About this Research Topic
Peritoneal dialysis (PD) is a renal replacement therapy whose use is becoming more prevalent around the world. The procedure involves the placement of a permanent catheter in the abdominal cavity through which fluid exchanges are performed with osmotic capacity generally based on glucose. The PD uses the peritoneal membrane (PM) as a semipermeable membrane to exchange solutes (uremic toxins) and water. The success of the procedure depends on the longevity of the PM. However, several exogenous and endogenous factors shorten the useful life of this exchange surface.
Considerable scientific efforts to protect the PM have been made in recent decades. This has led to the incorporation of new knowledge from basic sciences as well as recent technology. One of the greatest advances has been in the understanding of the mechanisms that lead to the fibrosis of the PM, which also leads to accumulation of components of the extracellular matrix angiogenesis and lymphangiogenesis. In advanced stages of this process encapsulating peritoneal sclerosis (EPS) occurs, which can lead to death due to intestinal obstruction and malnutrition. More than one decade ago, our group made a relevant contribution in this area by identifying the mesothelial mesenchymal transition (EMT) of the mesothelial cells (MC) that cover PM. These play a crucial role in the submesothelial fibroblasts pathogenesis (40-60 %), angiogenesis and lymphangiogenesis. Several groups have also achieved important advances in the prevention of peritoneal fibrosis taking EMT as a therapeutic target. The use of these drugs, together with the improvement in the biocompatibility of PD liquids replacing glucose as an osmotic agent, constitutes the future therapeutic measures.
Systemically, a concept is emerging that relates the products derived from the abdominal cavity in PD with the metabolic and cardiovascular disorders of uremia. The diabetes-like environment formed in the abdominal cavity by the action of PD fluids, the stimulation of the peritoneal immune system and the constant absorption of glucose by the peritoneum can induce dyslipidemia, hypertension and accelerated atherosclerosis.
Our goal is to convene a group of experts on the subject and achieve a mix of basic science and clinical topics that may be attractive to a diverse public (clinical and non-clinical). Our ultimate goal is to bring basic science to the clinic. We are also part of a European scientific consortium of studies in PD that includes a multidisciplinary staff that aims to delve into the complications associated with PD.
Guest editors of this Research Topic would like to dedicate this work to the memory of a dear friend and colleague, Dr. Abelardo Aguilera, who sadly passed away while working on this venture.
Considerable scientific efforts to protect the PM have been made in recent decades. This has led to the incorporation of new knowledge from basic sciences as well as recent technology. One of the greatest advances has been in the understanding of the mechanisms that lead to the fibrosis of the PM, which also leads to accumulation of components of the extracellular matrix angiogenesis and lymphangiogenesis. In advanced stages of this process encapsulating peritoneal sclerosis (EPS) occurs, which can lead to death due to intestinal obstruction and malnutrition. More than one decade ago, our group made a relevant contribution in this area by identifying the mesothelial mesenchymal transition (EMT) of the mesothelial cells (MC) that cover PM. These play a crucial role in the submesothelial fibroblasts pathogenesis (40-60 %), angiogenesis and lymphangiogenesis. Several groups have also achieved important advances in the prevention of peritoneal fibrosis taking EMT as a therapeutic target. The use of these drugs, together with the improvement in the biocompatibility of PD liquids replacing glucose as an osmotic agent, constitutes the future therapeutic measures.
Systemically, a concept is emerging that relates the products derived from the abdominal cavity in PD with the metabolic and cardiovascular disorders of uremia. The diabetes-like environment formed in the abdominal cavity by the action of PD fluids, the stimulation of the peritoneal immune system and the constant absorption of glucose by the peritoneum can induce dyslipidemia, hypertension and accelerated atherosclerosis.
Our goal is to convene a group of experts on the subject and achieve a mix of basic science and clinical topics that may be attractive to a diverse public (clinical and non-clinical). Our ultimate goal is to bring basic science to the clinic. We are also part of a European scientific consortium of studies in PD that includes a multidisciplinary staff that aims to delve into the complications associated with PD.
Guest editors of this Research Topic would like to dedicate this work to the memory of a dear friend and colleague, Dr. Abelardo Aguilera, who sadly passed away while working on this venture.
Keywords: Peritoneal dialysis, peritoneal membrane, abdominal cavity activation, cardiovacular complications, therapeutic measurement
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