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It has been suggested that frusemide affects plasma parathyroid hormone (PTH) concentrations. To further investigate this issue we analysed plasma intact PTH in 77 patients with chronic renal failure (CCr 8.0–89.8 ml/min per 1.73 m2) as a function of frusemide therapy. The rate of increase of plasma PTH observed with progression of renal failure was faster in patients who received frusemide as compared to patients who did not receive the drug. The slope of the regression line of PTH on CCr was steeper (P<0.02) for patients with frusemide (n = 40, slope −0.34) than without frusemide (n = 37, slope −0.20). This effect was specific for frusemide therapy since therapy with other antihyper-tensive drugs (including thiazides and β-blockers) was not correlated with PTH plasma concentrations. Frusemide therapy was also associated with a significantly greater urinary calcium excretion in uraemic patients but did not influence other parameters of calcium metabolism. To clarify mechanisms involved in the effect of frusemide on plasma PTH values, seven normal subjects were studied for 24 h before and for 24 h after oral administration of 80 mg frusemide. The main findings were: (1) Median PTH values were higher than on a control day (P<0.05) 3 h after frusemide (3.9 pmol/1 vs 1.8) and 6 h after frusemide (4.0 vs 2.6); (2) ionised plasma calcium did not change significantly, whereas mean calcium/creatinine ratio increased from 0.20 to 0.46 after frusemide treatment through an increase in absolute calcium excretion; (3) plasma 1α, 25-dihydroxyvitamin D3, catecholamines, and magnesium concentrations did not change significantly after frusemide. The effect of frusemide on elevation of plasma PTH was still present when propranolol was coadministered. Our results suggest that frusemide aggravates hyperparathyroidism in chronic renal insufficiency, probably through increased renal calcium excretion.