Dietary Phosphorus as a Marker of Mineral Metabolism and Progression of Diabetic Kidney Disease.

Phosphorus is an essential nutrient that is critically important in the control of cell and tissue function and body homeostasis. Phosphorus excess may result in severe adverse medical consequences. The most apparent is an impact on cardiovascular (CV) disease, mainly through the ability of phosphate to change the phenotype of vascular smooth muscle cells and its contribution to pathologic vascular, valvular and other soft tissue calcification. Chronic kidney disease (CKD) is the most prevalent chronic disease manifesting with the persistent derangement of phosphate homeostasis. Diabetes and resulting diabetic kidney disease (DKD) remain the leading causes of CKD and end-stage kidney disease (ESRD) worldwide. Mineral and bone disorders of CKD (CKD-MBD), profound derangement of mineral metabolism, develop in the course of the disease and adversely impact on bone health and the CV system. In this review we aimed to discuss the data concerning CKD-MBD in patients with diabetes and to analyze the possible link between hyperphosphatemia, certain biomarkers of CKD-MBD and high dietary phosphate intake on prognosis in patients with diabetes and DKD. We also attempted to clarify if hyperphosphatemia and high phosphorus intake may impact the onset and progression of DKD. Careful analysis of the available literature brings us to the conclusion that, as for today, no clear recommendations based on the firm clinical data can be provided in terms of phosphorus intake aiming to prevent the incidence or progression of diabetic kidney disease.

Elevated levels of Nε-homocysteinyl-lysine isopeptide in patients on long-term hemodialysis.

BACKGROUND: Nε-homocysteinyl-lysine (Nε-Hcy-Lys), a product of proteolysis of Nε-homocysteinylated proteins, has been discovered recently. We sought to investigate the presence of Nε-Hcy-Lys in patients on long-term hemodialysis (HD) and its association with markers involved in atherosclerotic vascular disease. METHODS: We studied 86 patients on long-term (median, 45 months) HD and 95 apparently healthy controls. Nε-Hcy-Lys and total homocysteine (tHcy) were assayed using high-performance liquid chromatography. Paraoxonase 1 (PON1), asymmetric dimethylarginine (ADMA), folate, 8-isoprostaglandin F2α(8-iso-PGF2α), plasminogen activator inhibitor-1 (PAI-1), C-reactive protein (CRP), together with antibodies against Nε-homocysteinylated albumin and hemoglobin, were also measured. RESULTS: Nε-Hcy-Lys was detected in 15 HD patients (17.4%). Those patients had 3.1-times lower PON1 (p<0.0001), 20% higher ADMA (p<0.0001), 30% higher PAI-1 (p<0.0001), 10% lower total cholesterol (p=0.001) and LDL-cholesterol (p<0.0001), together with 20% lower triglycerides (p<0.0001) compared with subjects without measurable Nε-Hcy-Lys. Nε-Hcy-Lys levels correlated with PON1 (r=-0.62, p<0.0001), ADMA (r=0.58, p<0.0001) and PAI-1 (r=0.59, p<0.0001). Folic acid supplementation, tHcy, folate, autoimmune response to Nε-Hcy-proteins, and oxidative stress were not associated with the presence of Nε-Hcy-Lys. PON1 is the only independent predictor of the presence of Nε-Hcy-Lys in HD patients. None of controls had measurable Nε-Hcy-Lys in serum. CONCLUSION: The presence of Nε-Hcy-Lys in HD patients is relatively infrequent and associated with lipid profile, endothelial dysfunction and impaired fibrinolysis, regardless of tHcy and folate levels.

Selenium status indices, laboratory data, and selected biochemical parameters in end-stage renal disease patients.

We investigated the relations between selenium status (SeS) parameters, indexes of nutrition, erythropoiesis, and uremic toxemia, serum electrolytes, and other biochemical markers in end-stage renal disease (ESRD) patients, as no multivariate statistical analysis concerning all of these parameters was performed so far. SeS was evaluated by plasma Se concentration (plSe) and glutathione peroxidase (plGSHPx) activity in 69 uremic patients treated with hemodialysis (HD) and 40 healthy controls. The hierarchical multivariate partial least squares model (PLS2) was employed to establish data structure and correlations between parameters investigated. plSe and plGSHPx activity were significantly lower in patients when compared with controls (p=0.000). plSe was positively associated with indexes of erythropoiesis and nutritional status, as well as serum electrolytes and parameters of uremic toxemia. plGSHPx was inversely dependent on the pair of parameters: intact parathyroid hormone (iPTH) and aluminum plasma concentration (Al). We conclude that (1) ESRD strongly decreases selenium status and (2) the PLS2 approach revealed the existence of significant interactions among plSe, plGSHPx, and selected biochemical parameters or groups of such parameters; some of these associations need further studies to be clarified.