الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
CKD is the 12th cause of death and the 17th cause of disability worldwide. The global incidence and prevalence of CKD, however, may be underestimated.
Therefore, prevention of CKD and of its progression to end-stage renal disease represents a major task in nephrology care. In addition to drug treatment, dietary management has a pivotal role in the therapy of CKD patients.
As patients progress through the stages of CKD, nutritional requirements are altered and metabolism of protein and other nutrients are affected. These nutritional derangements significantly affect the high morbidity and mortality rate observed in those patients. Much has been studied and reported about malnutrition in dialysed patients. However there is poverty of data concerning the nutrition status in the predialysis patients.
Though dietary protein restriction has been a relevant part of the management of CKD for years yet, reaching the principal goal of protein-restricted regimens of decreasing the accumulation of nitrogen waste products, hydrogen ions, phosphates, and inorganic ions while maintaining an adequate nutritional status to avoid deterioration is the current challenge.
Several nutritional markers have been introduced to assess nutritional status, however none of them has proven to be reliable
Leptin is a hormone regulating the body fat stores by controlling both the sensation of hunger, and energy expenditures. Adipose tissue is the primary site of its synthesis although leptin can be also secreted by other tissues. It reaches the brain, crosses the blood brain-barrier and triggers anorexigenic signals in hypothalamus nucleus. Leptin is cleared from the circulation by the kidney through glomerular filtration and metabolic degradation in renal tubules.
Visfatin is an exciting adipocytokine, it has been subject of intense research because of its pleiotropic actions. Interestingly it acts as an inflammatory cytokine and its levels are elevated in chronic inflammatory diseases. Visfatin plays an important role in the catabolic uremic milieu, and has been linked to systemic inflammation and uremic anorexia.
Patients with CKD generally have an abnormal plasma amino acid pattern. However, the mechanisms behind these abnormalities are not fully understood. Some of the changes are ascribed to derangements in AA metabolism, either because of deficient excretory and metabolic functions of the diseased kidneys or because of uremia per se. Inadequate nutritional intake and malnutrition may also contribute to plasma AA abnormalities. To some extent, the abnormal pattern of AAs seen in CKD patients resembles that seen in protein malnutrition, but the abnormal AA patterns are also observed in CKD patients with normal nutritional status. Because the biochemical changes that occur during inflammation exert a demand on AA metabolism it is hypothesized that the systemic inflammatory response seen in a large proportion of CKD patients may contribute to AA pattern disturbances.
The aim of this work was to assess the role of plasma amino acids, leptin and visfatin as nutritional biomarkers in predialysed chronic kidney disease patients and correlate the studied biomarkers with other traditional markers used to assess the nutritional status in CKD patients, also using these biomarkers in planning a continuously modified dietary program for these patients in attempt to delay their needs to hemodialysis while maintaining adequate nutritional status.
In order to achieve this goal 60 subjects were evaluated and divided into 3 groups. Group A were 20 patients in predialysis phase of CKD with good compliance to dietary protein restriction at 0.7gm/kg, group B were 20 patients in predialysis phase of CKD with poor compliance to dietary protein restriction at 0.7gm/kg (as estimated from dietary diaries), and 20 normal healthy controls.
Following proper selection of patients and control subjects, routine investigations, anthropometric measurements, plasma leptin, visfatin, amino acids, VAS for appetite and SGA were evaluated.
In the present study we found a significant increase of plasma leptin ,visfatin, non-essential amino acids, serum urea, creatinine and SGA in group A and B compared to the control group. Moreover our results showed a significant increase in these parameters in group B compared to group A.
Furthermore, there was a significant decrease in plasma essential amino acids (including valine) and VAS for appetite in group A and B compared to control group, also there was significant decrease in these parameters in group B compared to group A .
An interesting finding in this study was the significant positive correlation between plasma leptin, and creatinine, CRP, urea, SGA, visfatin and non-essential amino acids and the significant negative correlation between plasma leptin and essential amino acids.
Moreover, a positive significant correlation was found between plasma visfatin and CRP while no significant correlation was found with creatinine, urea, SGA, essential or non-essential amino acids
Furthermore, there was a negative correlation between plasma valine and creatinine, CRP, urea, leptin, visfatin and positive correlation with VAS.
An important finding was the ROC curve analysis that was applied to assess the performance of plasma Leptin and Valine in detecting malnutrition in predialysis CKD patients. Interstingly they showed high levels of sensitivity and specificity where plasma Leptin had a sensitivity of 100% and a specificity of 90%, while plasma Valine had a sensitivity of 90% and a specificity of 75% in detecting malnutrition in those patient population. Combined together plasma Leptin and Valine had a sensitivity of 90% and specificity of 95%.
Despite intense search, no single ideal biomarker for nutritional status for predialysis CKD patients has yet been approved, yet our study might introduce Leptin and Valine as potential markers for assessment of nutritional status in those patients.