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Background: Major public health risk was ‘Dengue infection’ initial discovery is critical to improving the existence in serious infection of dengue. Our objective in this study was to investigate the serum ferritin level to suppose biomarker in the diagnosis of dengue fever. Method: An observational and prospective study was conducted in the Hayatabad Medical Complex and it included one hundred nineteen cases related to dengue was diagnosed by using NSI Test antigen or serology test related to specific dengue that internment “ELISA”. At the time of diagnosis, serum ferritin was measured. Monitoring the clinical and platelets counts was done on daily bases, it also classified into two groups such as non-severe and severe groups by allowing WHO criteria in 2009. Result: Five out of 119 cases of dengue were severe, dengue patients had lower platelets when they are in severe condition, count the number of platelets (p less than 0.0001); Ferritin level almost high (p=0.02) and the value of hospital longer time period (p less than 0.0001) mostly in severe group as compare to non-severe group of dengue. Platelets count had negative value with age factor almost Positive correlations with ferritin levels (p=0.08 or r= 0.16) and a longer hospital stay (r= -0.427 and p 0.0001) were also found (r= 0.26, p= 0.004). These values indicate the severe risk of dengue infection/ disease. Negative value of serum ferritin that are related to the value of platelets (r=0.51 and p< 0.001). On day 4 of clinical infections, an elevated value of ferritin is seen in severe cases. Conclusion: In Clinical practice, a biomarker for determining the severity of dengue infection is increased serum ferritin concentrations. Keywords: Biomarkers, Serum ferritin, Severity, Dengue infection, Predicators

Metabolic acidosis, a common complication in patients with chronic kidney disease (CKD), results in a multitude of deleterious effects. Though the restoration of kidney function following transplantation is generally accompanied by a correction of metabolic acidosis, a subset of transplant recipients remains afflicted by this ailment and its subsequent morbidities. The vulnerability of kidney allografts to metabolic acidosis can be attributed to reasons similar to pathogenesis of acidosis in non-transplant CKD, and to transplant specific causes, including donor related, recipient related, immune mediated factors, and immunosuppressive medications. Correction of metabolic acidosis in kidney transplantation either with alkali therapy or through dietary manipulations may have potential benefits and the results of such clinical trials are eagerly awaited. This review summarizes the published evidence on the pathogenesis and clinical consequences of chronic metabolic acidosis in kidney transplant recipients.

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