Accelerated vascular calcification and relative hypoparathyroidism in incident haemodialysis diabetic patients receiving calcium binders.
BACKGROUND
Vascular calcification and low bone turnover with a relatively low parathyroid hormone (PTH) often coexist in diabetic patients undergoing haemodialysis. Since calcium salts (CaS) are used extensively as primary phosphate binders and have been associated with progressive vascular calcification, we studied the effects of CaS on coronary arteries and parathyroid activity in incident haemodialysis diabetic patients.


METHODS
We measured the change in coronary artery calcium scores (CACS) with sequential electron beam computed tomography (EBCT) in 64 diabetic and 45 non-diabetic patients, randomized to CaS or sevelamer within 90 days of starting haemodialysis. CACS measurements were repeated after 6, 12 and 18 months. Serum intact PTH (iPTH), calcium and phosphorus were serially tested.


RESULTS
During the study period, serum phosphate was similar in diabetic and non-diabetic patients. Serum calcium levels were similar at baseline (2.3+/-0.25 mmol/l for both) and increased significantly with CaS treatment (P<0.05) both in diabetic and non-diabetic patients but not with sevelamer. Diabetic patients treated with CaS showed a significantly greater CACS progression than sevelamer-treated patients (median increase 177 vs 27; P=0.05). During follow-up, diabetic patients receiving CaS were significantly more likely to develop serum iPTH values<16 pmol/l than diabetic patients treated with sevelamer (33% vs 6%, P=0.005) and had a lower mean iPTH level (24+/-16 vs 31+/-14 pmol/l; P=0.038).


CONCLUSIONS
The management of hyperphosphataemia with CaS in haemodialysis diabetic patients is associated with a significantly greater progression of CACS than with sevelamer. These effects are accompanied by iPTH changes suggestive of low bone turnover.
Galassi
Andrea
A
Ospedale San Paolo and Universita' di Milano, Department of Nephrology, Italy.
Spiegel
David M
DM
Bellasi
Antonio
A
Block
Geoffrey A
GA
Raggi
Paolo
P
D000085:Acetates / Q000378:metabolism* / Q000627:therapeutic use; D002114:Calcinosis / Q000188:drug therapy / Q000378:metabolism* / Q000628:therapy; D002118:Calcium / Q000097:blood; D002119:Calcium Carbonate / Q000378:metabolism* / Q000627:therapeutic use; D017610:Calcium Compounds / Q000378:metabolism / Q000627:therapeutic use; D003331:Coronary Vessels / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000378:metabolism* / Q000628:therapy*; D005260:Female; D006801:Humans; D007011:Hypoparathyroidism / Q000188:drug therapy / Q000378:metabolism* / Q000628:therapy; D007676:Kidney Failure, Chronic / Q000188:drug therapy / Q000378:metabolism / Q000628:therapy; D008297:Male; D008875:Middle Aged; D010758:Phosphorus / Q000097:blood; D011073:Polyamines / Q000627:therapeutic use; D006435:Renal Dialysis; D000069603:Sevelamer
D000085:Acetates; D017610:Calcium Compounds; D011073:Polyamines; D010758:Phosphorus; D000069603:Sevelamer; D002119:Calcium Carbonate; D002118:Calcium; C120662:calcium acetate