Abstract
Deficiency or excess exposure to manganese (Mn), an essential mineral, may have potentially adverse health effects. The kidneys are a major organ of Mn site-specific toxicity because of their unique role in filtration, metabolism, and excretion of xenobiotics. We hypothesized that Mn concentrations were associated with poorer blood pressure (BP) and kidney parameters such as estimated glomerular filtration rate (eGFR), blood urea nitrogen (BUN), and albumin creatinine ratio (ACR). We conducted a cross-sectional analysis of 1931 healthy U.S. adolescents aged 12–19 years participating in National Health and Nutrition Examination Survey cycles 2013–2014, 2015–2016, and 2017–2018. Blood and urine Mn concentrations were measured using inductively coupled plasma mass spectrometry. Systolic and diastolic BP were calculated as the average of available readings. eGFR was calculated from serum creatinine using the Bedside Schwartz equation. We performed multiple linear regression, adjusting for age, sex, body mass index, race/ethnicity, and poverty income ratio. We observed null relationships between blood Mn concentrations with eGFR, ACR, BUN, and BP. In a subset of 691 participants, we observed that a 10-fold increase in urine Mn was associated with a 16.4 mL/min higher eGFR (95% Confidence Interval: 11.1, 21.7). These exploratory findings should be interpreted cautiously and warrant investigation in longitudinal studies.
Highlights
Manganese (Mn) is an essential nutrient required for normal human development, with critical roles in energy metabolism, protection against oxidative stress, immunological system function, and nervous system function [1,2]
We observed differences in mean blood Mn levels based on self-identified race/ethnicity
We observed that a 10-fold increase in creatinine-adjusted urine Mn was associated with a 16.4 mL/min higher estimated glomerular filtration rate (eGFR) after adjusting for age, sex, Body mass index (BMI) z-score, race/ethnicity, and poverty-income ratio (PIR)
Summary
Manganese (Mn) is an essential nutrient required for normal human development, with critical roles in energy metabolism, protection against oxidative stress, immunological system function, and nervous system function [1,2]. Mn is an established neurotoxicant, but much less is known about nephrotoxic effects during critical periods of kidney function maturation from infancy to late adolescence. While evidence supports Mn nephrotoxicity at high doses [4,5], low-dose Mn exposure may be protective against preeclampsia or kidney disease [6,7]. Exposure to Mn by ingestion or inhalation among children poses higher risks compared to adults, due to metabolic differences in absorption and elimination [8]. The intestinal absorption rate of ingested Mn is higher in children and the high demand of iron linked
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