SummaryBackground and objectives IGF-1 deficiency links to malnutrition in CKD patients; however, it is not clear to what extent it associates with survival among these patients.Design, setting, participants, & measurements Serum IGF-1 and other biochemical, clinical (subjective global assessment), and densitometric (dual energy x-ray absorptiometry) markers of nutritional status and mineral and bone metabolism were measured in a cohort of 365 Swedish clinically stable CKD stage 5 patients (median age of 53 years) initiating dialysis between 1994 and 2009; in 207 patients, measurements were also taken after 1 year of dialysis. Deaths were registered during a median follow-up of 5 years. Associations of mortality with baseline IGF-1 and changes of IGF-1 after 1 year of dialysis were evaluated by Cox models.Results At baseline, IGF-1 concentrations associated negatively with age, diabetes mellitus, cardiovascular disease, poor nutritional status, IL-6, and osteoprotegerin and positively with body fat mass, bone mineral density, serum phosphate, calcium, and fibroblast growth factor-23. At 1 year, IGF-1 had increased by 33%. In multivariate regression, low age, diabetes mellitus, and high serum phosphate and calcium associated with IGF-1 at baseline, and in a mixed model, these factors, together with high fat body mass, associated with changes of IGF-1 during the first 1 year of dialysis. Adjusting for calendar year of inclusion, age, sex, diabetes mellitus, cardiovascular disease, IL-6, and poor nutritional status, a 1 SD higher level of IGF-1 at baseline associated with lower mortality risk (hazard ratio, 0.57; 95% confidence interval, 0.32 to 0.98). Persistently low or decreasing IGF-1 levels during the first 1 year on dialysis predicted worse survival (adjusted hazard ratio, 2.19; 95% confidence interval, 1.06 to 4.50). ConclusionIn incident dialysis patients, low serum IGF-1 associates with body composition and markers of mineral and bone metabolism, and it predicts increased mortality risk.

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Although a diet low in protein is well known to reduce the risk of progression in patients with chronic kidney disease (CKD), the impact of dietary fat content and fat quality has largely been ignored. As a reduced protein intake results in an obligatory reduction in energy intake, and as CKD patients often suffer from energy malnutrition, this issue deserves greater attention. The present review aims to summarize what is currently known about dietary fat intake in CKD and suggests areas for further study. We conclude that although overweight per se is an important risk factor for the development of CKD, the role of obesity as a risk factor for complications in manifest CKD remains unclear. Current data support a balanced increase in dietary fat intake in patients with CKD to compensate for reduced energy intake in protein-restricted diets and anorexic patients. However, patients who are obese should be encouraged to lose weight while maintaining or, preferably, increasing muscle mass.

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