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Let me start by thanking Dr Goldstein for his kind remarks and good wishes about the EMINEM project.

In response to his comments, I agree that lowering the calcium in the dialysate would be a stop-gap measure here if the hypercalcemia was symptomatic or severe, and endorse the approach of ruling out other causes for the hypercalcemia, and finding none would direct my attention to the management of the hyperparathyroidism.

I would also like to thank him for introducing the question of osteoporosis / osteopenia to the discussion forum.
What constitutes osteoporosis in patients with established renal bone disease is an area for controversy. Certainly it is accepted that standard bone mineral density parameters may not be reliable in this group, although loss of cortical bone at the distal radius is likely a true marker of bone dissolution. In an effort to compare osteoporotic dialysis patients with their non-osteoporotic counterparts, Barreto et al (KI 2006;69:1852) performed bone biopsies on a select group of 98 HD patients (only 9 diabetic patients). They had an a priori definition of osteoporosis as a ratio of bone volume to tissue volume (BV/TV)less than 1SD from the mean for males and females (controversial). White race, and the ratio of osteoprotegerin to RANK ligand, and duration of amenorrhea (in women) were independent determinants of a low BV/TV. Interestingly iPTH level was not associated with osteoporosis using the above definition (although the authors excluded patients with iPTH > ~ 100 pmol/L). Osteoporosis (by the authors' definition) was present in association with both high and low turnover renal bone diseases. 12.2% of patients had predominant hyperparathyroid bone disease on biopsy osteoporosis was rare in the hyperparathyroid patients.
  1.   about 14 years ago
Let me start by thanking Dr Goldstein for his kind remarks and good wishes about the EMINEM project.

In response to his comments, I agree that lowering the calcium in the dialysate would be a stop-gap measure here if the hypercalcemia was symptomatic or severe, and endorse the approach of ruling out other causes for the hypercalcemia, and finding none would direct my attention to the management of the hyperparathyroidism.

I would also like to thank him for introducing the question of osteoporosis / osteopenia to the discussion forum.
What constitutes osteoporosis in patients with established renal bone disease is an area for controversy. Certainly it is accepted that standard bone mineral density parameters may not be reliable in this group, although loss of cortical bone at the distal radius is likely a true marker of bone dissolution. In an effort to compare osteoporotic dialysis patients with their non-osteoporotic counterparts, Barreto et al (KI 2006;69:1852) performed bone biopsies on a select group of 98 HD patients (only 9 diabetic patients). They had an a priori definition of osteoporosis as a ratio of bone volume to tissue volume (BV/TV)less than 1SD from the mean for males and females (controversial). White race, and the ratio of osteoprotegerin to RANK ligand, and duration of amenorrhea (in women) were independent determinants of a low BV/TV. Interestingly iPTH level was not associated with osteoporosis using the above definition (although the authors excluded patients with iPTH > ~ 100 pmol/L). Osteoporosis (by the authors' definition) was present in association with both high and low turnover renal bone diseases. 12.2% of patients had predominant hyperparathyroid bone disease on biopsy osteoporosis was rare in the hyperparathyroid patients.
  1.   about 14 years ago
The use of cinacalcet in a patient in this sector of the grid is rational (see the PTH Management link above). Dr Weinstein has pointed out the issue in this group. Essentially it relates to the timing of parathyroidectomy in patients with autonomous parathytoid function when the PTH proves difficult to control by efforts to reign in phosphate and to lower PTH with vitamin D sterols or cinacalcet. Guidelines on the timing of parathyroidectomy are lacking, but I suspect that this manoeuvre is relatively underused (person bias).

Dr Anthony Hodsman, a member of the EMINEM working group has reviewed the New England Journal of Medicine article demonstraing the efficacy of cinacalcet is this population (New Engl. J. Med. 2004 Apr; 350: 1516-1525).
  1.   about 14 years ago
The use of cinacalcet in a patient in this sector of the grid is rational (see the PTH Management link above). Dr Weinstein has pointed out the issue in this group. Essentially it relates to the timing of parathyroidectomy in patients with autonomous parathytoid function when the PTH proves difficult to control by efforts to reign in phosphate and to lower PTH with vitamin D sterols or cinacalcet. Guidelines on the timing of parathyroidectomy are lacking, but I suspect that this manoeuvre is relatively underused (person bias).

Dr Anthony Hodsman, a member of the EMINEM working group has reviewed the New England Journal of Medicine article demonstraing the efficacy of cinacalcet is this population (New Engl. J. Med. 2004 Apr; 350: 1516-1525).
  1.   about 14 years ago
The efficacy of cinacalcet in Stage 3 and Stage 4 CKD has been the subject of a double-blind, randomized, placebo controlled trial (AJKD 2009;53:197-207). In this study, patients with iPTH > 100 pg/mL (stage 3) or 160 pg/mL (stage 4) were randomized to cinacalcet or placebo. More patients in the cinacalcet group achieved the primary end point (> 30% reduction in iPTH: 74% vs 28%). More patients in the cinacalcet group also achieved the stage-specific K/DOQI targets (44% vs 4%). Adverse events were more common with cinacalcet, but none were deemed severe. The finding of two consecutive hypocalcemic episodes was common with cinacalcet use (62%). As iPTH levels fell, the phosphaturic benefit of the PTH was lost, so phosphate levels rosein the cinacalcet treated group. The study did not look at hard end points, and was intermediate in length (32 weeks). No provision for bone biopsy was made. Patients in the cinacalcet group received more calcium carbonate (supplement for hypocalcemia and binder for hyperphosphatemia) and calcitriol (for hypocalcemia).
The clinical context is unclear. The better control of iPTH achieved by the cinacalcet may certainly be beneficial, but excess hyperphosphatemia is unlikely to be benificial and may be harmful. Certainly the Block data in hemodialysis patients ascribe a greater harmful effect to elevated phosphate than to elevated PTH except at severely high levels of PTH. The authors acknowledge that hard outcome data are required.
  1.   about 14 years ago
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