Calciphylaxis (calcific uremic arteriolopathy) is a severe complication of hemodialysis characterized by subcutaneous calcification of the small arteries and tissue necrosis. Our case report is focused on a woman receiving hemodialysis (HD) with diabetes mellitus for 20 years and severe secondary hyperparathyroidism, who presented painful subcutaneous nodules, skin necrosis and ulcerations. As the treatment of calciphylaxis is mainly empirical and controversial, we decided to administer cinacalcet with paricalcitol for the control of hyperparathyroidism and sodium thiosulfate to improve the calcification of the arterioles. Two months after the start of the therapy, parathyroid hormone (PTH) decreased significantly and the skin lesions nearly disappeared. Thus, we believe that the combination of sodium thiosulfate with cinacalcet and paracalcitol is effective for the treatment of calciphylaxis with secondary hyperparathyroidism.

This study determines the relationship between interdialytic water retention (IWR) and acid-base homeostasis in uremic patients under regular hemodialysis (HD). To this aim, in 33 regular bicarbonate HD sessions of 11 uremic patients (three HD sessions of 1 week for each patient), blood samples were received from arterial line immediately pre- and post-HD anaerobically in heparinized syringes and the HCO3-, pH, and pco2 were determined. Also in the studied HD sessions, the IWR was estimated and the apparent bicarbonate space percentage (ABS%) pre- and post-HD was calculated by Fernandez et al. (Eq. 1). The mean +/- SD values pre-HD (ABS% = 54.15 +/- 1.49, HCO3- = 18.54 +/- 2.0 mmol/L, pH = 7.32 +/- 0.02, pco2 = 35.44 +/- 3.10 mmHg) and post-HD (ABS% = 49.88 +/- 0.6, HCO3- = 26.33 +/- 1.6 mmol/L, pH = 7.44 +/- 0.02, pco2 = 37.69 +/- 3.00 mmHg) show metabolic acidosis pre-HD and slight alkalosis post-HD. There was a significant positive correlation between IWR and ABS% pre-HD (r = 0.650, p < .0001) and post-HD (r = 0.655, p < .0001), but a significant negative correlation between IWR and HCO3- pre-HD (r = -0.502, p < .003) and post-HD (r = -0.700, p < .001), as well as between IWR and pH pre-HD (r = -0.516, p < .002) and post-HD (r = -0.377, p < .03). In addition, there was a significantly negative correlation between IWR and pco2 post-HD (r = -0.656, p < .001), but not pre-HD (r = 0.0136, PNS). The significantly positive relationship between IWR and ABS% pre- and post-HD, in combination with the significantly negative correlation between HCO3- and pH pre- and post-HD, indicates that the IWR negatively influences the acid-base homeostasis in hemodialysis patients without residual renal function, and may worsen the cardiovascular physiology and tissue oxygenation of these patients.

Sevelamer hydrochloride (HCl) contains multiple amines that may cause a significant dietary acid load. To evaluate the impact of sevelamer on arterial blood gases, we followed two groups of stable hemodialysis patients for 24 months. The Sevelamer Group (n = 7) did not achieve the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) goals for phosporus and Ca x P product and was switched from a calcium-based to sevelamer-based regimen. The Calcium Group (n = 7) achieved those goals and remained on calcium salts. Following sevelamer administration, a deterioration of chronic metabolic acidosis was revealed, which lasted throughout the study. Sevelamer therapy was associated with reduced cholesterol levels, improved serum phosphate, and Ca x P product, which facilitated the management of secondary hyperparathyroidism. No significant changes in acid-base status or other parameter tested were found in the Control Group. In conclusion, sevelamer intake caused small but persistent acid-base disturbances, which did not neutralize sevelamer's beneficial effects on mineral and lipid metabolism.

Background. Lipoprotein(a), Lp(a), has been recognized as an atherogenic and thrombogenic lipoprotein in the general population and in hemodialysis (HD) patients. In addition, fibrinogen and fibronectin may promote atherothrombosis. The aim of this study was to investigate any possible relationship between Lp(a) and thrombogenic coagulation proteins in non-diabetic HD patients. Patients and Methods. Serum Lp(a) and plasma fibrinogen, plasminogen, and fibronectin levels were measured pre-HD in 60 uremic patients (30 male, 30 female) aged 58.6 AE 8.0 years who had been receiving HD treatment for 61.3 AE 50.7 months. The control group comprised 20 age-and sex-matched healthy subjects. All patients were receiving erythropoietin treatment. Results. The mean serum Lp(a) (33.88 AE 34.12 mg/dL) and plasma fibrinogen (329.45 AE 80.62 mg/dL) levels were significantly higher in the HD patients compared with those in the controls (16.70 AE 10.36 and 254.00 AE 43.34 mg/dL, respectively; p < .05 and p < .001, respectively). Plasminogen levels did not differ between the HD patients (11.64 AE 3.22 mg/dL) and the control group (10.67 AE 1.41 mg/dL, p>.05). Fibronectin levels were slightly increased in the HD patients (33.96 AE 5.49 mg/dL) versus in the control group (30.9 AE 5.80 mg/dL, p < .05). There was a significant positive correlation between Lp(a) and fibrinogen levels (r ¼ 0.305, p < .02), as well as between Lp(a) and fibronectin levels (r ¼ 0.360, p < .01). Moreover, there was a significant positive correlation between fibrinogen and fibronectin levels (r ¼ 0.587, p < .0001). Conclusions. According to our results, in non-diabetic HD patients, abnormal serum Lp(a) levels significantly correlated with abnormal levels of fibrinogen and fibronectin. There is a concern that the relationship between these atherogenic and thrombogenic acute-phase proteins may contribute to the increased incidence of atherosclerotic cardiovascular disease in this patient population.