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Pathogenesis and renal function in acute toxic nephropathies.

F C Reubi

    Contributions to Nephrology
    |January 1, 1978
    PubMed
    Summary
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    Acute toxic nephropathy, a kidney injury from poisons and drugs, can cause tubular necrosis or immune responses. Secondary acute renal failure may result from dehydration, shock, or electrolyte issues, but recovery is typical.

    Area of Science:

    • Nephrology
    • Toxicology
    • Immunology

    Background:

    • Acute toxic nephropathy results from diverse exogenous agents.
    • Poisons and medications are primary causes of kidney damage.

    Observation:

    • Cellular poisons like mercuric bichloride induce tubular necrosis.
    • Drugs can trigger immune responses, leading to interstitial nephritis, glomerulonephritis, or angiitis.
    • Non-nephrotoxic substances causing dehydration, shock, hemolysis, rhabdomyolysis, or electrolyte imbalances can lead to secondary acute renal failure.

    Findings:

    • Reduced renal blood flow, suppressed glomerular filtration, and increased tubular pressure contribute to functional kidney breakdown.
    • Obstruction and tubular leakage are key mechanisms in acute renal failure.

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  • Specific tubular functions may be impaired by toxic insults.

    • Implications:

    • Understanding the diverse mechanisms of toxic nephropathy is crucial for diagnosis and treatment.
    • Prompt identification of causative agents and supportive care can facilitate renal recovery.
    • Complete or incomplete recovery is the general outcome for patients with acute toxic nephropathy.