Disorders in calcium, phosphorus, and parathyroid hormone (PTH) are common in chronic kidney disease (CKD) and may be associated with poor outcomes including a higher rate of CKD progression and increased death risk. Although these abnormalities have been examined extensively in patients with CKD stage 5 who are receiving chronic maintenance dialysis, they have not been studied to the same extent at earlier stages of CKD, in spite of the much larger numbers of patients in the early CKD population. We summarize the available literature on outcomes associated with bone and mineral disorders in patients with CKD not yet receiving maintenance dialysis. We have reviewed novel data linking fibroblast growth factor 23 (FGF-23) to phosphorus and vitamin D homeostasis. More rapid CKD progression is linked to hyperphosphatemia and its associated hyperparathyroidism and vitamin D deficiency. Hence, hyperphosphatemia may play a central role in the diverse disorders characterizing CKD. We provide a brief overview of the available treatment recommendations for bone and mineral disorders, with an emphasis on areas needing further research.

Uremic malnutrition, also known as protein-energy wasting (PEW), is a common phenomenon in maintenance dialysis patients and a risk factor for poor clinical outcomes including worse quality of life and increased hospitalization and mortality. The paradoxical association between traditional cardiovascular risk factors and better outcomes in dialysis patients also referred to as "reverse epidemiology," is a good example of the powerful effect-modifying impact of the nutritional status in this population. Measures of food intake, body composition tools, nutritional scoring systems, and laboratory values such as serum albumin are used to diagnose PEW and to assess the degree of severity of PEW without clearly validated diagnostic criteria. Some observational studies suggest that inflammation is a missing link between the PEW and poor clinical outcomes in dialysis patients, although PEW per se may also predispose to illness and inflammation. Ongoing debate as to whether such surrogates as serum albumin or prealbumin concentrations are markers of nutritional status, inflammation, comorbidity, or other conditions has led to confusion and diagnostic and therapeutic nihilism. Irrespective of the cause of hypoalbuminemia in dialysis patients, evidence suggests that nutritional interventions can increase serum albumin in dialysis patients. Hence, we should continue assessing serum albumin and other surrogates of nutritional status to risk-stratify patients and to allocate nutritional therapy, while well-designed, large-scale, randomized, controlled trials of the effects of nutritional intake on clinical outcomes are awaited.

Obesity has become a worldwide epidemic, and its prevalence has been projected to grow by 40% in the next decade. This increasing prevalence has implications for the risk of diabetes, cardiovascular disease and also for Chronic Kidney Disease. A high body mass index is one of the strongest risk factors for new-onset Chronic Kidney Disease. In individuals affected by obesity, compensatory hyperfiltration occurs to meet the heightened metabolic demands of the increased body weight. The increase in intraglomerular pressure can damage the kidneys and raise the risk of developing Chronic Kidney Disease in the long-term. The incidence of obesity-related glomerulopathy has increased tenfold in recent years. Obesity has also been shown to be a risk factor for nephrolithiasis, and for a number of malignancies including kidney cancer. This year the World Kidney Day promotes education on the harmful consequences of obesity and its association with kidney disease, advocating a healthy lifestyle and health policy measures that make preventive behaviors an affordable option.

Increasing confusion exists as to which vitamin D compounds are more appropriate for persons with chronic kidney disease (CKD). Some opinion-based guidelines recommend administration of such nutritional vitamin D agents as ergocalciferol or cholecalciferol as the first therapy in hyperparathyroidism associated with low circulating levels of 25-hydroxy vitamin D (<30 ng/ml) in nondialysis dependent CKD patients. Insufficient to deficient levels of 25-hydroxy vitamin D have been reported in the majority of individuals with CKD, including both nondialysis dependent and maintenance dialysis patients. Epidemiologic studies have almost consistently indicated the survival benefit of active vitamin D agents across all stages of CKD, including among dialysis patients with 25-hydroxy vitamin D deficiency. To date, no large observational or interventional studies have shown any survival advantage of nutritional vitamin D in CKD patients. Several recent (postguideline) small studies have yielded mixed results regarding the potential benefits of ergocalciferol in CKD, including satisfactory to inadequate lowering of PTH level to target ranges, improving response to erythropoietin stimulating agents, and salutary effects on glycemic controls. Compared with nutritional vitamin D agents, active vitamin D compounds appear to more effectively lower the circulating levels of alkaline phosphatase, a conveniently available biomarker associated with increased mortality and coronary artery calcification in CKD patients. The ideal vitamin D therapy for CKD patients should be the one that improves survival irrespective of suggested or imposed target ranges for arbitrary or opinion-based surrogate end points. Randomized controlled trials are needed to verify which agents offer superior survival advantages.