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Published on: July 3, 2013
Contribution of lead to hypertension with renal impairment
Insights
Elevated lead levels, identified by the EDTA lead-mobilization test, were found in men with essential hypertension and reduced kidney function. This suggests lead exposure may contribute to hypertension-related renal disease.
Area of Science:
- Environmental Health
- Nephrology
- Cardiovascular Disease
Background:
- Essential hypertension, a common condition, has an unknown cause.
- Lead poisoning is a potential, though often overlooked, cause of hypertension.
- The EDTA lead-mobilization test effectively measures cumulative lead absorption.
Purpose of the Study:
- To investigate the association between cumulative lead absorption and essential hypertension.
- To determine if lead exposure plays a role in hypertension-related renal impairment.
Main Methods:
- Utilized the EDTA lead-mobilization test to assess lead body stores in 48 men with essential hypertension.
- Compared lead excretion in hypertensive patients with and without reduced renal function.
- Included a control group of 22 patients with renal impairment from other causes.
Main Results:
- Hypertensive patients with reduced renal function (serum creatinine >1.5 mg/dL) showed significantly higher mobilizable lead levels.
- Lead excretion in hypertensive patients was significantly greater than in control patients with similar renal impairment.
- These findings were not attributable to renal disease alone.
Conclusions:
- Cumulative lead absorption may be an etiologic factor in "essential" hypertension, particularly in cases with renal compromise.
- The EDTA test can identify patients with elevated lead burdens contributing to their hypertension.
- Re-evaluating the etiology of essential hypertension to include lead exposure is warranted.
Abstract:
Hypertension of unknown cause is generally termed "essential." Because hypertension has long been considered a possible complication of lead poisoning and the EDTA lead-mobilization test has proved to be a sensitive indicator of excessive body stores of lead, we used this test to evaluate cumulative past lead absorption in 48 men diagnosed as having essential hypertension. Patients who had hypertension with reduced renal function (i.e., serum creatinine level greater than 1.5 mg per deciliter [133 mumols per liter]) had significantly larger amounts of mobilizable lead than did patients who had hypertension without renal impairment. The increase in mobilizable lead was not due to the renal disease itself, since 22 control patients without a history of essential hypertension but with comparable renal impairment from known causes excreted significantly less lead chelate during the three-day test. These data suggest that lead may have an etiologic role in the renal disease of some patients usually designated as having "essential" hypertension.
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