Exposure to the environmental pollutant cadmium (Cd) is inevitable for most people because of its ubiquitous presence in the human diet. Concerningly, the risk of developing hypertension has been linked to dietary Cd exposure. The mechanisms involved are however, unclear. Because the kidneys play an indispensable role in long-term blood pressure regulation, and they are also the principal site of Cd accumulation and toxicity, a retrospective analysis was conducted to examine if the kidney damage and malfunction, reflected by urinary β2-microglobulin excretion (Eβ2M), and the estimated glomerular filtration rate (eGFR), are related to blood pressure variation and urinary Cd excretion (ECd). Data were obtained from 689 non-diabetic Thai subjects, chronically exposed to environmental Cd, of which 32.4% had hypertension. People in the top quartile of ECd had much higher risks of having β2-microglobulinuria [POR = 10.7 (95%CI:1.36, 83.4), p = 0.024), and hypertension [POR = 2.79 (95% CI:1.60, 4.87), p <0.001]. Only in subjects with an eGFR below 90 mL/min/1.73 m2, systolic blood pressure (SBP) and diastolic blood pressure (DBP) both increased linearly with Eβ2M (respective β = 0.182 and 0.192 for SBP and DBP) after adjustment for age, body mass index, gender, and smoking. The present study confirms the significant impact of Cd on risk of having hypertension, following GFR loss induced by Cd. A simple mediation model analysis has provided, for the first time, evidence that may link rising SBP and DBP in Cd-exposed people to the SH2B3-β2M axis of blood pressure regulation.
