SPON1 deficient mice have upregulated bone deposition and higher bone mass.[44] High concentrations of F-spondin are found in the human ovary, where it is known to stimulate vascular smooth muscle cell proliferation.[45] Given the negative Spearman correlation of Spondin-1 with eGFR and albuminuria, it follows that Spondin-1 levels were lower in those with higher eGFR, yet the Spondin-1-HF association was significantly stronger in these non-CKD patients. This evidence concerns the gene SPON1 and chronic kidney disease.