Results: Sal B attenuated the pathological damage of kidney and AVF venous segments tissues, improved calcium salt deposition, reduced the levels of Cr, BUN, and ALP, and inhibited the expression of BMP-2, p-Smad1, p-Smad5, Osterix, and Runx2 in AVF venous segments tissue (p < 0.05).Conclusion: The mechanism of Sal B inhibition of calcium salt deposition in rats of CKD-AVF may be related to the inhibition of the BMP2/Smads signaling pathway. Here, BMP2 is linked to chronic kidney disease.