The study used male rats that were fed a standard diet. In addition, 16 of the rats consumed drinking water treated with lead acetate for four weeks. The dose of lead administered resulted in mild toxicity and is similar or slightly lower than the levels observed in subjects with occupational 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 rodents 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. But low lead level 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 .
The study found 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.
"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," said Dr. Richard J Johnson, the senior researcher.
The study appears in the online edition of the American Journal of Physiology Renal Physiology