title: Impact of parathyroidectomy on neutrophil cytosolic calcium in chronic kidney disease patients: a prospective parallel group trial.
abstract: OBJECTIVE
  Polymorphonuclear leucocytes (PMNs) of chronic kidney disease (CKD) patients display elevated basal cytosolic calcium concentrations (iCa(2+)). As parathyroid hormone is considered to substantially contribute to the inappropriate cellular entry of calcium in uraemia, we hypothesized that parathyroidectomy lowers PMN iCa(2+).
  
  
  METHODS
  Prospective parallel group trial at a tertiary care centre. SUBJECTS, INTERVENTION AND MAIN OUTCOME MEASURES: Two patient cohorts (cohort 1: 14 CKD patients; cohort 2: 14 renal transplant recipients) underwent parathyroidectomy for uncontrolled secondary hyperparathyroidism. We assessed PMN iCa(2+) (primary objective) spectrofluorimetrically 1 day before and 20 days after intervention (secondary objective: PMN glucose uptake). Data were compared with those of 16 matched maintenance haemodialysis patients (cohort 3), and to 15 healthy subjects (cohort 4), by generalized estimating equations.
  
  
  RESULTS
  PMN iCa(2+) of cohort 1 decreased over time and was significantly higher than that of cohort 3 before but not after parathyroidectomy [mean difference before/after parathyroidectomy: 19.1 nmol L(-1) (95% confidence interval: 9.4-22.4), P =0.0003/-3.2 (-20.9-14.5), P = 0.71]. PMN iCa(2+) of cohort 2 decreased over time, but we found no significant difference in comparison with cohort 3 [mean difference before/after parathyroidectomy: 6.5 nmol L(-1) (-9.4-22.4), P = 0.4/-15.8 (-43.6-12.0), P = 0.25]. PMN iCa(2+) of all CKD patients was substantially higher in comparison with that of healthy subjects [cohort 4 vs. 3: -35.3 (-48.9-21.6), P < 0.001]. PMN glucose uptake increased significantly in both interventional cohorts in comparison with cohort 3.
  
  
  CONCLUSIONS
  Parathyroidectomy lowers, but does not normalize PMN iCa(2+) of CKD patients. Further variables, possibly uraemic retention solutes, control both PMN iCa(2+) and functional responses.
authors.affiliation: Department of Medicine III, Division of Nephrology and Dialysis, Medical University Vienna, Vienna, Austria.
authors.forename: R
authors.initials: R
authors.lastname: Deicher
authors.forename: B
authors.initials: B
authors.lastname: Kirsch
authors.forename: M
authors.initials: M
authors.lastname: Müllner
authors.forename: K
authors.initials: K
authors.lastname: Kaczirek
authors.forename: B
authors.initials: B
authors.lastname: Niederle
authors.forename: W H
authors.initials: WH
authors.lastname: Hörl
mesh_terms: D000328:Adult; D002118:Calcium / Q000032:analysis*; D003600:Cytosol / Q000378:metabolism; D003847:Deoxyglucose / Q000378:metabolism; D005260:Female; D006801:Humans; D006961:Hyperparathyroidism / Q000209:etiology / Q000601:surgery; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism / Q000601:surgery*; D016030:Kidney Transplantation / Q000379:methods; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism*; D010281:Parathyroid Hormone / Q000097:blood; D016105:Parathyroidectomy / Q000379:methods*; D011446:Prospective Studies
chemical_list: D010281:Parathyroid Hormone; D003847:Deoxyglucose; D002118:Calcium