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Renal function in patients with multiple myeloma.

R A DeFronzo, C R Cooke, J R Wright

    Medicine
    |March 1, 1978
    PubMed
    Summary
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    Bence Jones proteins in multiple myeloma directly harm kidney tubules, causing dysfunction and atrophy. This kidney damage occurs even when the glomerular filtration rate remains normal, highlighting tubular toxicity.

    Area of Science:

    • Nephrology
    • Oncology
    • Pathology

    Background:

    • Multiple myeloma frequently causes kidney disease.
    • The role of Bence Jones proteins in myeloma-related kidney damage is not fully understood.
    • Renal dysfunction is a common complication in multiple myeloma patients.

    Purpose of the Study:

    • To evaluate renal function and histopathology in multiple myeloma patients.
    • To correlate kidney function and pathology with Bence Jones proteinuria.
    • To elucidate the nephrotoxic mechanisms of Bence Jones proteins.

    Main Methods:

    • Assessed renal tubular and glomerular functions in 35 multiple myeloma patients.
    • Correlated renal function with histopathology and myeloma protein patterns.
    • Quantified Bence Jones proteinuria and creatinine clearance (CCr).

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    Main Results:

    • Patients without Bence Jones proteinuria had CCr > 50 ml/min.
    • 16/26 patients with Bence Jones proteinuria had CCr < 50 ml/min; proteinuria magnitude correlated with renal insufficiency.
    • Tubular dysfunction (acidifying, concentrating) and atrophy were prominent in Bence Jones proteinuric patients, while glomeruli appeared normal.

    Conclusions:

    • Bence Jones proteins exert a direct nephrotoxic effect on renal tubules.
    • Tubular dysfunction and atrophy are key features of myeloma kidney disease, independent of glomerular filtration rate.
    • Tubular atrophy, not obstructing casts, best correlated with renal dysfunction in these patients.