Publications by authors named "Raul G Carlini"

Venezuela is going through a humanitarian crisis that has severely impacted all programmes of kidney replacement therapy — dialysis coverage has decreased markedly, particularly in small towns and rural areas, and almost all peritoneal dialysis and deceased donor organ procurement for kidney transplantation have been discontinued.

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Globally, more than 5 million people die annually from lack of access to critical treatments for kidney disease - by 2040, chronic kidney disease is projected to be the fifth leading cause of death worldwide. Kidney diseases are particularly challenging to tackle because they are pathologically diverse and are often asymptomatic. As such, kidney disease is often diagnosed late, and the global burden of kidney disease continues to be underappreciated.

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The objective of this review is to evaluate the factors that determine the development or deterioration of Chronic Kidney Disease (CKD) after partial nephrectomy (PN). When current literature is reviewed, it is found that factors that influence renal function after partial nephrectomy, are multifactorial. Those are divided into pre-surgical factors, such as hypertension, diabetes mellitus, urolithiasis, obesity, metabolic syndrome among others; intra-surgical factors, like the surgical technique used, the remaining healthy tissue, the experience of the surgeon, the time and type of ischemia among others.

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The clinical practice guidelines for the prevention, diagnosis, evaluation and treatment of chronic kidney disease mineral and bone disorders (CKD-BMD) in adults, of the Latin American Society of Nephrology and Hypertension (SLANH) comprise a set of recommendations developed to support the doctor in the management of these abnormalities in adult patients with stages 3-5 kidney disease. This excludes changes associated with renal transplantation. The topics covered in the guidelines are divided into four chapters: 1) Evaluation of biochemical changes, 2) Evaluation of bone changes, 3) Evaluation of vascular calcifications, and 4) Treatment of CKD-MBD.

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It has been well established that a rapid decrease in bone mineral density (BMD) occurs in the first 6 to 12 mo after a successful renal transplantation and persists, albeit at a lower rate, for many years. This rapid BMD loss significantly increases the fracture risk of these patients to levels that are even higher than those of patients who have chronic kidney disease stage 5 and are on dialysis. The presence of low BMD in renal transplant patients as a predictor of risk fracture is controversial.

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Background: Iron sucrose (Fe-S) and low-molecular-weight iron dextran (Fe-D) have been used successfully in the treatment of anaemia in chronic kidney disease patients. However, some side effects, such as endothelial cell dysfunction have been reported. Mechanisms by which iron can induce endothelial cell damage have not been completely understood.

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Access to and coverage of renal replacement therapy in minorities and ethnic groups in Venezuela. Numerous studies have documented the presence of racial and minority disparities regarding the impact of renal disease and access to renal replacement therapy (RRT). This problem is less well documented in Latin America.

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Several studies have indicated that bone alterations after transplantation are heterogeneous. Short-term studies after transplantation have shown that many patients exhibit a pattern consistent with adynamic bone disease. In contrast, patients with long-term renal transplantation show a more heterogeneous picture.

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Background: Loss of bone mass after transplantation begins in the early periods after transplantations and may persist for several years, even in patients with normal renal function. While the pathogenesis of these abnormalities is still unclear, several studies suggest that preexisting bone disease, glucocorticoid therapy, and alterations in phosphate metabolism may play important roles. Recent studies indicate that osteoblast apoptosis and impaired osteoblastogenesis play important roles in the pathogenesis of glucocorticoid-induced osteoporosis.

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