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Persistent secondary hyperparathyroidism after renal transplantation may require parathyroidectomy (PTX). Clinical experience suggests that these patients commonly develop decreased renal function thereafter.To test this notion, we evaluated 76 transplant patients who underwent pararhyroidectomy between 1997 and 2003.In half the patients (47%), creatinine clearance decreased >20% (before vs after PTX, 57 ± 21 vs 38 ± 17 ml/min, P=0.001). The patients with decreased creatinine clearance had higher parathyroid hormone (PTH) concentrations before and lower values after PTX compared with those who did not (594 ± 392 vs 447 ± 234 pg/ml before PTX, P=0.03; 35 vs 123 pg/ml thereafter, P=0.002). They also had lower serum calcium concentrations after PTX (2.0 vs 2.2 mmol/l, P=0.005) and they required more calcium and vitamin D analogues. These patients also more commonly underwent total PTX with autotransplantation, compared with subtotal (75 vs 50%, P=0.03). However, in multivariate analysis, only the delta PTH decline (%) after PTX was a significant predictor of deteriorating renal function (P=0.005) and was correlated with the creatinine clearance decrease (R=0.369, P=0.001). Prospectively measured inulin and para-amino-hippuric acid (PAH) clearance decreased significantly after PTX in a subgroup of 19 patients (inulin before vs after PTX 67 vs 55 ml/min/1.73 m2, P=0.001; PAH 360 vs 289 ml/min/1.73 m2, P=0.001). Transplant biopsies revealed calcification in 70% of biopsied cases.Since PTH has a known positive regulatory effect on renal perfusion and glomerular filtration rate, we conclude that relative hypoparathyroidism after PTX is the main mechanism contributing to decreased renal function in these patients. There was no difference in 10-year-graft survival between the deteriorating and the non-deteriorating group.