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Introduction Catheter-related infections are an important clinical problem in maintenance hemodialysis patients. Catheter-related bloodstream infections have a negative effect on survival, hospitalization and cost of care. Tegaderm™ chlorhexidine gluconate (CHG) dressing may be useful to reduce catheter-related infection rates. Methods We performed a study to assess the efficacy of Tegaderm™ CHG dressing for reducing catheter-related infections. We designed a prospective randomized cross-over study with a scheme of two treatments, Tegaderm™ CHG dressing versus standard dressing, and two periods of six months. Catheter-related infection rate was the primary outcome. We enrolled 59 prevalent hemodialysis patients. Results Catheter-related infection rate per 1000 catheter days was reduced from 1.21 in patients using standard dressing to 0.28 in patients with Tegaderm™ CHG dressing (p = 0.02). Catheter-related bloodstream infection rate per 1000 catheter days was equal to 0.09 in patients with Tegaderm™ CHG dressing versus 0.65 in patients with standard dressing (p = 0.05). Annual total healthcare costs for catheter-related bloodstream infections were estimated equal to EUR62,459 versus EUR300,399, respectively, for patients with Tegaderm™ CHG versus standard dressing. Conclusions This is the first prospective study to show that Tegaderm™ CHG dressing significantly reduces catheter-related infection rates in hemodialysis patients.

Pregnancy-associated thrombotic microangiopathy (TMA) is a rare condition, but it is burdened by a significant perinatal and maternal morbidity as well as mortality. We describe the case of a 33-year-old woman, who developed a TMA at the 36th week of gestation characterized by increased LDH, haptoglobin consumption, schistocytes, thrombocytopenia and acute renal failure requiring dialysis. There were not gestational hypertension nor proteinuria until the day of hospitalization. ADAMTS 13 deficiency was ruled out and the patient did not have diarrhea. She was initially treated with caesarean section, plasma infusion and plasmapheresis with no benefit. Five days after the onset of TMA, a temptative diagnosis of atypical uremic syndrome (aHUS) was made and the patient was switched to eculizumab. Antibiotic prophylaxis and anti-meningococcal A,B, C, W135 and Y vaccination was performed. TMA rapidly resolved and renal function completely recovered. The newborn had a normal perinatal course. A complement dysregulation was ruled out by testing for mutations on CFH, CFHR3-R1, CFI, MCP, CFB, C3 and for anti CFH antibodies. In conclusion the differential diagnosis of aHUS with HELLP syndrome is often not straightforward. The severity and persistence of TMA, the high mortality associated to peripartum TMA and the risk for irreversible kidney failure require an early therapeutic decision as to the use of eculizumab.

High phosphate levels are associated with unfavorable outcomes in ESRD. Recent data suggested that phosphate levels within the normal range are equally associated with poor outcomes in the community and CKD stage 3 - 4. Several concept papers support the potential role of phosphate load as a first-line toxin in the beginning of CKD-MBD processes via the activation of FGF23 cascade. Phosphate load is thereafter involved in the progression of vascular calcification (VC) and bone disorder typical of CKD-MBD.Herein the authors cover the recent evidence on the pathophysiology of phosphate handling through the natural history of CKD, with particular emphasis on FGF23 cascade, its potential surrogate markers, VC and bone disorder. The major characteristics of lanthanum carbonate are therefore discussed, focusing on its potential advantages for the treatment of difficult cases in CKD-MBD.Lanthanum carbonate, being the most potent calcium-free phosphate binder available in clinical practice, could be decisive for those cases where controlling phosphate load is complicated by poor compliance to medications, stubborn high phosphorus intake, extended VC and bone disorders.

The involvement of vitamin D deficiency in cardiovascular morbidity and mortality is attracting great interest. In patients with chronic kidney disease this association is stronger because vitamin D levels decrease as a result of renal progressive impairment. In chronic kidney disease secondary hyperparathyroidism commonly occurs in response to persistent hypocalcemia and hyperphosphatemia; moreover, parathyroid gland volume increases, vascular calcification is accelerated, and structural and functional modifications of the left ventricle are observed. These alterations entail both cardiac and renal involvement, resulting in cardio-renal syndrome. Recent studies concluded that vitamin D administration seems to have cardioprotective and renoprotective effects and improve peripheral vascular disease, vascular calcification, cardiac outcome, and blood pressure control. In clinical practice, therefore, the use of this hormone may play an important role in cardio-renal syndrome prevention.