Your Family Physician

Saturday, May 9, 2009

Obesity Management in Adults With CKD

Case Presentation and Introduction

Case Presentation

A 22-year-old African American woman who has been dialysis dependent for 4 months because of hypertensive kidney disease is referred for kidney transplantation evaluation. Because of the recent occlusion of her left forearm arteriovenous graft, she currently is being dialyzed through a right internal jugular tunneled catheter. Her medications include methyldopa, 250 mg twice daily; calcium carbonate, 1,000 mg with each meal; and erythropoietin with dialysis. She is single without children, unemployed, and lives with her 38-year-old mother. She does not smoke or drink. Systems review findings are unremarkable. On physical examination, weight is 284 pounds (129 kg), height is 5 feet 2 inches (1.58 m), and body mass index (BMI) is 51.9 kg/m2. Blood pressure is 130/80 mm Hg, and cardiac and pulmonary examination findings are unremarkable. The surgeon believes she is a good candidate for transplantation, except she must lose weight before being listed. What advice should she be given regarding weight loss?

Introduction

This review addresses the identification and management of patients with chronic kidney disease (CKD) who may benefit from weight loss with lifestyle, pharmacological, and surgical therapies. Because of the existing controversy regarding obesity and mortality in this population, we have provided an overview of the definition of overweight and obesity in the general population and a discussion of the potential analytic problems in observational studies that try to determine BMI thresholds for mortality in populations with CKD. All adults will benefit from a healthy lifestyle regardless of kidney disease. Data also suggest that obese (BMI > 30 kg/m2 or waist circumference > 102 cm in men and > 88 cm in women) adults with CKD who are not being treated by dialysis will benefit from weight loss. For stable dependent dialysis patients, weight loss should be prescribed for persons who would be eligible for transplantation except for their degree of obesity. Otherwise, a more individualized approach is needed, and clinicians should evaluate nutritional needs along with comorbid conditions to determine the potential benefits. Multidisciplinary approaches are most effective for weight loss in any patient. However, if medical and nutritional interventions fail, bariatric surgery performed by an experienced surgeon at a certified center may be considered for a morbidly obese adult. Studies are urgently needed to determine safe approaches for effective and sustained weight loss in adults with CKD.

Overview of BMI and Mortality in the General Population

In the United States and most developed countries, the obesity epidemic substantially threatens the progress in health outcomes made during the past several decades[1] and likely will lead to growth in the number of adults with CKD. Compared with adults with BMI of 18.5 to 24.9 kg/m2, adults with BMI greater than 35 kg/m2 have a 7-fold increased odds of being given a diagnosis of diabetes and 6-fold increased odds of being hypertensive,[2] the 2 most common risk factors for CKD. A recent meta-analysis of observational studies reported that 24.2% and 33.9% of kidney disease in men and women may be attributed to overweight and obesity in the United States, respectively.[3] Although these effects are mediated largely by the development of diabetes and hypertension, increased fat mass itself may have independent effects on CKD incidence and progression.[4]

During the early part of the last century, life insurance companies were astute to the fact that obesity increases mortality. Until recently, the current standards used to classify "normal" or ideal weight, overweight, and obesity were based largely on the Metropolitan Life Insurance Company weight-for-height tables created from demographic data from adults who purchased life insurance from 1935 to 1954.[5] Groups of individuals not likely to purchase life insurance during this period were not well represented, including nonwhite adults and those with chronic medical conditions precluding life insurance eligibility.[6] Starting in 1995, the US Department of Agriculture and the US Department of Health and Human Services dietary guidelines suggested a BMI cutoff value of 25 kg/m2 or greater for defining overweight for men and women, but conceded the lack of credible evidence for a precise threshold and wide confidence intervals (CIs) for increased mortality.[5,7] These thresholds have largely been replaced by criteria published by the World Health Organization in 1997 that defined overweight as BMI of 25 kg/m2 or greater and included criteria for obesity stages I (BMI, 30 to 34.9 kg/m2), II (BMI, 35 to 39.9 kg/m2), and III (BMI ≥ 40 kg/m2)[8] ( Table 1 ).

Although a particular BMI threshold currently is used to define overweight and obesity for all individuals,[5] it remains a disputatious issue whether specific BMI cutoff values are appropriate for assessing cardiovascular and mortality risk for all age[9,10] and racial/ethnic groups.[11-14] Studies consistently have shown that obesity at a young age or during midlife decreases life expectancy.[15-17] However, the association between BMI and mortality in older adults may not mirror the associations in middle-aged or young adults.[13] A meta-analysis of studies limited to adults 65 years or older concluded that a wide range of BMI levels show no association with mortality in this group. Mortality risk does not appear to increase significantly until BMI exceeds 31 kg/m2.[18] In addition to age, the association between mortality and BMI also appears to be modified by race/ethnicity.[9,16,19,20]

Waist Circumference as a Predictor of Mortality in the General Population

Use of BMI as a proxy for degree of adiposity has become a routine part of clinical care. However, BMI reflects both fat-free mass and fat mass and does not provide information about body composition. Figure 1 shows how body fat may be preferentially distributed around the abdominal or hip area while some adults have an ideal BMI in the setting of abdominal obesity. Abdominal fat remains a strong predictor of mortality after adjustment for total body fat.[21] Thus, the adverse effects of abdominal fat largely mediate the increased cardiovascular risk associated with obesity. Although abdominal fat can be measured directly by using dual-energy X-ray absorptiometry, computed tomography, or magnetic resonance imaging, waist circumference can be measured reliably without cost and correlates highly with abdominal fat.[22-24] In the general population, adults with abdominal obesity, defined as waist circumference greater than 102 cm in men and greater than 88 cm in women, are more likely to have hypertension, diabetes, and increased cholesterol levels compared with those with a waist circumference less than these thresholds regardless of the presence of normal weight, overweight, or class I obesity.[25,26] These waist circumference cutoff values were selected from reference values associated with a BMI of 30 kg/m2 or greater in adults living in Scotland.[27] Although smaller waist circumference thresholds may be appropriate for certain racial/ethnic groups, such as Chinese or Japanese adults,[28] abdominal obesity, defined by increased waist circumference, increases the risk of cardiovascular disease and mortality regardless of BMI, age group, and race/ethnicity.

Adiposity Measures and Mortality

Adults With Stages 1 to 4 CKD

Obesity and abdominal obesity are common in adults with CKD and likely have a causal role for kidney disease incidence and progression.[31-35] However, it is unclear whether greater BMI increases mortality risk in this population. In adults with CKD, waist circumference correlates highly with abdominal fat[36] and may outperform BMI for prediction of future cardiovascular events and mortality. Elsayed et al[37] pooled data from the Atherosclerosis in Communities (ARIC) Study and the Cardiovascular Health Study (CHS) to examine the association between adiposity measures (BMI and waist-to-hip ratio) and mortality in adults with CKD. CHS participants were 65 years and older at the baseline visit, whereas the ARIC Study recruited adults aged 45 to 64 years. A total of 1,669 participants with CKD, defined as an estimated glomerular filtration rate of 15 to 60 mL/min/1.73 m2, were included in the analysis, and the primary outcome was myocardial infarction or cardiovascular death. After a mean follow-up of 9.3 years, no significant association was noted between overweight or obesity and cardiac events compared with an ideal BMI (20 to 24.9 kg/m2). Conversely, the highest waist-to-hip ratio (≥1.02 and ≥0.96 in men and women, respectively) had a 36% greater relative risk of cardiac events (95% CI, 1.02 to 1.85) compared with the group with the lowest waist-to-hip ratio (≤0.95 and 0.87 in men and women, respectively).[37] An additional analysis limited to ARIC Study participants with CKD showed that greater BMI in individuals with BMI in the normal range was associated with lower risk of mortality.[38] In contrast, no association was noted between BMI and mortality in participants with CKD and BMI of 25 kg/m2 or greater.[38] Madero et al[39] reported no association between sex-specific BMI quartiles and all-cause or cardiovascular mortality after a median follow-up of 10 years in 1,759 participants in the Modification of Diet in Renal Disease (MDRD) Study. Mean age of these adults with CKD was 51 years, and mean glomerular filtration rate was 39 ± 21 mL/min/1.73 m2.

Patients Treated by Dialysis

The issue of obesity in patients treated by dialysis presents a difficult dilemma. Although obese dialysis dependent patients face obstacles for transplantation, observational studies suggest that greater BMI is associated with improved survival in this population.[40-44] One of the largest studies, which included more than 400,000 dialysis dependent patients who initiated dialysis therapy from 1995 to 2000, noted substantial and significant differences in overall survival by BMI groups after a median follow-up of 2 years. The unadjusted annual cardiovascular mortality rate was approximately 2-fold greater in patients with BMI less than 22 kg/m2 compared with those with BMI of 37 kg/m2 or greater, and the all-cause mortality rate was more than 2-fold greater in patients with BMI less than 19 kg/m2 versus 37 kg/m2 or greater.[42] The prevalence of reported congestive heart failure was similar across BMI groups, but ischemic heart disease, myocardial infarction, peripheral vascular disease, previous stroke, and tobacco use were all lowest in the group with BMI of 37 kg/m2 or greater. After adjustment for these factors, BMI categories starting at BMI of 25 kg/m2 or greater, including the highest BMI category (≥37 kg/m2), were associated with decreased mortality compared with BMI of 22 to less than 25 kg/m2. Conversely, BMI less than 22 kg/m2 was associated with the greatest mortality risk.[42] When the investigators limited the analysis to incident dialysis dependent patients who had previously received a transplant, a potentially healthier group compared with the entire dialysis population, increased mortality was noted in those with BMI less than 22 kg/m2 and those with BMI of 37 kg/m2 or greater compared with the BMI group of 22 to less than 25 kg/m2.[42] Thus, morbid obesity did not appear to be protective in "healthier" patients receiving dialysis.

Beddhu et al[45] explored the potential confounding effects of muscle mass on the association between BMI and mortality in the dialysis population. A total of 70,028 patients who initiated dialysis therapy between 1995 and 1999 were stratified by level of urine creatinine excretion (>0.55 g/d [upper 25th percentile] versus ≤0.55 g/d) as reported on the US Renal Data System 2728 Form. Compared with the ideal-BMI group (18.5 to 24.9 kg/m2) with greater than 0.55 g/d of urine creatinine excretion, adults with BMI of 25 kg/m2 or greater and urine creatinine excretion of 0.55 g/d or less had a 14% increased risk of death (95% CI, 1.10 to 1.18), whereas those with BMI of 25 kg/m2 or greater and urine creatinine excretion greater than 0.55 g/d had 15% increased survival (95% CI, 0.83 to 0.87).[45] This analysis was criticized for potential confounding by differences in residual renal function.[44] However, regardless of BMI, those with high muscle mass had better survival than those with low muscle mass. This suggests that increasing muscle mass in hemodialysis dependent patients may improve survival.[46-48]

A major issue regarding studies examining the association between BMI and mortality in the dialysis population is the length of follow-up. Studies that show increased mortality in overweight and obese adults compared with normal BMI in the general population generally have follow-up durations that exceed 5 years.[9,12,49,50] Conversely, most studies examining BMI and mortality in dialysis dependent patients have average follow-up durations of 2 years or less.[40-43,45] In the short term, the presence of preexisting disease in those with BMI in the low end of normal will lead to greater mortality, and there may be incomplete ascertainment of these comorbid conditions. One team of investigators examined the association between BMI and mortality in 2 groups of adults living in The Netherlands. Hemodialysis dependent patients (n = 722) with a mean age of 66 ± 7 years made-up the first group, and the second group included 2,436 adults with a mean age of 62 ± 7 years not on dialysis therapy who were participants in the Hoorn Study, a population-based cohort. After 7 years of follow-up, a baseline BMI of 30 kg/m2 or greater in the hemodialysis dependent patients was associated with a 20% (95% CI, 0.8 to 1.7) increased risk of mortality compared with patients with ideal BMI. Similar results were noted in the Hoorn Study group, in which a baseline BMI of 30 kg/m2 or greater increased mortality risk by 30% (95% CI, 0.9 to 2.0) compared with an ideal BMI. The CIs for both populations crossed 1.0, most likely because of inadequate power, but the magnitude and direction of the association between obesity and 7-year mortality in these 2 groups did not differ substantially.[51]

Identification of Adults with CKD who will Benefit from Weight Loss

CKD Stages 1 to 4

The management of obesity requires identification of individuals who will benefit from weight loss. Studies show that intentional weight loss improves glucose control and decreases blood pressure in the general population,[52] 2 important factors for CKD progression.[53] Even moderate weight loss will reduce metabolic demands on the kidney[54] and may delay the progression of CKD. Weight loss has been shown to reduce proteinuria in patients with both diabetic and nondiabetic kidney diseases.[55] The National Kidney Foundation—Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) recently published clinical practice guidelines (for which evidence is strong) and clinical practice recommendations (for which evidence is limited) for diabetes and CKD.[56] Weight goals are addressed in the clinical practice recommendations section because of the dearth of evidence for the diabetic CKD population. Although these recommendations suggest that patients with CKD should maintain BMI in the range of 18.5 to 24.9 kg/m2, this is based largely on extrapolation from other populations. As such, the clinical practice recommendations strongly encourage the development of data-driven optimal BMI targets for patients with CKD.[56]

Maintaining behavioral changes for weight loss in obese individuals is very challenging, and such common CKD comorbid conditions as decreased exercise capacity only compound this difficulty. Because obtaining an ideal BMI may be especially challenging for many obese patients with CKD, clinicians should emphasize benefits of even modest weight loss and an overall healthy lifestyle encompassing diet, exercise, smoking cessation, and moderation of alcohol intake. The American College of Physicians guidelines for obesity in primary care state that clinicians should counsel all patients with BMI of 30 kg/m2 or greater on lifestyle changes for weight loss, and weight loss goals should be individually determined.[57] In adults with CKD, abdominal obesity, measured by waist circumference, should also be considered an indication for weight loss because of the strong association between abdominal obesity, metabolic syndrome, and CKD.[31,32,58] Suggested recommendations for patients with CKD who should receive interventions for weight loss are listed in Table 2 .

Regardless of BMI and waist circumference, all individuals with diabetes should receive medical nutrition therapy according to the American Diabetes Association guidelines.[59] Because many adults with CKD have diabetes, these recommendations apply to a large proportion of the CKD population and include reduced intake of total energy, saturated and trans fatty acids, cholesterol, and sodium and increased physical activity. Although BMI goals were not specified in these guidelines, they emphasize the likely benefits of a 5% to 10% weight loss, including improvements in blood pressure and cholesterol and glucose control.[59] Nutritional restrictions are discouraged for older adults in long-term care facilities because of the high risk of malnutrition in these individuals.[59]

Patients on Dialysis Therapy

Similar to the general population, increased visceral fat is associated with greater fasting plasma insulin and triglyceride levels and greater prevalence of carotid atherosclerosis in dialysis dependent patients without diabetes mellitus.[60-62] A small study of 197 adults with stage 5 CKD showed that presence of inflammation (C-reactive protein level ≥ 10 mg/L), regardless of nutritional status, was associated with significantly greater truncal body fat mass compared with no presence of inflammation.[65] Because inflammation is strongly linked to mortality in patients treated by dialysis,[66,67] adiposity itself is unlikely to confer a survival advantage.[68,69] The strength of the reported association between morbid obesity and survival does not equal the marked increase in survival associated with transplantation. One of the largest studies of obesity and mortality in the dialysis population showed a 20% greater adjusted mortality risk for patients with BMI of 22 to less than 25 kg/m2 compared with those with BMI greater than 37 kg/m2.[42] Conversely, dialysis dependent patients who receive a kidney transplant have adjusted total annual survival rates up to 200% greater than patients who remain on the transplant waiting list.[70,71]

The safety of intentional weight loss in stable dialysis dependent patients has not been studied, but many medical centers preclude kidney transplantation for patients with BMI of 35 kg/m2 or greater because of greater rates of surgical wound infections and dehiscence, delayed graft function, and acute rejection compared with kidney transplant recipients who are not obese.[72-75] The average hospital stay after kidney transplantation consequently is longer for obese patients compared with patients with ideal BMI.[72] The current reimbursement structure, which penalizes centers for performing transplantation on high-risk patients, along with other factors, may influence a center's decision to preclude transplantation for morbidly obese patients.[76] Differences in long-term allograft and patient survival between obese and nonobese kidney transplant recipients may vary by center.[74,77] However, 2 large studies, which together included data from more than 70,000 kidney transplant recipients, reported significantly greater rates of graft failure in adults with BMI of 35 kg/m2 or greater compared with patients with ideal BMI.[72,73] In the most recent study reported by Gore et al,[72] morbidly obese adults had a 22% (95% CI, 1.09 to 1.38) greater adjusted risk of graft failure compared with transplant recipients with ideal BMI. The magnitude of the association between morbid obesity and risk of graft failure was similar to the risk of graft failure associated with diabetes in this study population (hazard ratio, 1.28; 95% CI, 1.19 to 1.36).[72] Graft survival time exceeded 80 months in approximately 50% of morbidly obese transplant recipients versus 70% of transplant recipients with ideal BMI.[72] Thus, graft survival is negatively affected by the presence of morbid obesity. However, overall survival is substantially and significantly improved with kidney transplantation in obese dialysis dependent patients.[78] Using data from the US Renal Data System, Glanton et al[79] showed that cadaver and living donor transplantation reduced mortality incidence in obese adults by 61% and 77% compared with obese adults remaining on the transplant waiting list, respectively. Until transplant centers change their policy of using BMI thresholds for access to kidney transplantation, obesity in a patient who would otherwise be eligible for a kidney transplant must be viewed as the most important modifiable factor that can influence his or her overall survival. In stable dialysis dependent patients who are not eligible for transplantation for other reasons, benefits of weight loss need to be individually assessed based on the patient's comorbid conditions and nutritional status. Moreover, in the dialysis population, the focus should not simply be on weight loss, but on body composition, because interventions that increase muscle mass and improve overall fitness may improve survival.

Dietary Interventions

CKD Stages 1 to 4

The goal of a dietary intervention is to maximize sustained weight loss at an optimal level, yet long-term behavioral changes are the toughest obstacle for individuals trying to lose weight. Accordingly, 1 single dietary intervention cannot be broadly recommended. Instead, clinicians need to work with dieticians, nurses, psychologists, and social workers to determine the particular needs, motivations, and barriers for each patient. As food prices continue to increase, many patients may have difficulty affording healthy foods, an important consideration when determining a diet plan. Before recommending weight loss, the patient should be assessed for existing comorbid conditions caused by obesity, and medications that may contribute to weight gain should be delineated. A diet history should be obtained, and past experience with weight loss should be discussed.[80] There are a wide variety of healthy diets that can be considered, and these have been previously summarized in an excellent review.[81] A conservative approach is to restrict caloric intake by approximately 500 kcal/d, which in the absence of physical activity changes will lead to a weight loss of 1 lb/wk.[80] More restrictive diets (<1,200>[80] but may not be sufficient for the morbidly obese. Potential benefits of exercise to enhance weight loss and improve muscle mass in all adults with CKD, including persons who receive a kidney transplant, deserve further investigation.[82] Because weight gain is so common after kidney transplantation, dietary counseling for healthy diets with portion control should be provided before transplantation, with intensive and frequent follow-up after transplantation. Studies have documented that such interventions can ameliorate weight gain after kidney transplantation.[83,84]

The American Heart Association guidelines for a healthy lifestyle provide no specific recommendations for diet and state that the exact percentage of carbohydrates, protein, and fat within a given meal will not in itself influence weight management. Addressing portion size and reducing energy intake to less than energy expenditure is the only reliable method to facilitate weight loss.[63] High-protein diets for weight loss are extremely popular, and they appear to be useful for short-term weight loss in some individuals, but their long-term safety is unknown.[85] In adults with CKD, protein intake exceeding 20% of total calories is not recommended because of the potential detrimental effects on kidney damage and function.[86,87] The NKF—KDOQI guideline for nutritional management of patients with diabetes and CKD recommends that protein should meet, but not exceed, the Recommended Daily Allowance of 0.8 g/kg/d, with 50% to 75% of the protein derived from lean poultry, fish, and vegetables.[56] Diets that emphasize the consumption of such whole foods as fresh fruits and vegetables and whole grains, as well as the avoidance of processed foods, will provide additional benefits beyond those associated with weight loss. However, additional information about effects of specific nutrients on CKD initiation and progression is needed to better define optimal diets.

Patients Receiving Dialysis

Current guidelines for nutritional management of dialysis dependent patients recommend protein intake of 1.2 g/kg/d and 30 to 35 kcal/kg/d for stable patients.[88] However, obese dialysis dependent patients must reduce caloric consumption to levels less than energy expenditure to lose weight. Individualized treatment plans that encompass the nutritional requirements of the dialysis population are required to optimize patient outcomes. Consistent with behavioral interventions for any patient, dietary histories and food diaries are useful to determine sources of empty calories and areas in which behavioral modifications will be most helpful. Currently, evidence to support particular diets and interventions for weight loss in patients receiving dialysis is scant. A wide variety of methods may be used to create a caloric-restricted dietary plan to facilitate weight loss in this unique patient population. One conservative approach is to start with 25 kcal/kg/d based on the adjusted body weight (ideal body weight − [dry total body weight − ideal body weight]/4). This suggested caloric intake can be used as a starting point, but should be modified based on the patient's results with weight loss (personal communication, Judith Fitzhugh, Kovler Organ Transplant Center, Northwestern Memorial Hospital, August 17, 2008). Using the adjusted body weight is not as reliable as direct measures of resting energy expenditure.[6] Hence, research is needed to determine the efficacy and safety of using adjusted body weight to guide caloric intake, along with other potential methods.

Pharmacological Treatment of Obesity

After 6 to 12 months, recidivism becomes a difficult issue for even the most dedicated dieter. Most obese adults will have difficulty maintaining even a minimal to moderate weight loss and may not ever reach, let alone maintain, an ideal BMI. Weight loss medication may be used as an adjunctive therapy when diet and exercise alone have failed.[89] However, additional weight loss from pharmacological agents is usually modest.[57] Several drugs are used for the treatment of obesity, but none has been adequately tested in adults with stage 3 to 5 CKD. A tabulation of medications that have been investigated for weight loss in at least 1 randomized trial is listed in Table 3 . Some anorexic medications, which include phentermine, diethylpropion, and sibutramine along with other medications now off the market, have been associated with the development of primary pulmonary hypertension and valvular heart disease. These drugs also can increase blood pressure and should not be used in patients with a history of cardiovascular disease, cardiac arrhythmia, or stroke.[90] Considering the high prevalence of cardiovascular diseases in adults with CKD, these drugs probably should be avoided in adults with kidney disease, as well. To achieve weight loss with the selective serotonin reuptake inhibitors (fluoxetine and sertraline), high doses usually are required, which may not necessarily be safe in a patient with CKD for long-term use. Rimonabant antagonizes the CB-1 cannabinoid receptor, reduces consumption of sweet and high-fat foods, and enhances weight loss with caloric-restricted diets.[90] The drug was approved by the European Medical Agency in 2006 to aid weight loss with diet and exercise in obese adults, but because of increased risk of mood disorders, the drug has not been approved for use in the United States.[91]

Orlistat, a reversible inhibitor of gastric and pancreatic lipases, blocks approximately 30% of triglyceride gastrointestinal absorption and may be safe for use in many patients with CKD. The drug is characterized by very limited systemic absorption, with doses up to 800 mg/d yielding minimal plasma concentrations.[92] Studies have shown that the addition of orlistat to a caloric-restricted diet leads to greater weight reduction compared with the addition of a placebo.[93,94] Orlistat is available without a prescription, and the 60-mg tablet is taken 3 times daily within an hour of each meal. Because the drug interferes with cyclosporine absorption,[95,96] it should not be prescribed to patients using calcineurin inhibitors. Use of orlistat leads to incremental reductions in free fatty acid, total cholesterol, and low density lipoprotein cholesterol levels and improves insulin resistance beyond that expected with weight reduction.[92,97] This may be a function of the drug's beneficial effects on free fatty acids and subsequent improvements in insulin resistance.[97]

The social consequences of orlistat could be substantial for a given patient. Fat intake must be limited to less than 30% of total calories at each meal; otherwise, individuals are likely to experience diarrhea and fecal incontinence if the drug is taken with a high-fat meal. One study noted that 16% of persons using orlistat reported fecal incontinence,[93] but this side effect is usually temporary.[80] Fat-soluble vitamin deficiencies may also occur, and fat-soluble vitamin supplementation is usually required with long-term orlistat therapy.[93] Although warfarin use is not a contraindication for orlistat use, clinicians need to consider increasing the surveillance of prothombin times, especially when orlistat is used for a prolonged period. Orlistat use also was associated with acute kidney injury caused by renal oxalosis in an adult with CKD.[98] Thus, patients with CKD who use this drug should be monitored closely.

Bariatric Surgery

Facilitating weight loss in morbidly obese patients is frustrating because nonsurgical interventions fail in the majority.[99] For patients with BMI of 40 kg/m2 or greater or BMI of 35 kg/m2 or greater and diabetes or another obesity-related comorbid condition, bariatric surgery should be considered for treatment of obesity.[57,59,99,100] Bariatric surgery procedures (Fig 2) include those that divert food from the stomach into lower parts of the digestive tract, limiting absorption, and those that restrict gastric capacity.[99] The Roux-en-Y and biliopancreatic diversion both reduce stomach size and divert food from the stomach into the lower part of the digestive tract.[99] During adjustable gastric banding procedures, a band is placed around the upper part of the stomach, and the band may be adjusted by injecting or removing saline through a port positioned underneath the skin.[99] In 2006, Medicare agreed to provide coverage for open and laparoscopic Roux-en-Y gastric bypass, laparoscopic adjustable gastric banding, and open and laparoscopic biliopancreatic diversion with duodenal switch for adults with BMI of 35 kg/m2 or greater and at least 1 obesity-related comorbid condition in whom nonsurgical treatments failed. However, coverage is limited to procedures performed at facilities certified by the American College of Surgeons as a level 1 bariatric surgery center or certified by the American Society for Bariatric Surgery as a Bariatric Surgery Center of Excellence[99] because of substantially greater mortality rates when these procedures are performed by inexperienced surgeons and centers.[101] A list of approved facilities is listed on the Centers for Medicare & Medicaid Services website (www.cms.hhs.gov/center/coverage.asp).[99] Other procedures, such as intestinal bypass and gastric balloon procedures, are not covered because of safety concerns and efficacy.[99] Mortality rates after gastric bypass procedure are less than 2%, with greater rates in those with BMI greater than 50 kg/m2.[102,103] Laparoscopic gastric banding appears to be the safest, with mortality rates less than 0.5% in the hands of an experienced surgeon.[102,103]

Click to zoomFigure 2.

Graphic description of (A) Roux-en-Y gastric bypass procedure and (B) adjustable gastric banding. During a Roux-en-Y bypass procedure, staples are used to create a small stomach pouch that drains food directly into the lower intestine, limiting caloric absorption. Conversely, gastric banding reduces the functional size of the stomach by placing an adjustable band around the stomach neck. The stomal diameter may be changed by adjusting the inflatable silicone ring.

Figure 2.

Graphic description of (A) Roux-en-Y gastric bypass procedure and (B) adjustable gastric banding. During a Roux-en-Y bypass procedure, staples are used to create a small stomach pouch that drains food directly into the lower intestine, limiting caloric absorption. Conversely, gastric banding reduces the functional size of the stomach by placing an adjustable band around the stomach neck. The stomal diameter may be changed by adjusting the inflatable silicone ring.

Maximal weight loss is usually noted after 1 to 2 years regardless of the type of surgery.[103,104] Biliopancreatic diversion or duodenal switch procedures yield the greatest percentage of excess weight loss (70.1%), whereas excess weight loss associated with gastric banding procedures average 47.5%.[103] Intentional weight loss, even small to moderate amounts, is associated with multiple beneficial effects on such cardiovascular risk factors as fasting glucose level and blood pressure.[105] Reflecting the substantial weight loss that may occur with bariatric surgery, such chronic conditions as type 2 diabetes may resolve, defined by the presence of normal glucose levels without medications, in up to 98% of individuals undergoing gastric bypass and 48% undergoing gastric banding.[103] Both systolic and diastolic blood pressure are reduced after bariatric surgery, and the majority of hypertensive adults will have either improved or resolved hypertension.[103] Other comorbid conditions, including dyslipidemias, sleep apnea, and fatty liver, may also improve or resolve after bariatric surgery.[102] Most importantly, bariatric surgery appears to lengthen the survival of morbidly obese adults.[106,107]

Patients considering bariatric surgery for obesity management must be fully cognizant of the potential surgical complications associated with these procedures. In general, adults with CKD may be at greater risk of complications because of the propensity for infections[108] and the presence of comorbid conditions. Older adults and those with established cardiovascular disease are at high risk of complications,[107] with up to 20% of adults older than 65 years experiencing an adverse event after bariatric surgery.[109] The most common complications are gastrointestinal tract related, with more than half the bariatric surgical patients hospitalized for digestive disorders within a 5-year postoperative period in 1 series.[110] Nutritional complications, including iron, calcium, vitamin B, and fat-soluble vitamin deficiencies, are common after gastric bypass procedures, whereas nutritional deficiencies after banding procedures can usually be managed by using a multivitamin.[102]

Intestinal bypass procedures can result in enteric hyperoxaluria leading to kidney stones and renal oxalosis, with irreversible kidney damage.[111-114] Nasr et al[112] reported 11 cases of adults who developed oxalate nephropathy after Roux-en-Y gastric bypass procedures, and 8 of these patients eventually required dialysis. The majority of these patients had mild CKD at baseline;[112] thus, clinicians must be aware that CKD may worsen after gastric bypass procedures. The clinical effects of oxalate hyperabsorption in patients dialysis are uncertain; however, oxalate-induced anemia in a patient with enteric hyperoxaluria caused by Crohn disease has been reported.[115] One study from a single institution reported that of 491 patients who underwent gastric bypass surgery, acute kidney injury, defined as a 50% increase in serum creatinine level during the first 3 postoperative days or requirement of dialysis during the postoperative period, occurred in 8.5%. Two patients who developed acute kidney injury died while in the hospital.[116] Information for baseline kidney function in these patients was not delineated. Until a study systematically determines mortality and adverse-event rates by the presence of kidney disease, the overall safety of bariatric surgery in adults with CKD is unknown. Despite its potential risk, bariatric surgery has shown clinical benefit in adults with CKD. Successful kidney transplantation after facilitation of weight loss by means of bariatric surgery has been reported in morbidly obese dialysis dependent adults.[117] In 1 patient, kidney failure resolved after gastric bypass surgery in a morbidly obese patient with glomerulonephritis.[118] Bariatric surgery has also been useful in adults who gain substantial weight after kidney transplantation.[117,119,120]

Psychosocial Aspects of Obesity

Depression and other psychiatric disorders frequently accompany obesity, especially morbid obesity.[121-123] Up to 30% of adults seeking bariatric surgery report depression symptoms.[124] Facilitation of weight loss with bariatric surgery has been shown to improve symptoms of depression and self-esteem.[122,125,126] Although preoperative depression does not appear to negatively influence weight loss, all patients should be evaluated for depression and other mood disorders before surgery, and behavioral and/or pharmacologic therapy should be offered.[124] Persons with a history of chronic depression before surgery will probably have persistence of a mood disorder after surgery despite weight loss, and suicide risk may be heightened after surgery.[124] A multidisciplinary approach must be used to evaluate patients desiring bariatric surgery, and mood disorders must be included in the overall patient assessment.

Summary

All adults, including those with and without CKD, should receive counseling on the benefits of a healthy lifestyle, which includes a healthy diet, physical activity, and smoking cessation. In people with CKD who are overweight, but not obese, potential benefits of weight loss to the recommended "ideal" range are uncertain. Nevertheless, obesity is associated with increased inflammation, insulin resistance, hypertension, and dyslipidemia, and overweight adults with CKD should be counseled about the risks of weight gain. In persons with CKD and generalized or abdominal obesity, weight loss should be encouraged. For patients on dialysis therapy, survival can be greatly increased with kidney transplantation. Patients who are not eligible for transplantation because of obesity should receive lifestyle and medical interventions for weight loss. If nutritional and medical management fails, bariatric surgery by an experienced surgeon at a certified center may be considered. When eligibility for transplantation is not an issue for an obese patient on dialysis therapy, individualized approaches are needed and interventions should emphasize a healthy lifestyle and exercise that can increase muscle mass. Studies are urgently needed to define the benefits and risks of weight loss by means of lifestyle interventions, medications, and surgery for obese patients with CKD.

References

  1. Office of the Surgeon General (ed): The Surgeon General's Call to Action to Prevent and Decrease Overweight and Obesity. Rockville, MD, US Department of Health and Human Services PHS; Washington DC, US Government Printing Office, 2001
  2. Mokdad AH, Ford ES, Bowman BA, et al: Prevalence of obesity, diabetes, and obesity-related health risk factors, 2001. JAMA 289:76-79, 2003
  3. Wang Y, Chen X, Song Y, Caballero B, Cheskin LJ: Association between obesity and kidney disease: A systematic review and meta-analysis. Kidney Int 73:19-33, 2008
  4. Griffin KA, Kramer H, Bidani AK: Adverse renal consequences of obesity. Am J Physiol Renal Physiol 294:F685-F696, 2008
  5. Kuczmarski RJ, Flegal KM: Criteria for definition of overweight in transition: Background and recommendations for the United States. Am J Clin Nutr 72:1074-1081, 2000
  6. Harvey KS: Methods for determining healthy body weight in end stage renal disease. J Ren Nutr 16:269-276, 2006
  7. Nutrition and Your Health: Dietary Guidelines for Americans. Washington DC, US Department of Agriculture and US Department of Health and Human Services, 1995
  8. WHO: Obesity: Preventing and Managing the Global Epidemic: Report of a WHO Consultation on Obesity, Geneva, June 3-5, 1997. Geneva, Switzerland, World Health Organization, 1998
  9. Durazo-Arvizu RA, McGee DL, Cooper RS, Liao Y, Luke A: Mortality and optimal body mass index in a sample of the US population.Am J Epidemiol 147:739-749, 1998
  10. Calle EE, Thun MJ, Petrelli JM, Rodriguez C, Heath CW Jr: Body-mass index and mortality in a prospective cohort of U.S. adults. N Engl J Med 341:1097-1105, 1999
  11. Andres R, Elahi D, Tobin JD, Muller DC, Brant L: Impact of age on weight goals. Ann Intern Med 103:1030-1033, 1985
  12. Stevens J, Cai J, Pamuk ER, Williamson DF, Thun MJ, Wood JL: The effect of age on the association between body-mass index and mortality. N Engl J Med 338:1-7, 1998
  13. Grabowski DC, Ellis JE: High body mass index does not predict mortality in older people: Analysis of the Longitudinal Study of Aging. J Am Geriatr Soc 49:968-979, 2001
  14. Stevens J, Cai J, Juhaeri, Thun MJ, Williamson DF, Wood JL: Consequences of the use of different measures of effect to determine the impact of age on the association between obesity and mortality. Am J Epidemiol 150:399-407, 1999
  15. Adams KF, Schatzkin A, Harris TB, et al: Overweight, obesity, and mortality in a large prospective cohort of persons 50 to 71 years old. N Engl J Med 355:763-778, 2006
  16. Fontaine KR, Redden DT, Wang C, Westfall AO, Allison DB:Years of life lost due to obesity. JAMA289:187-193, 2003
  17. Peeters A, Barendregt JJ, Willekens F, Mackenbach JP, Al Mamun A, Bonneux L: Obesity in adulthood and its consequences for life expectancy: A life-table analysis. Ann Intern Med 138:24-32, 2003
  18. Heiat A, Vaccarino V, Krumholz HM: An evidencebased assessment of federal guidelines for overweight and obesity as they apply to elderly persons. Arch Intern Med 161:1194-1203, 2001
  19. Abell JE, Egan BM, Wilson PW, Lipsitz S, Woolson RF, Lackland DT: Differences in cardiovascular disease mortality associated with body mass between black and white persons.Am J Public Health 98:63-66, 2008
  20. Durazo-Arvizu R, Cooper RS, Luke A, Prewitt TE, Liao Y, McGee DL: Relative weight and mortality in U.S. blacks and whites: Findings from representative national population samples. Ann Epidemiol 7:383-395, 1997
  21. Bigaard J, Frederiksen K, Tjonneland A, et al: Waist circumference and body composition in relation to all-cause mortality in middle-aged men and women. Int J Obes 29:778-784, 2005
  22. Rankinen T, Kim SY, Perusse L, Despres JP, Bouchard C: The prediction of abdominal visceral fat level from body composition and anthropometry: ROC analysis. J Int Assoc Stud Obes 23:801-809, 1999
  23. Reeder BA, Senthilselvan A, Despres JP, et al: The association of cardiovascular disease risk factors with abdominal obesity in Canada. Canadian Heart Health Surveys Research Group. CMAJ 157:S39-S45, 1997 (suppl 1)
  24. Pouliot MC, Despres JP, Lemieux S, et al: Waist circumference and abdominal sagittal diameter: Best simple anthropometric indexes of abdominal visceral adipose tissue accumulation and related cardiovascular risk in men and women. Am J Cardiol 73:460-468, 1994
  25. Janssen I, Katzmarzyk PT, Ross R: Body mass index, waist circumference, and health risk: Evidence in support of current National Institutes of Health guidelines. Arch Intern Med 162:2074-2079, 2002
  26. Balkau B, Deanfield JE, Despres JP, et al: International Day for the Evaluation of Abdominal Obesity (IDEA): A study of waist circumference, cardiovascular disease, and diabetes mellitus in 168,000 primary care patients in 63 countries. Circulation 116:1942-1951, 2007
  27. Lean ME, Han TS, Morrison CE: Waist circumference as a measure for indicating need for weight management. BMJ 311:158-161, 1995
  28. Narisawa S, Nakamura K, Kato K, Yamada K, Sasaki J, Yamamoto M: Appropriate waist circumference cutoff values for persons with multiple cardiovascular risk factors in Japan: A large cross-sectional study. J Epidemiol 18:37-42, 2008
  29. Koster A, Leitzmann MF, Schatzkin A, et al: Waist circumference and mortality. Am J Epidemiol 167:1465-1475, 2008
  30. Zhang C, Rexrode KM, van Dam RM, Li TY, Hu FB: Abdominal obesity and the risk of all-cause, cardiovascular, and cancer mortality: Sixteen years of follow-up in US women. Circulation 117:1658-1667, 2008
  31. Chen J, Muntner P, Hamm LL, et al: Insulin resistance and risk of chronic kidney disease in nondiabetic US adults. J Am Soc Nephrol 14:469-477, 2003
  32. Chen J, Muntner P, Hamm LL, et al: The metabolic syndrome and chronic kidney disease in U.S. adults. Ann Intern Med 140:167-174, 2004
  33. Kramer H, Luke A, Bidani A, Cao G, Cooper R, McGee D: Obesity and prevalent and incident chronic kidney disease: The Hypertension Detection and Follow-up Program. Am J Kidney Dis 46:587-594, 2005
  34. Hsu CY, McCulloch CE, Iribarren C, Darbinian J, Go AS: Body mass index and risk for end-stage renal disease. Ann Intern Med 144:21-28, 2006
  35. Gelber RP, Kurth T, Kausz AT, et al: Association between body mass index and CKD in apparently healthy men. Am J Kidney Dis 46:871-880, 2005
  36. Sanches F, Avesani C, Kamimura M, et al: Waist circumference and visceral fat in CKD: A cross-sectional study. Am J Kidney Dis 52:66-73, 2008
  37. Elsayed EF, Tighiouart H,Weiner DE, et al:Waist-tohip ratio and body mass index as risk factors for cardiovascular events in CKD. Am J Kidney Dis 52:49-57, 2008
  38. Kwan BC, Murtaugh MA, Beddhu S: Associations of body size with metabolic syndrome and mortality in moderate chronic kidney disease. Clin J Am Soc Nephrol 2:992-998, 2007
  39. Madero M, Sarnak MJ, Wang X, et al: Body mass index and mortality in CKD. Am J Kidney Dis 50:404-411, 2007
  40. Leavey SF, McCullough K, Hecking E, Goodkin D, Port FK, Young EW: Body mass index and mortality in 'healthier' as compared with 'sicker' haemodialysis patients: Results from the Dialysis Outcomes and Practice Patterns Study (DOPPS). Nephrol Dial Transplant 16:2386-2394, 2001
  41. Fleischmann E, Teal N, Dudley J, MayW, Bower JD, Salahudeen AK: Influence of excess weight on mortality and hospital stay in 1346 hemodialysis patients. Kidney Int 55:1560-1567, 1999
  42. Johansen KL, Young B, Kaysen GA, Chertow GM: Association of body size with outcomes among patients beginning dialysis. Am J Clin Nutr 80:324-332, 2004
  43. Kalantar-Zadeh K, Kopple JD, Kilpatrick RD, et al: Association of morbid obesity and weight change over time with cardiovascular survival in hemodialysis population. Am J Kidney Dis 46:489-500, 2005
  44. Kalantar-Zadeh K: Obesity paradox in patients on maintenance dialysis, in Wolf G (ed): Obesity and the Kidney. Basel, Switzerland, Karger, 2006, pp 57-69
  45. Beddhu S, Pappas LM, Ramkumar N, Samore M: Effects of body size and body composition on survival in hemodialysis patients. J Am Soc Nephrol 14:2366-2372, 2003
  46. Beddhu S: The body mass index paradox and an obesity, inflammation, and atherosclerosis syndrome in chronic kidney disease. Semin Dial 17:229-232, 2004
  47. Kakiya R, Shoji T, Tsujimoto Y, et al: Body fat mass and lean mass as predictors of survival in hemodialysis patients [see comment]. Kidney Int 70:549-556, 2006
  48. Kalantar-Zadeh K, Kuwae N, Wu DY, et al: Associations of body fat and its changes over time with quality of life and prospective mortality in hemodialysis patients. Am J Clin Nutr 83:202-210, 2006
  49. Lindsted KD, Singh PN: Body mass and 26-year risk of mortality among women who never smoked: Findings from the Adventist Mortality Study. Am J Epidemiol 146:1-11, 1997
  50. McGee DL and Diverse Populations Collaboration: Body mass index and mortality: A meta-analysis based on person-level data from twenty-six observational studies. Ann Epidemiol 15:87-97, 2005
  51. de Mutsert R, Snijder MB, van der Sman-de Beer F, et al: Association between body mass index and mortality is similar in the hemodialysis population and the general population at high age and equal duration of follow-up. J Am Soc Nephrol 18:967-974, 2007
  52. Poirier P, Giles TD, Bray GA, et al: Obesity and cardiovascular disease: Pathophysiology, evaluation, and effect of weight loss: An update of the 1997 American Heart Association Scientific Statement on Obesity and Heart Disease from the Obesity Committee of the Council on Nutrition, Physical Activity, and Metabolism. Circulation 113:898-918, 2006
  53. Orchard TJ, Temprosa M, Goldberg R, et al: The effect of metformin and intensive lifestyle intervention on the metabolic syndrome: The Diabetes Prevention Program randomized trial. Ann Intern Med 142:611-619, 2005
  54. 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 14:1480-1486, 2003
  55. Morales E, Valero MA, Leon M, Hernandez E, Praga M: Beneficial effects of weight loss in overweight patients with chronic proteinuric nephropathies. Am J Kidney Dis 41:319-327, 2003
  56. National Kidney Foundation: KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease. Guideline 5: Nutritional management in diabetes and chronic kidney disease. Am J Kidney Dis 49:S95-S107, 2007 (suppl 2)
  57. Snow V, Barry P, Fitterman N, Qaseem A, Weiss K: Clinical Efficacy Assessment Subcommittee of the American College of Physicians. Pharmacologic and surgical management of obesity in primary care: A clinical practice guideline from the American College of Physicians. Ann Intern Med 142:525-531, 2005
  58. Bagby SP: Obesity-initiated metabolic syndrome and the kidney: A recipe for chronic kidney disease? J Am Soc Nephrol 15:2775-2791, 2004
  59. Bantle JP, Wylie-Rosett J, Albright AL, et al: Nutrition recommendations and interventions for diabetes: A position statement of the American Diabetes Association. Diabetes Care 31:S61-S78, 2008 (suppl 1)
  60. Kahraman S, Yilmaz R, Akinci D, et al: U-Shaped association of body mass index with inflammation and atherosclerosis in hemodialysis patients. J Ren Nutr 15:377-386, 2005
  61. Odamaki M, Furuya R, Ohkawa S, et al: Altered abdominal fat distribution and its association with the serum lipid profile in non-diabetic haemodialysis patients. Nephrol Dial Transplant 14:2427-2432, 1999
  62. Yamauchi T, Kuno T, Takada H, Nagura Y, Kanmatsuse K, Takahashi S: The impact of visceral fat on multiple risk factors and carotid atherosclerosis in chronic haemodialysis patients. Nephrol Dial Transplant 18:1842-1847, 2003
  63. Lichtenstein AH, Appel LJ, Brands M, et al, for the American Heart Association Nutrition Committee: Diet and lifestyle recommendations revision 2006: A scientific statement from the American Heart Association Nutrition Committee [erratum in Circulation 114:e629, 2006]. Circulation 114:82-96, 2006
  64. National Kidney Foundation: K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease: Evaluation, classification and stratification. Part 4. Definition and classification of stages of chronic kidney disease. Am J Kidney Dis 39:S72-S75, 2002 (suppl 1)
  65. Axelsson J, Rashid Qureshi A, Suliman ME, et al: Truncal fat mass as a contributor to inflammation in endstage renal disease.Am J Clin Nutr 80:1222-1229, 2004
  66. Hung CY, Chen YA, Chou CC, Yang CS: Nutritional and inflammatory markers in the prediction of mortality in Chinese hemodialysis patients. Nephron 100:c20-c26, 2005
  67. Yeun JY, Levine RA, Mantadilok V, Kaysen GA: C-Reactive protein predicts all-cause and cardiovascular mortality in hemodialysis patients. Am J Kidney Dis 35:469-476, 2000
  68. Beddhu S, Ramkumar N, Samore MH: The paradox of the "body mass index paradox" in dialysis patients: Associations of adiposity with inflammation. Am J Clin Nutr 82:909-910, 2005
  69. Stenvinkel P, Lindholm B: Resolved: Being fat is good for dialysis patients: The Godzilla effect: Con. J Am Soc Nephrol 19:1062-1064, 2008
  70. Rabbat CG, Thorpe KE, Russell JD, Churchill DN: Comparison of mortality risk for dialysis patients and cadaveric first renal transplant recipients in Ontario, Canada. J Am Soc Nephrol 11:917-922, 2000
  71. Wolfe RA, Ashby VB, Milford EL, et al: Comparison of mortality in all patients on dialysis, patients on dialysis awaiting transplantation, and recipients of a first cadaveric transplant. N Engl J Med 341:1725-1730, 1999
  72. Gore JL, Pham PT, Danovitch GM, et al: Obesity and outcome following renal transplantation. Am J Transplant 6:357-363, 2006
  73. Meier-Kriesche HU, Arndorfer JA, Kaplan B: The impact of body mass index on renal transplant outcomes: A significant independent risk factor for graft failure and patient death. Transplantation 73:70-74, 2002
  74. Jindal RM, Zawada ET Jr: Obesity and kidney transplantation. Am J Kidney Dis 43:943-952, 2004
  75. Johnson DW, Isbel NM, Brown AM, et al: The effect of obesity on renal transplant outcomes. Transplantation 74:675-681, 2002
  76. Kalil RS, Hunsicker LG: The disadvantage of being fat [comment]. JAm Soc Nephrol 19:191-193, 2008
  77. Chang SH, Coates PT, McDonald SP: Effects of body mass index at transplant on outcomes of kidney transplantation. Transplantation 84:981-987, 2007
  78. Pelletier SJ, Maraschio MA, Schaubel DE, et al: Survival benefit of kidney and liver transplantation for obese patients on the waiting list. Clin Transplants 77-88, 2003
  79. Glanton CW, Kao TC, Cruess D, Agodoa LY, Abbott KC: Impact of renal transplantation on survival in end-stage renal disease patients with elevated body mass index. Kidney Int 63:647-653, 2003
  80. Eckel RH: Clinical practice. Nonsurgical management of obesity in adults. N Engl J Med 358:1941-1950, 2008
  81. Packard DP, Milton JE, Shuler LA, Short RA, Tuttle KR: Implications of chronic kidney disease for dietary treatment in cardiovascular disease. J Ren Nutr 16:259-268, 2006
  82. Moinuddin I, Leehey DJ: A comparison of aerobic exercise and resistance training in patients with and without chronic kidney disease. Adv Chronic Kidney Dis 15:83-96, 2008
  83. Patel MG: The effect of dietary intervention on weight gains after renal transplantation. J Ren Nutr 8:137-141, 1998
  84. Guida B, Trio R, Laccetti R, et al: Role of dietary intervention on metabolic abnormalities and nutritional status after renal transplantation. Nephrol Dial Transplant 22:3304-3310, 2007
  85. Kennedy ET, Bowman SA, Spence JT, Freedman M, King J: Popular diets: Correlation to health, nutrition, and obesity. JAm Diet Assoc 101:411-420, 2001
  86. Friedman AN: High-protein diets: Potential effects on the kidney in renal health and disease. Am J Kidney Dis 44:950-962, 2004
  87. Uribarri J, Tuttle KR: Advanced glycation end products and nephrotoxicity of high-protein diets. Clin J Am Soc Nephrol 1:1293-1299, 2006
  88. National Kidney Foundation: K/DOQI Clinical Practice Guidelines for Nutrition in Chronic Renal Failure. Am J Kidney Dis 35:S1-S140, 2000 (suppl 2)
  89. Li Z, Maglione M, Tu W, et al: Meta-analysis: Pharmacologic treatment of obesity. Ann Intern Med 142:532-546, 2005
  90. Bray GA, Greenway FL: Pharmacological treatment of the overweight patient. Pharmacol Rev 59:151-184, 2007
  91. FDA: Briefing Document. NDA 21-888 Zimulti (rimonabant) Tablets, 20 mg Sanofi Aventis Advisory Committee 2007.Available at: http://www.fda.gov/ohrms/dockets/AC/07/
    briefing/2007-4306b1-fda-backgrounder.pdf. AccessedAugust 18, 2008
  92. Henness S, Perry CM: Orlistat: A review of its use in the management of obesity. Drugs 66:1625-1656, 2006
  93. Finer N, James WP, Kopelman PG, Lean ME, Williams G: One-year treatment of obesity: A randomized, double-blind, placebo-controlled, multicentre study of orlistat, a gastrointestinal lipase inhibitor. J Int Assoc Stud Obes 24:306-313, 2000
  94. Torgerson JS, Hauptman J, Boldrin MN, Sjostrom L: XENical in the prevention of Diabetes in Obese Subjects (XENDOS) Study: A randomized study of orlistat as an adjunct to lifestyle changes for the prevention of type 2 diabetes in obese patients. Diabetes Care 27:155-161, 2004
  95. Nagele H, Petersen B, Bonacker U, Rodiger W: Effect of orlistat on blood cyclosporin concentration in an obese heart transplant patient. Eur J Clin Pharmacol 55:667-669, 1999
  96. Zhi J, Moore R, Kanitra L, Mulligan TE: Pharmacokinetic evaluation of the possible interaction between selected concomitant medications and orlistat at steady state in healthy subjects. J Clin Pharmacol 42:1011-1019, 2002
  97. Kelley DE, Kuller LH, McKolanis TM, Harper P, Mancino J, Kalhan S: Effects of moderate weight loss and orlistat on insulin resistance, regional adiposity, and fatty acids in type 2 diabetes. Diabetes Care 27:33-40, 2004
  98. Singh A, Sarkar SR, Gaber LW, Perazella MA: Acute oxalate nephropathy associated with orlistat, a gastrointestinal lipase inhibitor.Am J Kidney Dis 49:153-157, 2007
  99. Phurrough S, Salive M, Brechner R, Tillman K, Harrison S, O'Connor D: Decision Memo for Bariatric Surgery for the Treatment of Morbid Obesity 2006. Available at http://www.cms.hhs.gov/mcd/viewdecisionmemo.asp?id=160. Accessed November 7, 2008
  100. Consensus Development Conference Panel: NIH conference: Gastrointestinal surgery for severe obesity. Ann Intern Med 115:956-961, 1991
  101. Flum DR, Salem L, Elrod JA, Dellinger EP, Cheadle A, Chan L: Early mortality among Medicare beneficiaries undergoing bariatric surgical procedures. JAMA 294:1903-1908, 2005
  102. Bouldin M, Ross L, Sumrall C, Loustalot F, Low A, Land K: The effect of obesity surgery on obesity comorbidity. Am J Med Sci 331:183-193, 2006
  103. Buchwald H,Avidor Y, Braunwald E, et al: Bariatric surgery: A systematic review and meta-analysis. JAMA 292:1724-1737, 2004
  104. Sjostrom L, Lindroos AK, Peltonen M, et al: Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med 351:2683-2693, 2004
  105. Anderson J, Konz E: Obesity and disease management: Effects of weight loss on co-morbid conditions. Obes Res 9:S326-S334, 2001 (suppl 11)
  106. Flum DR, Dellinger EP: Impact of gastric bypass operation on survival: A population-based analysis. J Am Coll Surg 199:543-551, 2004
  107. Sjostrom L, Narbro K, Sjostrom CD, et al: Effects of bariatric surgery on mortality in Swedish obese subjects. N Engl J Med 357:741-752, 2007
  108. Eleftheriadis T, Antoniadi G, Liakopoulos V, Kartsios C, Stefanidis I: Disturbances of acquired immunity in hemodialysis patients. Semin Dial 20:440-451, 2007
  109. Livingston EH, Langert J: The impact of age and Medicare status on bariatric surgical outcomes. Arch Surg 141:1115-1120, 2006
  110. Christou NV, Sampalis JS, Liberman M, et al: Surgery decreases long-term mortality, morbidity, and health care use in morbidly obese patients. Ann Surg 240:416-423, 2004
  111. Asplin JR, Coe FL: Hyperoxaluria in kidney stone formers treated with modern bariatric surgery. J Urol 177:565-569, 2007
  112. Nasr SH, D'AgatiV, Said SM, et al: Oxalate nephropathy complicating Roux-en-Y gastric bypass:An underrecognized cause of irreversible renal failure. Clin J Am Soc Nephrol 2008 Aug 13 [Epub ahead of print]
  113. Sinha MK, Collazo-Clavell ML, Rule A, et al: Hyperoxaluric nephrolithiasis is a complication of Rouxen-Y gastric bypass surgery. Kidney Int 72:100-107, 2007
  114. Nelson WK, Houghton SG, Milliner DS, Lieske JC, Sarr MG: Enteric hyperoxaluria, nephrolithiasis, and oxalate nephropathy: Potentially serious and unappreciated complicationsof Roux-en-Y gastric bypass. Surg Obes Relat Dis 1:481-485, 2005
  115. Bernhardt WM, Schefold JC, Weichert W, et al: Amelioration of anemia after kidney transplantation in severe secondary oxalosis. Clin Nephrol 65:216-221, 2006
  116. Thakar CV, Kharat V, Blanck S, Leonard AC: Acute kidney injury after gastric bypass surgery. Clin J Am Soc Nephrol 2:426-430, 2007
  117. Koshy A: Laparoscopic gastric banding surgery performed in obese dialysis patients prior to kidney transplantation. Am J Kidney Dis 52:e15-e17,2008
  118. Soto FC, Higa-Sansone G, Copley JB, et al: Renal failure, glomerulonephritis and morbid obesity: Improvement after rapid weight loss following laparoscopic gastric bypass. Obes Surg 15:137-140, 2005
  119. Newcombe V, Blanch A, Slater GH, Szold A, Fielding GA: Laparoscopic adjustable gastric banding prior to renal transplantation. Obes Surg 15:567-570, 2005
  120. Alexander JW, Goodman H: Gastric bypass in chronic renal failure and renal transplant. Nutr Clin Pract 22:16-21, 2007
  121. Petry NM, Barry D, Pietrzak RH, Wagner JA: Overweight and obesity are associated with psychiatric disorders: Results from the National Epidemiologic Survey on Alcohol and Related Conditions. Psychosom Med 70:288-297, 2008
  122. Schowalter M, Benecke A, Lager C, et al: Changes in depression following gastric banding: A 5- to 7-year prospective study. Obes Surg 18:314-320, 2008
  123. Onyike CU, Crum RM, Lee HB, Lyketsos CG, Eaton WW: Is obesity associated with major depression? Results from the Third National Health and Nutrition Examination Survey.Am J Epidemiol 158:1139-1147, 2003
  124. Wadden TA, Sarwer DB, Fabricatore AN, Jones L, Stack R,Williams NS: Psychosocial and behavioral status of patients undergoing bariatric surgery: What to expect before and after surgery. Med Clin North Am 91:451-469, 2007
  125. Dixon JB, Dixon ME, O'Brien PE: Depression in association with severe obesity: Changes with weight loss. Arch Intern Med 163:2058-2065, 2003
  126. Emery CF, Fondow MD, Schneider CM, et al: Gastric bypass surgery is associated with reduced inflammation and less depression: A preliminary investigation. Obes Surg 17:759-763, 20
Source : http://www.medscape.com/viewarticle/586404_10
posted by hermandarmawan93 at 22:12

0 Comments:

Post a Comment

<< Home