Although intradialytic parenteral nutrition (IDPN) is a method used widely to combat protein-calorie malnutrition in hemodialysis patients, its effect on survival has not been thoroughly studied. We conducted a prospective, randomized trial in which 186 malnourished hemodialysis patients received oral nutritional supplements with or without 1 year of IDPN. IDPN did not improve 2-year mortality (primary end point), hospitalization rate, Karnofsky score, body mass index, or laboratory markers of nutritional status. Instead, both groups demonstrated improvement in body mass index and the nutritional parameters serum albumin and prealbumin (P < 0.05). Multivariate analysis showed that an increase in prealbumin of >30 mg/L within 3 months, a marker of nutritional improvement, independently predicted a 54% decrease in 2-year mortality, as well as reduced hospitalizations and improved general well-being as measured by the Karnofsky score. Therefore, although we found no definite advantage of adding IDPN to oral nutritional supplementation, this is the first prospective study demonstrating that an improvement in prealbumin during nutritional therapy is associated with a decrease in morbidity and mortality in malnourished hemodialysis patients.

Metformin (dimethylbiguanide) has been used for more than 30 years as an antihyperglycemic agent in the treatment of diabetes mellitus, but its effect on gluconeogenesis is still controversial. In isolated hepatocytes from fasted rats, a significant inhibition of glucose production from lactate/pyruvate (10: 1, mol/mol), fructose, alanine or glutamine, following metformin addition, is observed. Moreover, in hepatocytes perifused with dihydroxyacetone as the gluconeogenic substrate and treated with 0.5 mM metformin, an inhibition of the glucose flux and a simultaneous stimulation of the lactate/pyruvate flux were observed. This enhancement of lactate/pyruvate formation appears to be due to an effect on the pyruvate‐kinase enzyme. A direct effect of metformin on pyruvate kinase cannot explain this result, since pyruvate‐kinase activity was not affected by metformin at this concentration. In contrast, the addition of metformin caused a significant decrease in the cellular ATP concentration, a known allosteric inhibitor of this enzyme. This could explain the stimulation of pyruvate‐kinase activity following metformin addition and thus the inhibition of gluconeogenesis.

The Kidney Disease Outcomes Quality Initiative (K/DOQI) guidelines recommend that serum parathyroid hormone (PTH) concentration of patients with chronic kidney disease (CKD) should be measured regularly and maintained within target ranges that are defined according to the stage of CKD (e.g., 150–300 pg/ml in patients with CKD stage 5). The quality of the PTH assay is of paramount importance, as it contributes to the therapeutic decision. Indeed, when the PTH concentration is above these target values, drugs that decrease PTH secretion, such as active vitamin D compounds or calcimimetic agents, may be given and the doses are then adapted according to the evolution of the PTH concentration. By contrast, if the PTH concentration is below the target range, any treatment that may decrease PTH secretion is stopped to avoid adynamic bone disease and associated extra-skeletal calcifications. The aim of this article is to discuss the main features and pitfalls related to PTH measurement in the setting of CKD.