Nephron Clinical Practice最新文献

Background: Haemodialysis patients have a high risk of malnutrition which is associated with increased mortality. Nocturnal haemodialysis (NHD) is associated with a significant increase in protein intake compared with conventional haemodialysis (CHD). It is unclear whether this leads to improved nutritional status. Therefore, we studied whether 1 year of NHD is associated with a change in body composition.

Methods: Whole-body composition using dual-energy X-ray absorptiometry (DEXA) and normalised protein catabolic rate (nPCR) were measured in 11 adult patients before and 1 year after the transition from CHD (12 h dialysis/week) to NHD (28-48 h dialysis/week). Similar measurements were performed in a matched control group of 13 patients who stayed on CHD. Differences between groups were analysed with linear mixed models.

Results: At baseline, nPCR, total mass, fat-free mass, and fat mass did not differ significantly between the CHD and NHD groups. nPCR increased in the NHD group (from 0.96 ± 0.23 to 1.12 ± 0.20 g/kg/day; p = 0.027) whereas it was stable in the CHD group (0.93 ± 0.21 at baseline and 0.87 ± 0.09 g/kg/day at 1 year, n.s.). The change in nPCR differed significantly between the two groups (p = 0.027). We observed no significant differences in the course of total mass, fat-free mass, and fat mass during the 1-year observation period between the NHD and CHD groups.

Conclusions: One year of NHD had no significant effect on body composition in comparison with CHD, despite a significantly higher protein intake in patients on NHD.

The immune system is among the key pathogenic factors in acute kidney injury (AKI). Various immune cells, including dendritic cells, natural killer T cells, T and B lymphocytes, neutrophils and macrophages are involved. Conventional CD4+ lymphocytes are well established to participate in early injury, and CD4+CD25+FoxP3 regulatory T cells are protective and can accelerate repair. A newly identified kidney T cell receptor + CD4-CD8- (double-negative) T cell has complex functions, including potentially anti-inflammatory roles in AKI. In this mini review, we summarize the data on the role of lymphocytes in AKI and set the stage for further mechanistic studies as well as interventions to improve outcomes.

Pyruvate is a key intermediary in both aerobic and anaerobic energy metabolisms. In addition, a burgeoning body of experimental literature indicates that it can also dramatically impact oxidant, proinflammatory, and cytoprotective pathways. In sum, these actions can confer protection against diverse forms of tissue damage. However, the fate of pyruvate during the evolution of acute kidney injury (AKI) has remained ill defined. Recent experimental studies have indicated that following either ischemic or nephrotoxic renal injury, marked and sustained pyruvate depletion results. While multiple potential mechanisms for this pyruvate loss may be involved, experimental data suggest that a loss of lactate (a dominant pyruvate precursor) and enhanced gluconeogenesis (i.e. pyruvate utilization) are involved. The importance of pyruvate depletion for AKI pathogenesis is underscored by observations that pyruvate therapy can attenuate diverse forms of experimental AKI. This protection may stem from reductions in tissue inflammation, improved anti-inflammatory defenses, and an enhanced cellular energy metabolism. The pieces of information that give rise to these conclusions are discussed in this brief report.

Acute kidney injury (AKI) is a common medical problem, especially in patients undergoing cardiovascular procedures. The risk of kidney damage has multiple determinants and is often related to or exacerbated by intravenous or intra-arterial iodinated contrast. Contrast-induced AKI (CI-AKI) has been associated with an increased risk of subsequent myocardial infarction, stroke, the development of heart failure, rehospitalization, progression of chronic kidney disease, end-stage renal disease, and death. Statins have been studied extensively in the setting of chronic kidney disease and they have been shown to reduce albuminuria, but they have had no effect on the progressive reduction of glomerular filtration or the need for renal replacement therapy. Several meta-analyses have shown a protective effect of short-term statin administration on CI-AKI and led to two large randomized controlled trials evaluating the role of rosuvastatin in the prevention of CI-AKI in high-risk patients with acute coronary syndrome and diabetes mellitus. Both trials showed a benefit of rosuvastatin prior to contrast administration in a statin-naive patient population. In aggregate, these studies support the short-term use of statins specifically for the prevention of CI-AKI in patients undergoing coronary angiography with or without percutaneous coronary intervention.

Fibroblast growth factor-23 (FGF23) is a bone-derived hormone that regulates phosphate and 1,25-hydroxyvitamin D [1,25(OH)2D] metabolism. FGF23 binds to FGF receptor 1 with its coreceptor Klotho and maintains serum phosphate levels within the normal range by increasing renal phosphate excretion. In addition, FGF23 reduces the synthesis and accelerates the degradation of 1,25(OH)2D to reduce intestinal phosphate absorption. Moreover, FGF23 acts at the parathyroid gland to decrease parathyroid hormone synthesis and secretion. In chronic kidney disease (CKD), serum FGF23 levels rise exponentially as renal function declines long before a significant increase in serum phosphate concentration occurs. Although there is room for argument, FGF23 and Klotho are recently reported contributors to vascular calcification. Finally, prospective observational studies have shown that serum FGF23 concentrations predict mortality not only among dialysis patients but among predialysis CKD patients. In addition to being a coreceptor for FGF23, Klotho circulates as an endocrine substance and exerts a multitude of effects. This review describes recent advances in research on the FGF23-Klotho axis in CKD. © 2014 S. Karger AG, Basel.