Clinical and preclinical studies have shown that reduction in parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23) can ameliorate anemia associated with chronic kidney disease (CKD). Additionally, clinical studies have demonstrated that salmon calcitonin (sCT) effectively reduces secondary hyperparathyroidism (SHPT) and FGF23. Thus, this study aimed to investigate the potential of sCT to improve renal anemia in a rat model. Male Wistar rats (N=24) were orally administered with adenine (100 mg/kg/day) for 28 days to induce renal anemia. Subsequently, subcutaneous administration of sCT (20 IU/kg/day) or recombinant human erythropoietin (rhEPO) (30 IU/kg/day) was carried out for 21 days. Hematological, biochemical parameters, and histopathological analysis were measured at the end of study (Day 50) with primary objective of investigating the effect of sCT on serum EPO levels. Adenine exposure resulted in reduced (EPO) serum levels, decreased total red blood cell (RBC) counts, hemoglobin (Hb), and hematocrit (Hct), accompanied by elevated serum levels of blood urea nitrogen (BUN), creatinine, PTH, and FGF23. In adenine-treated wistar rats, both sCT and rhEPO administrations successfully increased EPO serum levels, total RBC counts, Hb, and Hct, while decreasing serum BUN, creatinine, FGF23, and PTH levels. Histopathological analysis revealed characteristic kidney damage indicative of CKD in adenine-treated rats, which was notably absent in rats treated with sCT or rhEPO. The study concludes that sCT successfully mitigated renal anemia in rats suggesting its potential as a promising therapeutic strategy for CKD-related anemia. These findings support the translational potential of sCT for improving anemia in CKD patients.

Background and Purpose: Corticosteroid therapy is still controversial to use for treatment of coronavirus disease-2019 (COVID-19). The results of multiple randomized clinical trials (RCTs) and observational studies are very diverse and contradictory, which arising difficulty in the clinical decision-making. The objective of this study is to investigate the effect of corticosteroids on mortality by systematic review and meta-analysis. External Approach: A systematic search was performed on different databases namely Medline/PubMed, Cochrane and Google scholar on 10 February 2022, according to PRISMA guidelines. The 28-days mortality was considered as outcome of study. A pooled estimate was calculated with random effects and fixed effects models. Cochran’s Q test and the I2 statistic were conducted for statistical heterogeneity. Key Results: 38 studies were included, having sample size of 87,781 patients. Amongst them, 16437 patients received corticosteroid therapy (intervention group) while 71344 patients were standard (noncorticosteroids) therapy (control group). 12.68% (2084) mortality observed in the intervention group while 5.93% (4227) mortality observed in the control group. The overall pooled estimate showed a significantly (OR2.305;95%CI: 2.1810 to 2.4370) increased mortality in intervention group. A pooled fold change estimation showed significantly increased in the mortality in methylprednisolone (OR 1.206;95%CI: 1.0770 to 1.3500) and dexamethasone (OR 1.388;95% CI:1.1870 to 1.6220) therapy. Conclusion and Implication: In conclusion, corticosteroid therapy produced a negative prognosis as depicted by increased mortality among COVID-19 patients. The possible reasons might be delay in virus clearance and secondary infection due to initiation of the corticosteroids at high dose in the early stage of infection.