Mobilizable lead in patients with chronic renal failure

Abstract

Blood lead (Pb) and urinary Pb before and after i.v. infusion of 1 g of Na2Ca EDTA were determined (atomic absorption) in 46 control subjects and 91 patients with various stages of renal failure (median serum creatinine 2.5 mg dl-1). Under baseline conditions, patients with renal failure had higher blood Pb levels (112 ng ml-1, range 44-272 vs. 76; 36-187 in controls; P less than 0.001) and lower urinary Pb (16.2 nmol 24 h-1 1.73 m-2, 4.86-66.8 vs. 33; 11-91 in controls; P = 0.001). The increment in urinary Pb after EDTA infusion (mobilizable Pb) was higher (795 nmol 4 days-1 1.73 m-2, range 155-5611 vs. 307; 131-1587 in controls; P = 0.001). In 12 patients with renal failure (13%) mobilizable Pb was above the highest value in controls. Mobilizable urinary Pb correlated (r = 0.68) significantly (P = 0.001) with blood Pb, but only marginally with serum creatinine (r = 0.32; P less than 0.007). Mobilizable Pb was higher in patients with renal failure and a history of smoking or occupational Pb exposure and tended to be higher in patients with alcoholism. Ten of 91 patients had gout; increased mobilizable Pb was present in three of the 10. The data confirm relatively high prevalence of elevated body Pb burden in European patients with chronic renal failure. The question is unresolved whether Pb plays a role in the progression of renal failure.

Occult lead intoxication as a cause of hypertension and renal failure

“…It would be useless to compare only healthy controls and 'CRF patients' as the latter would represent a mixture of patients with CRF of known and unknown aetiologies, all of them with or without overt Pb exposure. With the study designs used by a number of authors [4,5,[22][23][24] it is only possible to state that some CRF patients have high levels of Pb burden, but it is impossible to clearly discern what proportion of CRF is a consequence of the excessive Pb burden.…”

“…Its long-term effects as an environmental pollutant and poison have only become a matter of concern in the last few years and is thought to be a world-wide risk for all populations. The idea of Pb-associated renal disease is an ancient concept [1], but still some degree of controversy persists even today as to the role of chronic Pb intoxication as a cause of chronic renal failure (CRF) [2][3][4][5]. Available reports, based in most cases on occupationally exposed workers [6][7][8][9][10][11][12][13], generally involve Pb as a cause of CRF, but still some do not find such a relationship [14,15].…”

“…In other words, Pb may indeed be the cause of some cases of CRF of uncertain aetiology. Conversely, some reports pose the question whether CRF itself may be the cause of excessive Pb accumulation [4,5,16].…”

Hyperparathyroidism and abnormal 1,25(OH)2vitamin D3 metabolism in experimental lead intoxication

“…Finally, low-level exposure to Pb has recently been discussed in the genesis of hypertension [35,36]. This concept is based upon the finding that a significant correlation is noted between blood Pb levels and arterial blood pressure in the general population [37,38] and that Pb in several animal studies increased blood pressure and pressor responsiveness [39].…”

The conceptual structure of the integrated exposure uptake biokinetic model for lead in children.

“…The transfer coefficient for blood to urine, which was estimated by the process described above, is the blood lead mass divided by the rate at which lead is eliminated from the blood through the urine. A literature review revealed seventeen adult studies for evaluating this coefficient (46,51,(76)(77)(78)(79)(80)(81)(82)(83)(84)(85)(86)(87)(88)(89)(90). The adult value was allometrically scaled to children 0 to 84 months of age, based on proportionality between the blood volume and glomerular filtration rate for that age group.…”