EVALUATION OF THE EFFECTS OF SALMON CALCITONIN AGAINST
EXPERIMENTALLY-INDUCED RENAL ANEMIA
Abstract
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.