Background: Kidney injury molecule-1 (KIM-1) is a biomarker useful for detecting early tubular damage and has been recently reported as a useful marker for evaluating kidney injury in IgA nephropathy (IgAN). We therefore investigated whether treatment decreases urinary KIM-1 excretion in IgAN.
Methods: We prospectively enrolled 37 patients with biopsy-proven IgAN. Urinary KIM-1 was assessed before and after treatment, which included low salt diet, blood pressure control, pharmacotherapy with angiotensin receptor blockers and/or angiotensin converting enzyme inhibitors, and immunosuppressive agents as necessary. The median treatment duration was 24 months.
Results: Urinary KIM-1/creatinine (Cr) was significantly decreased in patients with IgAN after treatment compared to baseline (P < 0.0001, 1.16 [0.51-1.83] vs 0.26 [0.12-0.65] ng/mg). There was a decrease in the amount of proteinuria after treatment, but it was not statistically significant (P = 0.052, 748.1 [405-1569.7] vs 569.2 [252.2-1114] g/d). Estimated glomerular filtration rate (eGFR) did not change with treatment (P = 0.599, 79.28 ± 30.56 vs 80.98 ± 32.37 ml/min/1.73 m2). Urinary KIM-1 was not correlated with proteinuria baseline or follow up (pre-: R = - 0.100, P = 0.577, post-: R = 0.001, P = 0.993). In patients with higher baseline urinary KIM-1, both urinary KIM-1 level and proteinuria were significantly decreased following treatment.
Conclusions: Treatment decreases urinary KIM-1/Cr in patients with IgAN. It also reduces proteinuria in patients with higher baseline urinary KIM-1. These results suggest a potential role for urinary KIM-1 as a biomarker for predicting treatment response in IgAN, however, further study is needed to verify this.