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Related Experiment Videos

Persistent pituitary-thyroid dysfunction patients following renal transplantation.

P Bratusch-Marrain, H Kopsa, P Pils

    Clinical Nephrology
    |August 1, 1980
    PubMed
    Summary

    Kidney transplant recipients show altered pituitary-thyroid function, with some experiencing reduced thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH). Corticoid treatment may contribute to these persistent changes.

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    Area of Science:

    • Nephrology
    • Endocrinology
    • Immunology

    Background:

    • Chronic renal insufficiency is known to alter pituitary-thyroid function.
    • Successful kidney transplantation aims to restore normal physiological functions.
    • Persistent abnormalities in pituitary-thyroid axis post-transplant require further investigation.

    Purpose of the Study:

    • To evaluate pituitary-thyroid function after successful kidney transplantation.
    • To compare thyroid function in kidney transplant recipients with healthy controls.
    • To identify factors influencing altered thyroid function post-transplant.

    Main Methods:

    • Assessed thyrotropin (TSH) response to thyrotropin-releasing hormone (TRH) in 36 kidney transplant recipients and 15 healthy subjects.
    • Measured serum thyroxine and triiodothyronine levels.

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  • Correlated TSH response and thyroid hormone levels with transplant function, duration of renal insufficiency, hemodialysis, and prednisolone dosage.

    • Main Results:

    • Twenty-four patients had low-normal TSH response, while 12 had markedly decreased response.
    • Patients with decreased TSH response exhibited reduced thyroxine and triiodothyronine levels compared to controls.
    • TSH response was unrelated to transplant function, renal insufficiency duration, or hemodialysis duration.
    • A negative correlation was found between prednisolone dose and TSH responsiveness/triiodothyronine levels (P < 0.05).

    Conclusions:

    • Kidney transplantation does not fully restore normal pituitary-thyroid function in all patients.
    • Corticoid treatment, specifically prednisolone, may partially explain altered TSH secretion and peripheral thyroxine to triiodothyronine conversion.
    • Individual patient variability in pituitary response to immunosuppressive therapy is suspected as a major cause of persistent abnormalities.