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Peritoneal dialysis is the most common modality for home dialysis and to ensure patients have access to dialysis at home, training programs have to ensure that the fellows attain clinical competency in the care of such patients. The limited data available however are sobering; about 10 years ago, 44% of nephrologists reported that they did not feel competent in the care of patients undergoing peritoneal dialysis. There are recognizable challenges in ensuring clinical competency of trainees that may need creative solutions. It is important for training program directors to evaluate the state of training at their institution, identify their unique barriers, and work to overcome them in the interest of ensuring that fellows are trained in all aspects of nephrology.

Over the past two decades in the United States, there has been a inexorable increase in the mean estimated glomerular filtration rate (eGFR) at which patients are starting maintenance dialysis. Data from observational studies using eGFR derived from serum creatinine-based estimating equations has suggested that initiating dialysis at higher levels of kidney function may be associated with increased incidence of adverse clinical outcomes including mortality. At the same time, observational studies using time urinary clearances to measure eGFR have not demonstrated the same relationship, and instead of shown either no association between eGFR at dialysis initiation and subsequent outcomes, or increased survival with higher native renal clearances. There are numerous potential harms from the dialysis procedure itself, including adverse effects on cardiac structure and function, hemodynamic disturbances, increased oxidative stress, and risk for infection due to the presence of foreign objects such as dialysis catheters. Notwithstanding these potential harms, the IDEAL trial, the only controlled clinical trial published to date examining this question, showed no effect of eGFR on any of the examined clinically relevant outcomes at the start of maintenance dialysis. Thus, the available data do not support the use of renal function as the primary guide for determining timing of initiation of chronic renal replacement therapy. The nephrology community should transition to examining other potential approaches to addressing this important question. One potential area of interest is uremic symptomatology and health-related quality of life, though currently available data are indeterminate regarding which symptoms improve with the start of dialysis. Further research is needed to identify patient-centered approaches for decision making around dialysis initiation that will optimally improve survival and other important outcomes.

Correction of metabolic acidosis is an important goal in the management of patients with chronic kidney disease (CKD). However, there is no consensus as to what constitutes an optimal correction of metabolic acidosis in this setting - various expert groups from around the world have set different goals for serum bicarbonate levels for patients with CKD. Accumulating evidence seems to indicate that achieving an arterial pH closer to the upper limit of the reference range may have even greater benefits than maintaining the arterial pH closer to the lower limit of the reference range. This benefit seems to be particularly relevant for patients with protein-energy wasting and we present a review of the evidence that supports this argument. Routine measurement of arterial pH, however, is not feasible in clinical practice; using the Henderson equation, a high-normal arterial pH is generally expected to be associated with a serum bicarbonate level of 24-30 mEq/l and should be the therapeutic goal for chronic kidney disease patients with protein-energy wasting.

Vascular calcification is an active, cell-mediated process that can involve either the intima or media of the blood vessels. The current methods used to clinically measure vascular calcification cannot distinguish between intimal (invariably atherosclerotic) and medial calcification. The high calcification scores seen in patients with end-stage renal disease likely represent a composite of high calcification burden in both sites. The severity of vascular calcification has been associated with a variety of findings including left ventricular hypertrophy and angiographic vascular stenosis as well as with all-cause and cardiovascular mortality. There is increasing evidence that disordered mineral metabolism participates in the process of vascular calcification and is one of the mechanisms whereby hyperphosphatemia, hypercalcemia, and hyperparathyroidism enhance cardiovascular and all-cause mortality of end-stage renal disease patients. There are no studies showing improved outcomes of ESRD patients with aggressive control of disordered mineral metabolism. However, the preponderance of evidence argues strongly in favor of aggressive management of these abnormalities from starting early in the course of chronic kidney disease in the hope of improving patient outcomes.

Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.

Recent dramatic decreases in US medical graduate and International Medical Graduate interest in nephrology as a career suggest that delivery of care to the vulnerable population of dialysis patients in the United States could be negatively affected in coming years. Demographic shifts and changes to national health policy are also likely to exacerbate challenges to provide adequate care to people on dialysis or at risk of end-stage renal disease. Training an adequate number of nephrologists is imperative and will require both reconfiguring current approaches to training and certain aspects of care delivery as well as highlighting bright spots of innovation within the field of nephrology.

Over the last decade, individuals with end-stage renal disease (ESRD) in the United States are starting maintenance dialysis therapy at progressively higher estimated glomerular filtration rate (eGFR). Moreover, several observational studies have demonstrated an association of a higher risk of death with higher serum creatinine-based estimates of GFR at the time of initiation of dialysis. In contrast, studies in which renal function has been measured by timed urinary collection show either a lower risk of death or no significant association with higher GFR at the time of initiation of dialysis. There are numerous potential sources of bias in such observational studies, particularly in those that use serum creatinine-based eGFR. The only randomized controlled clinical trial to have examined this question did not demonstrate either benefit or harm with initiation of dialysis at higher level of renal function. Thus, the data to date suggest that eGFR should not be the sole consideration when assessing the need for initiating maintenance dialysis in patients with advanced chronic kidney disease. Given the high societal costs of starting renal replacement therapy earlier in the course of the disease, these considerations also suggest that dialysis can be safely be postponed in otherwise asymptomatic individuals with advanced chronic kidney disease. By the same token, dialysis should not be denied to individuals who could clearly benefit from renal replacement therapy simply because the GFR is too high (viz., volume overload, refractory hyperkalemia). Finally, there is a compelling need to reexamine the symptoms that could be attributed to uremia and clearly improve upon initiation of dialysis to better guide clinical decision-making.

The major payer of dialysis services in the United States, Medicare, has established incentives to encourage the use of home dialysis. However, this modality remains underutilized. We think that a major cause of this situation is ineffective education of the prospective dialysis population regarding the choices of kidney replacement modalities. We discuss the value of patient education and the consequences of failing to educate prospective dialysis patients. We then explore approaches to achieve patient education goals and the physician's and education team's roles in the development of an individual patient's life plan.

Recent dramatic decreases in US medical graduate and International Medical Graduate interest in nephrology as a career suggest that delivery of care to the vulnerable population of dialysis patients in the United States could be negatively affected in coming years. Demographic shifts and changes to national health policy are also likely to exacerbate challenges to provide adequate care to people on dialysis or at risk of end-stage renal disease. Training an adequate number of nephrologists is imperative and will require both reconfiguring current approaches to training and certain aspects of care delivery as well as highlighting bright spots of innovation within the field of nephrology.

Correction of metabolic acidosis is an important goal in the management of patients with chronic kidney disease (CKD). However, there is no consensus as to what constitutes an optimal correction of metabolic acidosis in this setting - various expert groups from around the world have set different goals for serum bicarbonate levels for patients with CKD. Accumulating evidence seems to indicate that achieving an arterial pH closer to the upper limit of the reference range may have even greater benefits than maintaining the arterial pH closer to the lower limit of the reference range. This benefit seems to be particularly relevant for patients with protein-energy wasting and we present a review of the evidence that supports this argument. Routine measurement of arterial pH, however, is not feasible in clinical practice; using the Henderson equation, a high-normal arterial pH is generally expected to be associated with a serum bicarbonate level of 24-30 mEq/l and should be the therapeutic goal for chronic kidney disease patients with protein-energy wasting.

Vascular calcification is an active, cell-mediated process that can involve either the intima or media of the blood vessels. The current methods used to clinically measure vascular calcification cannot distinguish between intimal (invariably atherosclerotic) and medial calcification. The high calcification scores seen in patients with end-stage renal disease likely represent a composite of high calcification burden in both sites. The severity of vascular calcification has been associated with a variety of findings including left ventricular hypertrophy and angiographic vascular stenosis as well as with all-cause and cardiovascular mortality. There is increasing evidence that disordered mineral metabolism participates in the process of vascular calcification and is one of the mechanisms whereby hyperphosphatemia, hypercalcemia, and hyperparathyroidism enhance cardiovascular and all-cause mortality of end-stage renal disease patients. There are no studies showing improved outcomes of ESRD patients with aggressive control of disordered mineral metabolism. However, the preponderance of evidence argues strongly in favor of aggressive management of these abnormalities from starting early in the course of chronic kidney disease in the hope of improving patient outcomes.

Metabolic acidosis, a common condition in patients with renal failure, may be linked to protein-energy malnutrition (PEM) and inflammation, together also known as malnutrition-inflammation complex syndrome (MICS). Methods of serum bicarbonate measurement may misrepresent the true bicarbonate level, since the total serum carbon dioxide measurement usually overestimates the serum bicarbonate concentration. Moreover, the air transportation of blood samples to distant laboratories may lead to erroneous readings. In patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD), a significant number of endocrine, musculoskeletal, and metabolic abnormalities are believed to result from acidemia. Metabolic acidosis may be related to PEM and MICS due to an increased protein catabolism, decreased protein synthesis, endocrine abnormalities including insulin resistance, decreased serum leptin level, and inflammation among individuals with renal failure. Evidence suggests that the catabolic effects of metabolic acidosis may result from an increased activity of the adenosine triphosphate (ATP)-dependent ubiquitin-proteasome and branched-chain keto acid dehydrogenase. In contrast to the metabolic studies, many epidemiologic studies in maintenance dialysis patients have indicated a paradoxically inverse association between mildly decreased serum bicarbonate and improved markers of protein-energy nutritional state. Hence metabolic acidosis may be considered as yet another element of the reverse epidemiology in ESRD patients. Interventional studies have yielded inconsistent results in CKD and ESRD patients, although in peritoneal dialysis patients, mitigating acidemia appears to more consistently improve nutritional status and reduce hospitalizations. Large-scale, prospective randomized interventional studies are needed to ascertain the potential benefits of correcting acidemia in malnourished and/or inflamed CKD and maintenance hemodialysis patients. Until then, all attempts should be made to adhere to the National Kidney Foundation Kidney Disease and Dialysis Outcome Quality Initiative guidelines to maintain a serum bicarbonate level in ESRD patients of at least 22 mEq/L.