Zum topochemischen Quecksilbernachweis in der Niere bei experimenteller Sublimatvergiftung

Woeckel, W; He, Stegner; Jaenisch, W

doi:10.1007/bf00964794

Cited by 16 publications

(1 citation statement)

References 9 publications

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“…Previous studies have failed to demonstrate this heterogeneous distribution of the metal, although they clearly demonstrate an early glomerular accumulation of mercury. Wockel et a1 (17) reported mercury deposits in glomeruli and on the brush border of S2 segments of proximal tubules within 15 min of administration. At later time-points, they saw an increase in lumenal tubular staining.…”

Section: Discussionmentioning

confidence: 96%

Metal Accumulation and Nephron Heterogeneity in Mercuric Chloride-Induced Acute Renal Failure

Wilks

Gregg²,

Bach

1994

Toxicol Pathol

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h S T R A ( J TThe present siudy was designed to assess the effects of mercury on glomerular integrity during the early phase of acute renal failure. The silver amplification method showed distribution of mercury in midcortical and juxtamedullary glomeruli and on the brush border of the S2 segment of the proximal tubule 15 min after treatment. At 30 min, there was a decrease in glomerular staining and increased mercury in the proximal tubule. After 3 hr, mercury was no longer detectable in glomeruli but was widespread in the lumen of the proximal tubule. By 24 hr, mercury was prominent in all proximal tubular segments throughout the cortex. The presence of mercury in glomeruli was not related to hemodynamic changes, as there was no evidence for blood redistribution toward juxtamedullary glomeruli as assessed by the filling of the microvascular system with Monastral Blue B. The reduced activity of horseradish peroxidase (administered iv 90 sec and 10 min before sacrifice) in juxtamedullary glomeruli 30 min after mercury administration suggests a decreased uptake of horseradish peroxidase or an increased glomerular protein filtration. These data support glomerular filtration as the predominant excretory route for mercury, highlight the marked nephron heterogeneity in the distribution of this metal, and show that impairment of glomerular integrity occurs before necrosis of the proximal tubules and acute renal failure.

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Section: Discussionmentioning

confidence: 96%

Metal Accumulation and Nephron Heterogeneity in Mercuric Chloride-Induced Acute Renal Failure

Wilks

Gregg²,

Bach

1994

Toxicol Pathol

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Renal Injury and Urinary Excretion

Magós

Clarkson

1977

Comprehensive Physiology

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The sections in this article are: Acute Renal Failure Nephrotic Syndrome and Tubular Dysfunction Inorganic Mercury Atomic Mercury Vapor Organomercurials Uranium Cadmium Chronic Nephritis Proteinuria and Excretion of Heavy Metals Factors Affecting Renal Toxicity and Excretion Storage Capacity of the Tubular Cells Tolerance Complexing Agents Summary

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Pathophysiology of Ischemic/ Toxic Acute Renal Failure

Andreucci¹

1984

Acute Renal Failure

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Zum topochemischen Quecksilbernachweis in der Niere bei experimenteller Sublimatvergiftung

Cited by 16 publications

References 9 publications

Metal Accumulation and Nephron Heterogeneity in Mercuric Chloride-Induced Acute Renal Failure

Metal Accumulation and Nephron Heterogeneity in Mercuric Chloride-Induced Acute Renal Failure

Renal Injury and Urinary Excretion

Pathophysiology of Ischemic/ Toxic Acute Renal Failure

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