Introduction:
Nephrocalcinosis has become a growing problem in Norwegian hatcheries for salmonids. The disease is considered an important cause of reduced welfare, reduced growth and increased mortality. Poor-performing fish, often referred to as "losers," also represent a significant problem in the hatchery phase in salmon (Salmo salar) and rainbow trout (Oncorhynchus mykiss) farming . The underlying causes are multifactorial and remain poorly understood.
The primary aim of this study is to investigate histological and hematological changes in rainbow trout (Oncorhynchus mykiss) during the hatchery phase, with the goal of identifying factors associated with nephrocalcinosis and the development of the loser phenotype.
Material, methods and results:
Kidney and blood samples were collected from 15 loser fish (98 ±31 g) and 15 apparently healthy fish (201 ± 36 g) from local hatcheries (Fig. 1 ). B leeding was not detected in any of the fish. Histological evaluation revealed well-developed nephrocalcinosis in all loser fish, corresponding to grade 2 or 3 lesions. Among the healthy fish, 6 of 15 displayed mild mineral precipitation and dilation of Bowman’s capsule. Additionally, two individuals exhibited grade 2 or 3 nephrocalcinosis, despite being classified as healthy (Fig. 2). Hematological analysis revealed a significantly lower hematocrit (HCT) in loser fish (19 ± 4%) compared to healthy individuals (29 ± 3%; p < 0.05; Fig. 3) . Plasma c ortisol levels were also markedly elevated in loser fish (17.9 ± 7.3 ng/mL) relative to healthy controls (4.4 ± 2.5 ng/mL, p < 0.001). However, plasma glucose concentrations did not differ significantly between the groups.
Conclusion:
These results indicate a strong association between advanced nephrocalcinosis, reduced hematocrit, and the loser phenotype. Impaired excretory function and anemia may contribute to the syndrome’s development. To further explore causative mechanisms, subsequent analyses will include comprehensive blood chemistry profiling, stress biomarker evaluation, and measurements of erythropoietin levels. In the next phase, we will longitudinally monitor the progression of nephrocalcinosis, loser syndrome, and hematopoietic disturbances from early juvenile stages (20 g) up to 200 g. These observations will be correlated with detailed renal histopathology, and the potential influence of seawater transfer and vaccination will also be assessed.