Abstract

SUMMARY 1. The biological half-life of minocycline in serum has been studied in twenty-one patients and shown to have no relationship to renal function. There is very little excretion of minocycline by the kidney, and practically none is removed by dialysis. 2. In normal subjects, minocycline therapy is not accompanied by a significant rise in blood urea concentration or urinary urea excretion. However, high doses may produce a marked increase in urea excretion. 3. Of eight patients with impaired renal function who were treated with a normal therapeutic dose of minocycline (200 mg/day), one showed a significant increase in urea excretion and a rise in plasma urea concentration. Two patients with severe unstable renal failure required dialysis following therapy. 4. Minocycline is unlikely to accumulate in patients with renal failure due to its predominantly gastrointestinal excretion and is therefore safe to use. However, its protein catabolic effect is dose dependent and if renal function is impaired, even a small increase in urea production may be sufficient to aggravate uraemia. In such patients the normal therapeutic dose (200 mg/day) should not be exceeded and monitoring of renal function is advisable.

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