What are the Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines for prevention of osteoporosis after renal transplantation?

Updated: Jul 02, 2020
  • Author: Carmel M Fratianni, MD, FACE; Chief Editor: George T Griffing, MD  more...
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The Kidney Disease Outcomes Quality Initiative (KDOQI) has published comprehensive Clinical Practice Guidelines for interventions for the prevention of bone disease following renal transplantation. [70]

During the first week after kidney transplantation, serum levels of phosphorus should be monitored daily due to high urinary excretion rates associated with improving renal function. While there is not an absolute consensus as to the level of hypophosphatemia necessitating replacement, kidney transplant recipients demonstrating persistently low serum phosphate levels (< 2.5 mg/dL [< 0.81 mmol/L]) should probably receive supplemental phosphate. [71]

Since phosphate supplementation may worsen hyperparathyroidism—with a decrease in serum calcium, increase in PTH, and decrease in 1,25-dihydroxyvitamin D—KDOQI guidelines suggest that calcitriol or vitamin D analog therapy may be necessary if phosphate supplementation is required.

In the first 3 months following renal transplant, levels of calcium and phosphate should be monitored at least weekly to achieve a desired phosphorus target range of 2.5-4.5 mg/dL (0.81-1.45 mmol/L). More than 3 months after transplant, K/DOQI guidelines state that PTH, calcium, and phosphorus are to be measured at a frequency clinically appropriate to the achieved glomerular filtration rate (GFR).

While PTH levels usually return nearly to normal by 1 year following renal transplant, hypercalcemia due to preexisting hyperparathyroidism is not rare after renal transplant. Persistent hyperparathyroidism has been associated with higher pretransplant PTH and calcium levels, in addition to a longer period of dialysis preceding transplantation. [72]

Hypercalcemia usually improves as hypertrophic parathyroid glands involute with improving GFR. Since hypercalcemia that requires parathyroidectomy may persist in up to 5% of renal transplant recipients, monitoring of calcium is prudent. The development of spontaneous fractures in a kidney transplant recipient in the presence of hyperparathyroidism is thought by many experts to be an additional indication for parathyroid resection (K/DOQI guidelines).

As in ESRD, metabolic acidosis may persist following renal transplant, inducing bone calcium loss and inhibiting osteoblast function. [73] In addition, systemic metabolic acidosis blunts the anabolic effects of insulin-like growth factor 1(IGF-1), the downstream mediator of growth hormone action, [74] and reduces synthesis of 1,25-dihydroxyvitamin D at the proximal renal tubules, thereby limiting dietary calcium absorption. [75] Correction of metabolic acidosis may be advisable since bone acts as a buffer for correction of acidosis, further compromising the at risk skeleton of the transplant recipient.

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