Pulse wave velocity (PWV) is a main parameter for arterial stiffness. In patients with end-stage renal disease (ESRD), PWV is known to be associated with increased mortality. But factors related to the increased PWV in ESRD patients are not well defined. In addition, the carotid-femoral PWV (cfPWV) measurement, which traditionally has been used to evaluate arterial stiffness, has low reproducibility. Recently, brachial-ankle PWV (baPWV) measurement, which can be performed more easily than cfPWV measurement, has become available as a means of measuring PWV. The aim of this study is to investigate the clinical factors associated with increased baPWV in ESRD patients. BaPWV was examined for 65 ESRD patients on maintenance hemodialysis during the period between the 7th to the 11th of February in 2005 using VP-1000. The clinical factors included age, sex, smoking history, blood pressure, diabetes, body mass index, interdialytic weight gain, duration of dialysis, lipid profile, uric acid, albumin, creatinine, C-reactive protein, calcium, phosphate, intact parathyroid hormone, and hematocrit were analyzed regarding associations (or to determine associations) with baPWV. The median age was 53.8±12.0, 31 males and 34 females. BaPWV was 18.9±5.2 m/s and there was no significant difference between gender (18.1±4.4 m/s vs 19.4±5.9 m/s, p=NS). In multiple regression models, age, predialysis systolic blood pressure, and diabetes were independent variables. In conclusion, age, systolic blood pressure, and diabetes were correlated with baPWV in ESRD patients. Thus baPWV measured by simple, noninvasive methods may become available for screening high risk groups in ESRD patients, although further longitudinal studies are necessary.

• Atherosclerosis
• renal dialysis
• blood pressure

Plasma calcium concentration is maintained within a narrow range (8.5-10.5 mg/dL) by the coordinated action of parathyroid hormone (PTH), 1,25(OH)(2)D(3), calcitonin, and ionized calcium (iCa2+) itself. The kidney plays a key role in this process by the fine regulation of calcium excretion. More than 95% of filtered calcium is reabsorbed along the renal tubules. In the proximal tubules, 60% of filtered calcium is reabsorbed by passive mechanisms. In the thick ascending limb, 15% of calcium is reabsorbed by paracellular diffusion through paracellin-1 (claudin-16). The calcium sensing receptor (CaSR) in the basolateral membrane of the thick ascending limb senses the change in iCa2+ and inhibits calcium reabsorption independent to PTH and 1,25(OH)(2)D(3). The fine regulation of calcium excretion occurs in the distal convoluted tubules and connecting tubules despite the fact that only 10-15% of filtered calcium is reabsorbed there. Transient receptor potential vanilloid 5 (TRPV5) and 6 (TRPV6) in the apical membrane act as the main portal of entry, calbindin-D(28K) delivers Ca2+ in the cytoplasm, and then Na2+/Ca2+ exchanger (NCX1) and plasma membrane Ca2+-ATPase in the basolateral membrane serve as an exit. In the cortical collecting duct, TRPV6 is expressed, but the role might be negligible. In addition to PTH and 1,25(OH)(2)D(3), acid-base disturbance, diuretics, and estrogen affect on these calcium channels. Recently, klotho and fibroblast growth factor 23 (FGF23) are suggested as new players in the calcium metabolism. Klotho is exclusively expressed in the kidney and co-localized with TRPV5, NCX1, and calbindin-D(28K). Klotho increases calcium reabsorption through trafficking of TRPV5 to the plasma membrane, and also converts FGF receptor to the specific FGF23 receptor. FGF23:klotho complex bound to FGF receptor inhibits 1α-hydroxylase of vitamin D, and contributes to calcium reabsorption and phosphate excretion in the kidney.

• Kidney
• TRPV cation channels
• klotho
• fibroblast growth factor 23

The serum phosphorus level is maintained through a complex interplay between intestinal absorption, exchange intracellular and bone storage pools, and renal tubular reabsorption. The kidney plays a major role in regulation of phosphorus homeostasis by renal tubular reabsorption. Type IIa and type IIc Na+/Pi transporters are important renal Na+-dependent inorganic phosphate (Pi) transporters, which are expressed in the brush border membrane of proximal tubular cells. Both are regulated by dietary Pi intake, vitamin D, fibroblast growth factor 23 (FGF23) and parathyroid hormone. The expression of type IIa Na+/Pi transporter result from hypophosphatemia quickly. However, type IIc appears to act more slowly. Physiological and pathophysiological alteration in renal Pi reabsorption are related to altered brush-border membrane expression/content of the type II Na+/Pi cotransporter. Many studies of genetic and acquired renal phosphate wasting disorders have led to the identification of novel genes. Two novel Pi regulating genes, PHEX and FGF23, play a role in the pathophysiology of genetic and acquired renal phosphate wasting disorders and studies are underway to define their mechanism on renal Pi regulation. In recent studies, sodium-hydrogen exchanger regulatory factor 1 (NHERF1) is reported as another new regulator for Pi reabsorption mechanism.

• Phosphorus
• sodium-phosphate cotransporter proteins
• PHEX
• fibroblast growth factor 23
• sodium-hydrogen exchanger regulatory factor 1

Magnesium is the second most common intracellular divalent cation. Magnesium balance in the body is controlled by a dynamic interplay among intestinal absorption, exchange with bone, and renal excretion. Intestinal magnesium absorption proceeds in both a passive paracellular and an active transcellular manner. Regulation of serum magnesium concentrations is achieved mainly by control of renal magnesium reabsorption. Only 20% of filtered magnesium is reabsorbed in the proximal tubule, whereas 60% is reclaimed in the cortical thick ascending limb (TAL) and another 5-10% in the distal convoluted tubule (DCT). The passive paracellular transport of magnesium in the TAL is closely related with the mutations in claudin-16/paracellin-1 and is responsible for familial hypomagnesemia with hypercalciuria and nephrocalcinosis. The active transcellular transport of magnesium in the DCT was similarly enhanced by the realization that defects in transient receptor potential melastatin 6 (TRPM6) cause hypomagnesemia with secondary hypocalcemia. This channel regulates the apical entry of magnesium into epithelia and alters whole-body magnesium homeostasis by controlling urinary excretion. TRPM6 is regulated at the transcriptional level by acid-base status, 17β-estradiol, and both FK506 and cyclosporine. The molecular identity of the protein responsible for the basolateral exit of magnesium from the epithelial cell remains unidentified.

• Magnesium
• homeostasis
• paracellular transport
• transcellular transport
• transient receptor potential channels