Encapsulating Peritoneal Sclerosis: Case report and Current Status

Encapsulating peritoneal sclerosis (EPS), is a rare but devastating complication of long-term peritoneal dialysis (PD) with a high mortality rate. The incidence is between 0.5 and 3.3%, decreasing with time. EPS is defi ned as a clinical syndrome with major signs of gastrointestinal obstruction, infl ammatory parameters, radiological and macroscopic changes. Duration of treatment and cessation of PD are the main risk for development of EPS: about 75% of EPS occurred in patients transferred on hemodialysis or in the two years after kidney transplantation. Morphological alterations are disappearance of mesothelial layer, sub-mesothelial fi brosis, interstitial sclerosis and vasculopathy, ultrafi ltration failure, fast transport status of the peritoneal membrane, and loss of sodium sieving are the most predicting functional abnormalities. Some biomarkers could be found in the peritoneal effl uent. The pathophysiology is probably a consequence of a multiple-hit process in which expression of growth factors and cytokines play a role. Medical strategies (corticosteroids, immunosuppressive drugs, tamoxifen) in association with parenteral nutrition and/or surgery (enterolysis) are discussed. Prevention is the use of physiological peritoneal solutions, icodextrine instead of high glucose concentration solution, and peritoneal lavage fter peritoneal dialysis cessation for any reason

Use of Iron Therapy in Chronic Kidney Disease

Anemia is a common complication in patients with chronic kidney disease (CKD), and increases with the progression of renal dysfunction [1]. The main cause of anemia is the inadequate production of erythropoietin (EPO), a glycoprotein mainly produced by the kidney responsible for the growth of erythroid cells in the bone marrow [2]. Iron deficiency is another common cause of anemia in these patients and is a major cause of hyporesponsiveness to erythropoiesis-stimulating agents (ESAs) [3]. Approximately, 50% of patients with CKD, who have anemia and are not receiving ESA or iron supplementation show depleted iron stores in their bone marrow [4]. Although the use of intravenous iron in hemodialysis patients has significantly increased during the last decade [5], the appropriate iron dosing strategy in CKD remains debatable.</p

Encapsulating Peritoneal Sclerosis: Case report and Current Status

Encapsulating peritoneal sclerosis (EPS), is a rare but devastating complication of long-term peritoneal dialysis (PD) with a high mortality rate. The incidence is between 0.5 and 3.3%, decreasing with time. EPS is defi ned as a clinical syndrome with major signs of gastrointestinal obstruction, infl ammatory parameters, radiological and macroscopic changes. Duration of treatment and cessation of PD are the main risk for development of EPS: about 75% of EPS occurred in patients transferred on hemodialysis or in the two years after kidney transplantation. Morphological alterations are disappearance of mesothelial layer, sub-mesothelial fi brosis, interstitial sclerosis and vasculopathy, ultrafi ltration failure, fast transport status of the peritoneal membrane, and loss of sodium sieving are the most predicting functional abnormalities. Some biomarkers could be found in the peritoneal effl uent. The pathophysiology is probably a consequence of a multiple-hit process in which expression of growth factors and cytokines play a role. Medical strategies (corticosteroids, immunosuppressive drugs, tamoxifen) in association with parenteral nutrition and/or surgery (enterolysis) are discussed. Prevention is the use of physiological peritoneal solutions, icodextrine instead of high glucose concentration solution, and peritoneal lavage fter peritoneal dialysis cessation for any reason

Are oxyphil cells responsible for the ineffectiveness of cinacalcet hydrochloride in haemodialysis patients?

International audienceParathyroid glands consist primarily of chief cells. In some cases, the proportion of parathyroid oxyphil cells increases in patients with chronic kidney disease. We describe a case of secondary hyperparathyroidism (SHPT) in a patient treated with haemodialysis who initially received large doses of vitamin D and calcium (Ca) supplements, as well as high doses of cinacalcet hydrochloride (C-HCl), but without any effect on parathyroid hormone levels. Following a successful parathyroidectomy, histopathological examination revealed that two of the parathyroid glands consisted of 40% of oxyphil cells. Oxyphil cells have significantly more Ca-sensing receptors (CaSRs) than chief cells, suggesting that CaSRs are involved in the transdifferentiation of chief cells to oxyphil cells. C-HCl treatment leads to a significant increase in parathyroid oxyphil cell content. This case suggests that C-HCl may induce specific phenotypic alterations in hyperplastic parathyroid glands in patients with severe SHPT