Search PubMed⌕ Search

Biomedical subjects

R P Wedeen

Publications and source records attributed to R P Wedeen.

At least 19 recordsLinked to original sources
PubMed1997

Occupational and environmental renal disease.

Occupational renal diseases provide models for understanding environmental renal diseases. Kidney damage in a few workers induced by heavy exposure to identifiable toxins indicates what to expect among the large population exposed to low levels of toxins dispersed in the larger environment. Occupational and environmental renal diseases present a unique opportunity for primary prevention as well as the diagnostic challenge of long latency and multifactorial etiology. The occupational and environmental toxins that cause chronic renal disease include the heavy metals (Pb, Cd, Hg, As, Cr, U), organic compounds sometimes referred to as solvents, silica, and beryllium. Toxins encountered as medicinal agents such as germanium, gold, and aluminum will not be considered. This review will update major contributions to the subject which have appeared over the past half decade.

Animals↗
PubMed1995

Lead poisoning.

Explore the source record for details and available documents.

Adult↗
PubMed1994

Sharing the toxic burden in New Jersey.

As toxic pollution spreads throughout New Jersey, the environment induces illness and the fear of illness in an ever-increasing population. The questions to ask physicians and residents of New Jersey are: Who will share the burden? What is the cost of this burden?

Environmental Exposure↗
PubMed1992

Laser microprobe mass spectrometric identification of cyclosporin-induced intrarenal microliths in rat.

Using laser microprobe mass analysis (LAMMA), the composition of 'micro-calcifications (dystrophic type)' or 'metastatic calcifications', previously described in rats given high doses of cyclosporin, have been identified. Female Wistar rats given 12.5, 25 or 50 mg kg-1 per day of cyclosporin in olive oil by gastric gavage developed intrarenal calcifications detected by silver nitrate staining (von Kossa) in the outer medulla after two weeks. The calcifications stained red with periodic acid-Schiff reagent and appeared to be intraluminal microliths with concentric laminations. They could be identified by LAMMA as calcium phosphate (hydroxyapatite), indistinguishable from undecalcified bone. These studies indicate that intraluminal obstruction by calcium phosphate microliths, similar to that seen with magnesium depletion or high phosphate diets, may contribute to renal damage in rats given high-dose cyclosporin. LAMMA appears to be an appropriate technique for identifying both the elemental and organic moieities of intrarenal calcium deposits.

Administration, Oral↗
PubMed1992

Removing lead from bone: clinical implications of bone lead stores.

The chelating agent, CaNa2EDTA, has proven useful for both the diagnosis and treatment of lead poisoning. The EDTA lead-mobilization test has demonstrated the presence of excessive body lead stores when blood concentrations were "normal." The EDTA lead-mobilization test is, however, impractical because it requires injections and timed urine collections. Bone lead measured in biopsy specimens by atomic absorption spectroscopy shows a good correlation with chelatable lead. Over 95% of the body stores of lead are retained in bone with a biological half-life approximating two decades. The half-life of lead in blood, on the other hand, approximates one month. Bone, therefore, provides a good estimate of cumulative lead absorption. In vivo tibial K x-ray fluorescence (XRF) is a safe, specific and reliable technique for the non-invasive measurement of elevated bone lead concentrations. K XRF measures lead to a depth of about 2 cm in cortical bone and is largely independent of geometric factors because lead is measured relative to bone calcium. In vivo tibial K XRF can therefore replace the EDTA lead-mobilization test and bone biopsies for assessing body lead stores and for following the efficacy and endpoint of deleading during chelation therapy.

Bone and Bones↗
PubMed1992

Environmental hazards and public health: lessons for the practice of medicine and for public policy.

The separation of occupational and environmental disease from the mainstream of medical practice has deep roots in the culture of the profession. Medical practice centered on individual patient care as nineteenth-century science yielded the therapeutic triumphs of the twentieth century. Social issues seemed remote to medical practitioners as the rewards of scientifically based therapies upstaged the unglamorous aspects of preventive medicine. Public health was left to politicians and bureaucrats. Victorian ambivalence toward the less successful members of society reinforced the isolation of medicine from public policy. As a consequence, physicians are largely ignored in contemporary debates about environmental hazards, to the detriment of both society and the profession.

Environmental Exposure↗
PubMed1991

Chromium-induced kidney disease.

Kidney disease is often cited as one of the adverse effects of chromium, yet chronic renal disease due to occupational or environmental exposure to chromium has not yet been reported. Occasional cases of acute tubular necrosis (ATN) following massive absorption of chromate have been described. Chromate-induced ATN has been extensively studied in experimental animals following parenteral administration of large doses of potassium chromate (hexavalent) (15 mg/kg body weight). The chromate is selectively accumulated in the convoluted proximal tubule where necrosis occurs. An adverse long-term effect of low-dose chromium exposure on the kidneys is suggested by reports of low molecular weight (LMW) proteinuria in chromium workers. Excessive urinary excretion of beta 2-microglobulin, a specific proximal tubule brush border protein, and retinol-binding protein has been reported among chrome platers and welders. However, LMW proteinuria occurs after a variety of physiologic stresses, is usually reversible, and cannot by itself be considered evidence of chronic renal disease. Chromate-induced ATN and LMW proteinuria in chromium workers, nevertheless, raise the possibility that low-level, long-term exposure may produce persistent renal injury. The absence of evidence of chromate-induced exposure may produce persistent renal injury. The absence of evidence of chromate-induced chronic renal disease cannot be interpreted as evidence of the absence of such injury. Rather, it must be recognized that no prospective cohort or case-control study of the delayed renal effects of low-level, long-term exposure to chromium has been published.

Animals↗
PubMed1991

Environmental renal disease: lead, cadmium and Balkan endemic nephropathy.

The similarity of lead and cadmium nephropathy to Balkan endemic nephropathy warrants careful reevaluation of the possibility that these nephrotoxic metals contribute to the production of the endemic renal disease. Low-level environmental exposure may result in a relationship between the concentration of the metals in tissue storage sites and biological fluids that differs from that encountered after occupational exposure. Urine and blood concentrations may therefore be inadequate measures of exposure. Lead is accumulated in the skeleton and cadmium in the liver and kidneys with biological half lives approximating a decade. Non-invasive in vivo x-ray fluorescence or neutron activation analysis can therefore be used to measure cumulative tissue stores. Multiple regression analysis of epidemiologic data could reveal the relative contribution of causal factors, including lead and cadmium, and help to distinguish Balkan endemic nephropathy from other renal diseases using rigorous diagnostic criteria. As long as Balkan endemic nephropathy remains a diagnosis of exclusion, the accuracy of the diagnosis of other renal disease determines the reliability of identification of the endemic disease.

Balkan Nephropathy↗
PubMed1989

Were the hatters of New Jersey "mad"?

Conventional wisdom holds that the "Mad Hatter" of Alice's Adventures in Wonderland earned his name because he exhibited psychotic behavior from mercury poisoning. The first description of mercurialism in hatters was published by J. Addision Freeman, M.D., in Transactions of the Medical Society of New Jersey in 1860, just 5 years before Lewis Carrol's famous tale. But it is unlikely that Alice's creator was aware of this obscure provincial report. Numerous subsequent studies of hatters in New Jersey showed that the hatters' shakes were rampant among the immigrant workers. The pathologic shyness of mercurialism, however, was not noted in New Jersey hatters until 1912. The idea that hatters were "mad" stemmed from popular perceptions more than from medical knowledge. Nor did medical studies lead to elimination of mercury in felt hat manufacturing. The hatters' occupational disease was curbed only in 1941 when mercury was required for the manufacture of detonators in World War II. The hatters of New Jersey were not only not mad, but neither were they, the physicians, nor the public of the period sufficiently angry to control the conditions under which the hatters worked.

Clothing↗
PubMed1989

Reducing bone lead content by chelation treatment in chronic lead poisoning: an in vivo X-ray fluorescence and bone biopsy study.

A stained-glass artist with longstanding exposure to lead presented with neuropsychiatric symptoms. He was evaluated before and after chelation treatment by the CaNa2 EDTA lead mobilization test, iliac crest bone lead measurement, and in vivo tibial X-ray fluorescence (XRF). The three methods showed a progressive fall in body lead stores during chelation therapy in association with improvement in symptoms and a fall in blood lead and zinc protoporphyrin levels. In vivo tibial XRF is a safe, rapid, and noninvasive technique for detecting excessive body lead burdens. XRF measurement of bone lead content is a practical method for monitoring the efficacy of therapy as well as for establishing the diagnosis.

Biopsy↗
PubMed1988

Bone lead in dialysis patients.

We measured lead and calcium in multiple bone biopsies from 11 cadavers without known excessive past exposure to lead. Paired iliac crest, transiliac and tibial bone biopsies from these cadavers indicated that in bone biopsy specimens the lead/calcium ratio is more reproducible than the absolute lead concentration. There were no significant differences between the lead/calcium ratios from the iliac crest, transiliac, or tibial specimens. Transiliac bone biopsies from 35 patients (13 patients showing symptoms of slight or moderate degree of renal failure, medical history of gout and/or arterial hypertension and 22 lead workers with chelatable lead in excess of 1000 micrograms) indicated that the lead and the lead/calcium ratio in bone biopsies reflect body lead stores as estimated by the EDT A test (r = 0.87 and 0.83, respectively). Chemical and histological studies of transiliac biopsies previously obtained from 153 dialysis patients (from 8 dialysis centers from Belgium, France and Germany) for studies of aluminum-induced bone disease showed that chronic renal failure and dialysis do not cause accumulation of lead in bone and elevated bone lead does not appear to alter trabecular bone histomorphometry. We found that in 5% of the hemodialysis population studied, bone lead concentrations approximated levels found in active lead workers.

Adult↗
PubMed1988

Intrarenal distribution of exchangeable calcium in HgCl2-induced acute tubular necrosis.

We used autoradiography to localize 45Ca accumulated in vitro by rat kidney that had been injured by HgCl2 in vivo. HgCl2, 1 mg/kg, was administered IV to male Sprague-Dawley rats and nephrectomies were performed from 15 min-30 days later. Kidney slices were incubated in KRB buffer containing 2 mM 45Ca at 25 degrees C for 180 min. The 45Ca slice-to-medium concentration ratio (S/M) increased significantly from a control mean of 0.8 +/- 0.04 SD (n = 4) to 1.6 +/- 0.3 (n = 4) after 1 day and reached 4.6 +/- 4.2 (n = 6) after 3 days. The serum creatinine increased more rapidly, from a control mean of 0.4 +/- 0.1 mg/dl to 0.7 +/- 0.1, 3.3 +/- 0.2, 7.2 +/- 1.6 after 4 hr, 1 day, and 3 days, respectively. Autoradiographic localization of 45Ca was first evident in necrotic proximal tubule (PT) straight segments after 1 day and was maximal at 3 days. 45Ca uptake was increased by slice incubation with N2 instead of O2, but anoxia did not alter the intrarenal distribution pattern. Necrotic PTs showing 45Ca by autoradiography were also positive by the von Kossa stain. Autoradiographs prepared from paraffin or Epon sections showed the same intrarenal distribution of 45Ca as section freeze-dry autoradiographs. Increased tissue 45Ca was due primarily to uptake by nephrocalcinotic PT segments; 40Ca accumulated in vivo exchanged for 45Ca during in vitro incubation. The exchangeable intrarenal calcium observed in this autoradiographic study was due to HgCl2-induced nephrocalcinosis.

Acute Kidney Injury↗