While lead exposure has long been associated with hypertension, arteriolosclerosis and kidney disease, a new animal study from the University of Florida, Gainesville indicates that even low level exposure to lead accelerates chronic renal disease–primarily by raising blood pressure and accelerating injury to kidney tissues and blood vessels.
The study used male rats which were fed a standard diet. In addition, 16 of the rats were given water with lead acetate at a dosage resulting in similar or slightly lower than the levels observed in subjects with occupational lead exposure. Thereafter they underwent remnant kidney (RK) surgery and afterwards continued on the lead acetate for 12 more weeks.
A control group also underwent RK surgery but without lead acetate. At eight and 12 weeks after surgery, the body weight of all the rats was measured and systolic blood pressure was assessed. Twelve weeks after RK surgery, kidney tissue was collected for histologic and molecular biologic studies from both groups.
Lead treatment was well tolerated and resulted in modest elevations in whole blood lead levels. However, the lead exposure reduced body weight, increased blood pressure and worsened renal dysfunction.
Specifically, lead exposure:
- was associated with higher systolic blood pressure and worse renal function, and with a tendency for greater urinary protein; and
- while scarring in the renal capillary system tended to be worse in lead treated rats, the most striking finding was that kidney tissue disease (arteriolar disease, peritubular capillary loss, tubulointerstitial damage and macrophage infiltration) worsened with lead exposure. These developments were associated with the significantly increased renal expression of monocyte chemoattractant protein-1 mRNA.
According to Dr. Richard J. Johnson, the seior researcher, "This study examined the effect of mild, chronic lead intoxication in an experimental model of chronic renal disease. The dose of lead administered resulted in mild toxicity. This degree of lead poisoning was sufficient to cause higher blood pressures and accelerate the progression of renal failure."
Source: American Journal of Physiology—Renal Physiology (Online Edition)