2001

Allograft Dysfunction and Nephrocalcinosis following Parathyroidectomy. An under estimated complication.

Maharajan Raman1, Rajkumar Chinnadurai1,Grahame Wood1, Jamil Choudhury2, Philip Kalra1, Rachel Middleton1

Department of Renal Medicine1 and Pathology2, Salford Royal NHS Foundation Trust

Background: Hungry Bone Syndrome (HBS) is a recognised problem following Parathyroidectomy. The incidence of HBS is more common in renal hyperparathyroidism than in primary hyperparathyroidism. HBS can be associated with seizure, coma and fractures. Hence patients are pre loaded with calcium and active vitamin D supplements.

We report a case of iatrogenic hypercalcaemia following Parathyroidectomy causing graft dysfunction and Nephrocalcinosis with calcium casts.

Patient: A renal transplant recipient with tertiary hyperparathyroidism underwent Parathyroidectomy(PTX), as her calcium levels remained elevated despite being on a high dose of Cinacalcet (90mg). As per local protocol patient was pre loaded with calcium and active vitamin D supplements. Post operatively she required intravenous calcium for symptomatic hypocalcaemia, which was then followed by high doses of calcium and active vitamin D supplements. Our patient was also on weekly maintenance dose of Cholecalciferol for native vitamin D deficiency. Post operatively Cinacalcet was discontinued.Trends in Creatinine (Cr),Corrected Calcium (C.Ca), Phosphate (Po4), Alkaline Phosphatase (A. Phos) and Parathyroid Hormone levels (PTH) pre and four months post surgery are shown in Table 1.

Pre PTX / Post 1st month / Post 2nd month / Post 3rd month / Post 4th month
Cr (umol/L) / 113 / 167 / 132 / 169 / 284
C.Ca (mmol/L) / 2.73 / 2.62 / 2.55 / 2.71 / 2.67
Po4 (mmol/L) / 0.77 / 1.32 / 1.20 / 1.32 / 1.45
A. Phos (u/L) / 139 / 116 / 87 / 79 / 69
PTH (ng/L) / 329 / - / 54 / - / -

(Table 1)

Management: All other causes for graft dysfunction were explored and excluded. A renal biopsy was performed as it was difficult establish the cause for renal dysfunction, which showed evidence of Nephrocalcinosis with calcium cast and inflammation with no evidence of rejection. Patient’s calcium, vitamin D and cholecalciferol were stopped following the biopsy and the prednisolone dose was transiently increased in view of the inflammation seen on the biopsy. Two months following this creatinine improved to baseline and calcium normalised.

Conclusion: Our patient had hypercalcaemia prior to Parathyroidectomy with a stable renal function. Following Parathyroidectomy patient developed graft dysfunction and Nephrocalcinosis, which can only be explained by iatrogenic causes. Monitoring of urinary calcium may help us guide the amount of calcium given to such patients. Perhaps aiming for lower levels of calcium post Parathyroidectomy rather than normal levels to alleviate symptoms and signs of hypocalcaemia needs to be evaluated to prevent Nephrocalcinosis. We plan to evaluate outcomes following all Parathyroidectomies in our centreover the last five years and report it as a case series.