SPP1 and nephrocalcinosis: Additionally, TA treatment effectively suppressed the glyoxylate‐induced up‐regulation of renal osteopontin (OPN) expression (Figure 4J), pointing to a mitigation of renal damage.[23] When compared to mice afflicted with nephrocalcinosis, TA‐treated mice displayed decreased levels of plasma BUN, serum creatinine, and a reduced kidney/body weight ratio (Figure 4D–F), which collectively suggest improved excretory kidney function.