Environmental lead exposure has been linked with reduced kidney function. However, evidence about its role in diabetic kidney damage, especially when considering the nutritional status of
vitamin D, is sparse. In this observational study, we investigated the association between low-level lead exposure and urinary
albumin-to-
creatinine ratio (UACR) and assessed potential impact of
vitamin D among 4033 diabetic patients in Shanghai, China. Whole blood lead was measured by
graphite furnace atomic absorption spectrometry. Serum
25-hydroxyvitamin D [25(
OH)D] was tested using a chemiluminescence immunoassay. The associations of blood lead with UACR and
albuminuria, defined as UACR ≥30 mg/g, according to 25(
OH)D levels were analyzed using linear and Poisson regression models. A doubling of blood lead level was associated with a 10.7% higher UACR (95% CI, 6.19%-15.5%) in diabetic patients with 25(
OH)D < 50 nmol/L, whereas the association was attenuated toward null (2.03%; 95% CI, -5.18% to 9.78%) in those with 25(
OH)D ≥ 50 nmol/L. Similarly, the risk ratios of prevalent
albuminuria per doubling of blood lead level between the two groups were 1.09 (95% CI, 1.03-1.15) and 0.99 (95% CI, 0.86-1.14), respectively. Joint analysis demonstrated that a combination of high blood lead and low 25(
OH)D corresponded to significantly higher UACR. Among diabetic patients with 25(
OH)D < 50 nmol/L, the increment of UACR relative to blood lead was more remarkable in those with reduced estimated glomerular filtration rate (<60 mL/min/1.73 m2). These results suggested that higher blood lead levels were associated with increased urinary
albumin excretion in diabetic patients with
vitamin D deficiency. Further prospective studies are needed to validate our findings and to determine whether
vitamin D supplementation yields a benefit.