الفهرس 
Chronic Kidney Disease (CKD)Only 14 pages are availabe for public view
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Abstract
chronic kidney disease (CKD) in children is defined by the presence of kidney damage or by a glomerular filtration rate that has remained below 60 ml/min/1.73 m2 for more than 3 months. End-stage kidney or renal disease (ESRD) is the final stage of chronic kidney disease in which the kidneys no longer function well enough to meet the needs of daily life. Progression of CKD to end-stage renal disease (ESRD) requires dialysis or transplantation for survival (Inker et al., 2014).
The main etiologic factors of CKD in children are represented by congenital anomalies of kidney and urinary tract(CAKUT), steroid-resistant nephrotic syndrome (SRNS), chronic glomerulonephritis (e.g. lupus nephritis, Alport syndrome) and renal cystic ciliopathies, that account for approximately 49.1,10.4,8.1 and 5.3% of cases, respectively (Vivante and Hildebrandt, 2016).
Less common causes of CKD in children include thrombotic microangiopathies (especially atypical haemolytic uraemic syndrome), nephrolithiasis/ nephrocalcinosis, Wilm’s tumor, infectious and interstitial diseases and other structural causes (e.g. renal hypoplasia or posterior urethral valves) predominate in younger patients, the incidence of glomerulo-nephritis increases in those >12 years old (Harambat et al., 2012).
Chronic kidney disease (CKD), in fact, is not only a localized disease, but also affects virtually all organ systems, especially at the late stage of the disease. Among these, respiratory system disorders are one of the most prevalent complications in ESRD patients (Rezaeetalab et al., 2015).
A variety of pulmonary abnormalities, including pulmonary edema, pleural effusion, acute respiratory distress syndrome, pulmonary fibrosis and calcification, pulmonary hypertension, hemosiderosis, pleural fibrosis, and sleep apnea syndrome, have been documented in those patients (Vincenti et al., 2016).
Impaired pulmonary function may be the direct result of circulating uremic toxins or may indirectly result from fluid overload, anemia, immune suppression, extra osseous calcification, malnutrition, electrolyte disorders, and/or acid-base imbalances, which are common issues in ESRD patients (Yilmaz et al., 2016).
Many studies have been published on functional changes affecting the respiratory system in patients with ESRD. These studies have focused on changes in arterial oxygen and spirometric parameters. Reduction of arterial oxygen content has been shown in association with hemodialysis, although the etiology is not clarified. It is believed to be due to diffusion of carbon dioxide (CO2) into the dialysate, which may cause alveolar hypoventilation and reduction of partial pressure of oxygen (PaO 2) (Turcios, 2012).
Patients with ESRD undergo different types of dialysis: regular hemodialysis and hemodiafiltration. Haemodialysis is based on the diffusive transport of solutes across a semipermeable membrane and is effective in removing small solutes, such as urea, and correcting electrolyte, acid–base and fluid imbalances. However, it is poorly suited to the effective removal of larger solutes, such as β2-microglobulin, even when high-flux membranes are used because solute diffusion coefficients decrease rapidly with the increasing molecular size (Tattersall et al., 2013).
Hemodiafiltration is a treatment designed to remove accumulated metabolic products from blood by a combination of diffusive and convective transport through a semi-permeable membrane of high-flux type. Fluid is removed by ultrafiltration and the volume of filtered fluid exceeding the desired weight loss is replaced by sterile, pyrogen-free infusion solution. Hemodiafiltration provides a better elimination of higher-molecular weight solutes than hemodialysis (Grooteman et al., 2012).
Hemodiafiltration is the most efficient way of doing renal replacement therapy. It is called continuous veno-venous hemofiltration or (CVVH), as opposed to continuous veno-venous hemodialysis (CVVHD) (Ramin, 2014).
Endothelin-1(ET-1) is a middle molecule and most of it is secreted in the lungs by the endothelium and smooth muscles of airway epithelium. ET-1 is also found circulating in the plasma. Since the discovery of ET-1, investigators from different parts of the world have performed numerous studies because of its prolonged vasoconstrictive effect even after a single-dose injection to rats. Also, ET-1causes bronchoconstriction and pulmonary artery hypertension. Moreover, it has been shown that ET-1 has an important role in stabilizing blood pressure (Safa et al., 2014).
The kidney is an important site of endothelin-1(ET-1) production and is particularly susceptible to ET-1 action, its renal effect include increase in renal vascular resistance decrease in GFR and increase in Na reabsorption (Ganong and Ganong, 1995).