695–702. [21] Coupaye M, Flamant M, Sami O, et al. Determinants of evolution of glomerular filtration rate after bariatric surgery: a 1-year observational study. Obes Surg 2017;27(1):126–33.
[22] Hou CC, Shyu RS, Lee WJ, Ser KH, Lee YC, Chen SC. Improved renal function 12 months after bariatric surgery. Surg Obes Relat Dis 2013;9(2):202–6. [23] Favre GA, Esnault VL, Van Obberghen E. Modulation of glucose metabolism by the renin-angiotensin-aldosterone system. Am J Physiol Endocrinol Metab 2015;308(6):E435–49. [24] Neels JG, Olefsky JM. Inflamed fat: what starts the fire? J Clin Invest 2006;116(1):33–5. [25] Guo G, Morrissey J, McCracken R, Tolley T, Liapis H, Klahr S. Contributions of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis. Am J Physiol Renal Physiol 2001;280 (5):F777–85. [26] Wolf G, Ziyadeh FN. Leptin and renal fibrosis. Contrib Nephrol 2006;151:175–83. [27] Sharma K. Obesity, oxidative stress, and fibrosis in chronic kidney disease. Kidney Int Suppl (2011) 2014;4(1):113–7. [28] Sarafidis PA. Obesity, insulin resistance and kidney disease risk: insights into the relationship. Curr Opin Nephrol Hypertens 2008;17 (5):450–6. [29] Park HS, Park JY, Yu R. Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. Diabetes Res Clin Pract 2005;69(1):29–35. [30] Adami GF, Scopinaro N, Cordera R. Adipokine pattern after bariatric surgery: beyond the weight loss. Obes Surg 2016;26(11):2793–801. [31] Salazar DE, Corcoran GB. Predicting creatinine clearance and renal drug clearance in obese patients from estimated fat-free body mass. Am J Med 1988;84(6):1053–60. [32] Navaneethan SD, Malin SK, Arrigain S, Kashyap SR, Kirwan JP, Schauer PR. Bariatric surgery, kidney function, insulin resistance, and adipokines in patients with decreased GFR: a cohort study. Am J Kidney Dis 2015;65(2):345–7. [33] Lemoine S, Guebre-Egziabher F, Sens F, et al. Accuracy of GFR estimation in obese patients. Clin J Am Soc Nephrol 2014;9 (4):720–7. [34] Okada R, Yasuda Y, Tsushita K, Wakai K, Hamajima N, Matsuo S. The number of metabolic syndrome components is a good risk indicator for both early- and late-stage kidney damage. Nutr Metab Cardiovasc Dis 2014;24(3):277–85. [35] Lovell A, Game P, Wittert G, Thompson C. Estimating renal function in morbidly obese patients. Obes Surg 2013;23(9):1427–30. [36] Navaneethan SD, Yehnert H. Bariatric surgery and progression of chronic kidney disease. Surg Obes Relat Dis 2009;5(6):662–5. [37] Kovesdy CP, Kopple JD, Kalantar-Zadeh K. Management of proteinenergy wasting in non-dialysis-dependent chronic kidney disease: reconciling low protein intake with nutritional therapy. Am J Clin Nutr 2013;97(6):1163–77. [38] Windsor JA, Hill GL. Protein depletion and surgical risk. Aust N Z J Surg 1988;58(9):711–5.
Editorial comment
Comment on: determinants associated with the correction of glomerular hyperfiltration one year after bariatric surgery Metabolic surgery offers the opportunity to durably address several obesity-related co-morbidities, many of which have complex interactions and deleterious end-organ effects [1]. The destructive potential of type 2 diabetes, for
instance, on renal function in morbidly obese patients is well known and need not be summarized for this audience. Patients with impaired renal function are common in bariatric practices/programs and may present anywhere
Hyperfiltration in Severe Obesity / Surgery for Obesity and Related Diseases 13 (2017) 1760–1767
along the chronic kidney disease spectrum, even including dialysis-dependent patients seeking bariatric surgery as a potential bridge to renal transplant [2]. Because of this, most bariatric surgeons are comfortable with the nuances and challenges patients with chronic kidney disease can pose. However, what is less understood is the magnitude of benefit weight loss surgery can impart on renal function, what mechanisms govern this, and what (if any) predictive variables for renal function improvement may exist. Both direct and indirect mechanisms can contribute to renal insufficiency in obesity. Indirect mechanisms are well established and are more related to the increased incidence of nephrotoxic diseases (type 2 diabetes, hypertension) in the morbidly obese. However, there are direct ways in which obesity leads to chronic kidney disease, and one of the major proposed mechanisms is related to hyperfiltration of a fixed number of nephrons dealing with increased volume demands [3]. Not surprisingly, surgical weight loss has been shown to be capable of decreasing hyperfiltration and increasing glomerular filtration rate (GFR) in the morbidly obese, highlighting yet another profound effect of metabolic surgery [4]. As with type 2 diabetes, it is of significant benefit to identify predictive factors of renal disease amelioration after bariatric surgery, especially when that is the primary motivation for seeking surgery [5]. Herein, the authors present a relatively novel way to indirectly assess the pre- and postsurgical effects on GFR given the logistical challenges of obtaining direct GFR measurements. This method aims to adjust for fluctuations in lean body mass after surgical weight loss and its effect on the accuracy of GFR calculations because serum creatinine is dependent on muscle mass. Interestingly, they report 3 independent determinants associated with a reduction in
1767
hyperfiltration reduction after metabolic surgery: (1) low baseline C-reactive protein levels, (2) low baseline brachial circumference, and (3) high reduction rate of fat mass. The largest corrections in GFR were observed in severely obese patients, and this appeared to be limited by chronic inflammation. Although further work is needed, this study is a great starting point in trying to establish which patients may benefit most when seeking bariatric surgery with a primary goal of improvement of kidney function. As with most disease processes, not every patient will achieve the desired outcome, and it is important to establish predictive variables for both success and failure. Christopher R. Daigle, M.D., F.R.C.S.C. Cleveland Clinic Akron General The Bariatric Center Akron, Ohio
References [1] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes - 5-year outcomes. N Engl J Med 2017;376(7):641–51. [2] Jamal MH, Corcelles R, Daigle CR, et al. Safety and effectiveness of bariatric surgery in dialysis patients and kidney transplantation candidates. Surg Obes Relat Dis 2015;11(2):419–23. [3] Helal I, Fick-Brosnahan GM, Reed-Gitomer B, et al. Glomerular hyperfiltration: definitions, mechanisms and clinical implications. Nat Rev Nephrol 2012;8(5):293–300. [4] Hou CC, Shyu RS, Lee WJ, et al. Improved renal function 12 months after bariatric surgery. Surg Obes Relat Dis 2013;9(2):202–6. [5] Lee MH, Lee WJ, Chong K, et al. Predictors of long-term diabetes remission after metabolic surgery. J Gastrointest Surg 2015;19 (6):1015–21.
G. Favre et al. / Surgery for Obesity and Related Diseases 13 (2017) 1760–1767
[7] Tomaszewski M, Charchar FJ, Maric C, et al. Glomerular hyperfiltration: a new marker of metabolic risk. Kidney Int 2007;71 (8):816–21. [8] Bosma RJ, Kwakernaak AJ, van der Heide JJ, de Jong PE, Navis GJ. Body mass index and glomerular hyperfiltration in renal transplant recipients: cross-sectional analysis and long-term impact. Am J Transplant 2007;7(3):645–52. [9] Ruggenenti P, Porrini EL, Gaspari F, et al. Glomerular hyperfiltration and renal disease progression in type 2 diabetes. Diabetes Care 2012;35(10):2061–8. [10] Kwakernaak AJ, Toering TJ, Navis G. Body mass index and body fat distribution as renal risk factors: a focus on the role of renal haemodynamics. Nephrol Dial Transplant 2013;28(Suppl 4):iv42–9. [11] Iannelli A, Martini F, Rodolphe A, et al. Body composition, anthropometrics, energy expenditure, systemic inflammation, in premenopausal women 1 year after laparoscopic Roux-en-Y gastric bypass. Surg Endosc 2014;28(2):500–7. [12] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes - 5-year outcomes. N Engl J Med 2017;376(7):641–51. [13] Ozmen S, Kaplan MA, Kaya H, et al. Role of lean body mass for estimation of glomerular filtration rate in patients with chronic kidney disease with various body mass indices. Scand J Urol Nephrol 2009;43(2):171–6. [14] Jesudason DR, Clifton P. Interpreting different measures of glomerular filtration rate in obesity and weight loss: pitfalls for the clinician. Int J Obes (Lond) 2012;36(11):1421–7. [15] Navaneethan SD, Yehnert H, Moustarah F, Schreiber MJ, Schauer PR, Beddhu S. Weight loss interventions in chronic kidney disease: a systematic review and meta-analysis. Clin J Am Soc Nephrol 2009;4 (10):1565–74. [16] Chagnac A, Weinstein T, Herman M, Hirsh J, Gafter U, Ori Y. The effects of weight loss on renal function in patients with severe obesity. J Am Soc Nephrol 2003;14(6):1480–6. [17] Iannelli A, Anty R, Schneck AS, Tran A, Gugenheim J. Inflammation, insulin resistance, lipid disturbances, anthropometrics, and metabolic syndrome in morbidly obese patients: a case control study comparing laparoscopic Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy. Surgery 2011;149(3):364–70. [18] Engeli S, Bohnke J, Gorzelniak K, et al. Weight loss and the reninangiotensin-aldosterone system. Hypertension 2005;45(3):356–62. [19] Lieske JC, Collazo-Clavell ML, Sarr MG, Rule AD, Bergstralh EJ, Kumar R. Gastric bypass surgery and measured and estimated GFR in women. Am J Kidney Dis 2014;64(4):663–5. [20] Brochner-Mortensen J, Rickers H, Balslev I. Renal function and body composition before and after intestinal bypass operation in obese patients. Scand J Clin Lab Invest 1980;40(8):695–702. [21] Coupaye M, Flamant M, Sami O, et al. Determinants of evolution of glomerular filtration rate after bariatric surgery: a 1-year observational study. Obes Surg 2017;27(1):126–33.
[22] Hou CC, Shyu RS, Lee WJ, Ser KH, Lee YC, Chen SC. Improved renal function 12 months after bariatric surgery. Surg Obes Relat Dis 2013;9(2):202–6. [23] Favre GA, Esnault VL, Van Obberghen E. Modulation of glucose metabolism by the renin-angiotensin-aldosterone system. Am J Physiol Endocrinol Metab 2015;308(6):E435–49. [24] Neels JG, Olefsky JM. Inflamed fat: what starts the fire? J Clin Invest 2006;116(1):33–5. [25] Guo G, Morrissey J, McCracken R, Tolley T, Liapis H, Klahr S. Contributions of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis. Am J Physiol Renal Physiol 2001;280 (5):F777–85. [26] Wolf G, Ziyadeh FN. Leptin and renal fibrosis. Contrib Nephrol 2006;151:175–83. [27] Sharma K. Obesity, oxidative stress, and fibrosis in chronic kidney disease. Kidney Int Suppl (2011) 2014;4(1):113–7. [28] Sarafidis PA. Obesity, insulin resistance and kidney disease risk: insights into the relationship. Curr Opin Nephrol Hypertens 2008;17 (5):450–6. [29] Park HS, Park JY, Yu R. Relationship of obesity and visceral adiposity with serum concentrations of CRP, TNF-alpha and IL-6. Diabetes Res Clin Pract 2005;69(1):29–35. [30] Adami GF, Scopinaro N, Cordera R. Adipokine pattern after bariatric surgery: beyond the weight loss. Obes Surg 2016;26(11):2793–801. [31] Salazar DE, Corcoran GB. Predicting creatinine clearance and renal drug clearance in obese patients from estimated fat-free body mass. Am J Med 1988;84(6):1053–60. [32] Navaneethan SD, Malin SK, Arrigain S, Kashyap SR, Kirwan JP, Schauer PR. Bariatric surgery, kidney function, insulin resistance, and adipokines in patients with decreased GFR: a cohort study. Am J Kidney Dis 2015;65(2):345–7. [33] Lemoine S, Guebre-Egziabher F, Sens F, et al. Accuracy of GFR estimation in obese patients. Clin J Am Soc Nephrol 2014;9 (4):720–7. [34] Okada R, Yasuda Y, Tsushita K, Wakai K, Hamajima N, Matsuo S. The number of metabolic syndrome components is a good risk indicator for both early- and late-stage kidney damage. Nutr Metab Cardiovasc Dis 2014;24(3):277–85. [35] Lovell A, Game P, Wittert G, Thompson C. Estimating renal function in morbidly obese patients. Obes Surg 2013;23(9):1427–30. [36] Navaneethan SD, Yehnert H. Bariatric surgery and progression of chronic kidney disease. Surg Obes Relat Dis 2009;5(6):662–5. [37] Kovesdy CP, Kopple JD, Kalantar-Zadeh K. Management of proteinenergy wasting in non-dialysis-dependent chronic kidney disease: reconciling low protein intake with nutritional therapy. Am J Clin Nutr 2013;97(6):1163–77. [38] Windsor JA, Hill GL. Protein depletion and surgical risk. Aust N Z J Surg 1988;58(9):711–5.
Editorial comment
Comment on: determinants associated with the correction of glomerular hyperfiltration one year after bariatric surgery Metabolic surgery offers the opportunity to durably address several obesity-related co-morbidities, many of which have complex interactions and deleterious end-organ effects [1]. The destructive potential of type 2 diabetes, for
instance, on renal function in morbidly obese patients is well known and need not be summarized for this audience. Patients with impaired renal function are common in bariatric practices/programs and may present anywhere
Hyperfiltration in Severe Obesity / Surgery for Obesity and Related Diseases 13 (2017) 1760–1767
along the chronic kidney disease spectrum, even including dialysis-dependent patients seeking bariatric surgery as a potential bridge to renal transplant [2]. Because of this, most bariatric surgeons are comfortable with the nuances and challenges patients with chronic kidney disease can pose. However, what is less understood is the magnitude of benefit weight loss surgery can impart on renal function, what mechanisms govern this, and what (if any) predictive variables for renal function improvement may exist. Both direct and indirect mechanisms can contribute to renal insufficiency in obesity. Indirect mechanisms are well established and are more related to the increased incidence of nephrotoxic diseases (type 2 diabetes, hypertension) in the morbidly obese. However, there are direct ways in which obesity leads to chronic kidney disease, and one of the major proposed mechanisms is related to hyperfiltration of a fixed number of nephrons dealing with increased volume demands [3]. Not surprisingly, surgical weight loss has been shown to be capable of decreasing hyperfiltration and increasing glomerular filtration rate (GFR) in the morbidly obese, highlighting yet another profound effect of metabolic surgery [4]. As with type 2 diabetes, it is of significant benefit to identify predictive factors of renal disease amelioration after bariatric surgery, especially when that is the primary motivation for seeking surgery [5]. Herein, the authors present a relatively novel way to indirectly assess the pre- and postsurgical effects on GFR given the logistical challenges of obtaining direct GFR measurements. This method aims to adjust for fluctuations in lean body mass after surgical weight loss and its effect on the accuracy of GFR calculations because serum creatinine is dependent on muscle mass. Interestingly, they report 3 independent determinants associated with a reduction in
1767
hyperfiltration reduction after metabolic surgery: (1) low baseline C-reactive protein levels, (2) low baseline brachial circumference, and (3) high reduction rate of fat mass. The largest corrections in GFR were observed in severely obese patients, and this appeared to be limited by chronic inflammation. Although further work is needed, this study is a great starting point in trying to establish which patients may benefit most when seeking bariatric surgery with a primary goal of improvement of kidney function. As with most disease processes, not every patient will achieve the desired outcome, and it is important to establish predictive variables for both success and failure. Christopher R. Daigle, M.D., F.R.C.S.C. Cleveland Clinic Akron General The Bariatric Center Akron, Ohio
References [1] Schauer PR, Bhatt DL, Kirwan JP, et al. Bariatric surgery versus intensive medical therapy for diabetes - 5-year outcomes. N Engl J Med 2017;376(7):641–51. [2] Jamal MH, Corcelles R, Daigle CR, et al. Safety and effectiveness of bariatric surgery in dialysis patients and kidney transplantation candidates. Surg Obes Relat Dis 2015;11(2):419–23. [3] Helal I, Fick-Brosnahan GM, Reed-Gitomer B, et al. Glomerular hyperfiltration: definitions, mechanisms and clinical implications. Nat Rev Nephrol 2012;8(5):293–300. [4] Hou CC, Shyu RS, Lee WJ, et al. Improved renal function 12 months after bariatric surgery. Surg Obes Relat Dis 2013;9(2):202–6. [5] Lee MH, Lee WJ, Chong K, et al. Predictors of long-term diabetes remission after metabolic surgery. J Gastrointest Surg 2015;19 (6):1015–21.