Title
The Kidney In Lead Poisoning
Author
Radosevic, Saric, Beritic and Knezevic
Publication
British Journal of Industrial Medicine, July 1961, 18(3), p. 222-230
Link
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1038152/
Abstract
Kidney damage due to lead is still an interesting problem of industrial toxicology. In spite of abundant literature data, much still remains to be explained. There are controversial opinions, not only on the type of renal lesions due to lead, but also on whether lead affects the kidney at all.
In this paper our clinical observations on the effect of lead upon the kidney in 53 patients suffering from lead poisoning are presented. In 44 patients (40 men and four women) lead poisoning was due to occupation, and in nine (five men and four women) to the use of lead-glazed pottery. The length of exposure varied from two months to 35 years. In all cases the diagnosis of lead poisoning was made clinically and confirmed by laboratory tests.
Permanent changes in the form of chronic nephropathy were observed in only two patients. These were the two cases in which exposure to lead was the longest and most intense. Twenty-three patients showed functional renal lesions tending to normalize. In addition to the cases of organic nephropathy, blood pressure was persistently raised in one further patient; in two patients a raised blood pressure was observed only in the acute stage of poisoning.
On the basis of these findings we consider that lead intoxication can cause renal lesions. These lesions are for the most part functional and temporary. In cases of long and severe exposure and repeated lead intoxication, organic renal lesions seem possible. The disturbances of renal function observed in this study may be ascribed to disordered intrarenal circulation, due to the spastic effect of lead on intrarenal blood vessels, and to a direct toxic or indirect hypoxic effect of lead on the tubules.
Title
Renal Effects of Environmental and Occupational Lead Exposure
Author
- K. Rastogi
Publication
Indian Journal Occupational Environmental Medicine, Dec 2008, p.103–106
Link
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796746/
Abstract
Lead is one of the most useful elements in industry, but serves no useful function in the human body. Environmental and industrial lead exposures continue to pose major public health problems in the exposed population. Over the years, it has become increasingly evident that low-level lead exposure resulting in blood lead levels between 10 and 15 μg/dL can lead to deleterious effects like cognitive impairment and behavioral deficits, high blood pressure (BP) and impaired renal function. Lancereaux provided the first description of kidney disease and interstitial nephritis by postmortem examination of a lead-poisoned artist. It was not until the late 1920s when an epidemic of chronic nephritis in Queensland, Australia, was linked to childhood lead poisoning that the full spectrum of lead-induced nephropathy became apparent. This was followed by cases of renal diseases from the US in individuals consuming lead-contaminated illegally distilled moonshine whisky.
Title
Effects of Lead Exposure on Renal Function in Young Rats
Author
D.R. Johnson & L.I. Kleinman
Publication
Toxicology and Applied Pharmacology, Volume 48, Issue 3, May 1979, Pages 361–367
Link
http://www.sciencedirect.com/science/article/pii/0041008X79904198
Abstract
Renal function was evaluated in young rats, 35–50 days old, exposed to lead before weaning via mother’s milk and after weaning in their solid diet. Lead-exposed rats had blood lead concentrations of 120±21 μg Pb/100 ml, compared to 10±2 μg Pb/100 ml for pair-fed, age-matched controls. There was no significant difference between the control and lead-exposed groups in body weight, kidney weight, glomerular filtration rate, renal plasma flow, extraction of paraaminohippurate, and fractional excretion of amino acids or phosphate. However, significant differences between control and lead-exposed rats were observed in 24-hr urinary volume excretion and in fractional excretion of sodium following extracellular volume expansion. The elevation in 24-hr urine volume was subsequently demonstrated to be associated with increased water intake in the lead-exposed rats. The results of these studies indicate that in young rats with elevated blood lead concentrations, resting renal function is similar to that found in non-lead-exposed animals. Significant differences in water and electrolyte excretion during stress (water deprivation or extracellular volume expansion) were observed between the control and lead-exposed rats. However, the role of the kidney in the mechanisms involved in these altered responses in unknown.
Title
Erythrophagocytosis of Lead-Exposed Erythrocytes by Renal Tubular Cells: Possible Role in Lead-Induced Nephrotoxicity
Author
So-Youn Kwon, Ok-Nam Bae, Ji-Yoon Noh, Keunyoung Kim, Seojin Kang, Young-Jun Shin, Kyung-Min Lim, and Jin-Ho Chung
Publication
Environmental Health Perspectives, Volume 123, Issue 2, February 2015
Link
http://dx.doi.org/10.1289/ehp.1408094
Abstract
Background: Nephrotoxicity associated with lead poisoning has been frequently reported in epidemiological studies, but the underlying mechanisms have not been fully described.
Objectives: We examined the role of erythrocytes, one of the major lead reservoirs, in lead-associated nephrotoxicity.
Methods and Results: Co-incubation of lead-exposed human erythrocytes with HK-2 human renal proximal tubular cells resulted in renal tubular cytotoxicity. Morphological and flow cytometric analyses revealed that HK-2 cells actively phagocytized lead-exposed erythrocytes, which associated with phosphatidylserine (PS) externalization on the erythrocyte membrane and generation of PS-bearing microvesicles. Increased oxidative stress and up-regulation of nephrotoxic biomarkers, such as NGAL, were observed in HK-2 cells undergoing erythrophagocytosis. Moreover, TGF-β, a marker of fibrosis, was also significantly up-regulated. We examined the significance of erythrophagocytosis in lead-induced nephrotoxicity in rats exposed to lead via drinking water for 12 weeks. We observed iron deposition and generation of oxidative stress in renal tissues of lead-exposed rats, as well as the histopathological alterations such as tubulointerstitial lesions, fibrosis, and up-regulation of KIM-1, NGAL, and TGF-β.
Conclusions: Our data strongly suggest that erythrophagocytosis and subsequent iron deposition in renal tubular cells could significantly enhance nephrotoxicity following lead exposure, providing insight on lead-associated kidney damages.
Title
Chronic Kidney Disease Associated With Environmental Toxins and Exposures
Author
Peter Soderland, Shachi Lovekar, Daniel E. Weiner, Daniel R. Brooks, James S. Kaufman
Publication
Advances in Chronic Kidney Disease Journal, Volume 17, Issue 3, May 2010, Pages 254-264
Link
http://dx.doi.org/10.1053/j.ackd.2010.03.011
Abstract
People are exposed to various potentially toxic agents and conditions in their natural and occupational environments. These agents may be physical or chemical, may enter the human body through oral, inhalational, or transdermal routes, and may exert effects on all organ systems. Several well-known as well as lesser known associations exist between chronic kidney disease (CKD) and both environmental agents and conditions, such as heavy metals, industrial chemicals, elevated ambient temperatures, and infections. The effects of these agents may be modulated by genetic susceptibility and other comorbid conditions and may lead to the development of acute and CKD. In this article, we present environmental factors that are associated with CKD.