NDT Advance Access originally published online on April 19, 2005
Nephrology Dialysis Transplantation 2005 20(7):1499-1500; doi:10.1093/ndt/gfh836
© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Teaching Point
Pseudohypocalcaemia in an elderly patient with advanced renal failure and renovascular disease
Patrick B. Mark1,
Emmanouil Mazonakis1,
David Shapiro2,
Richard J. Spooner2 and
R. Stuart C. Rodger1
1 Renal Unit, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, UK and 2 Department of Biochemistry, Gartnavel General Hospital, Great Western Road, Glasgow G12 0YN, UK
Correspondence and offprint requests to: Patrick B. Mark, Renal Unit, Western Infirmary, Dumbarton Road, Glasgow G11 6NT, UK. Email: pm124p{at}clinmed.gla.ac.uk
Keywords: atherosclerotic renovascular disease; calcium; chronic renal failure; gadolinium; magnetic resonance angiography
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Introduction
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Hypocalcaemia is a common clinical problem in patients with
advanced renal failure, frequently related to abnormal vitamin
D metabolism. However, not all causes are due to 1,25-dihydroxycholecalciferol
deficiency and in this case we would like to demonstrate the
confusion which may be caused by iatrogenic pseudohypocalcaemia.
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Case report
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An 84-year-old man with advanced chronic renal failure (glomerular
filtration rate
15 ml/min) was admitted due to rapid deterioration
of his kidney function and was established on haemodialysis.
There were no obvious precipitating factors for this deterioration.
He had known renovascular disease (50–70% ostial stenosis
of his right renal artery and ‘irregular’ left renal
artery). On admission his adjusted serum calcium level was 1.99
mmol/l (normal range 2.1–2.6 mmol/l; uncorrected calcium
1.92 mmol/l, serum albumin 39 g/l; correction formula used:
[adjusted calcium] = [measured calcium] + 0.0171 (43 –
albumin), with 43 g/l being the mean normal albumin) and phosphate
level was 1.84 mmol/l. His parathyroid hormone level, measured
2 months earlier, was 10 pmol/l. Although he had not been prescribed
oral supplementation with a vitamin D analogue, he was already
on calcium carbonate 1.25 g three times daily, which had been
doubled the day of admission. One week later, after his second
dialysis session (at which point his adjusted calcium level
had decreased to 1.91 mmol/l), a magnetic resonance angiogram
(
Figure 1) of his renal arteries showed no difference in the
degree of the stenoses. The morning following the magnetic resonance
angiogram, his adjusted calcium level was 1.12 mmol/l and his
phosphate level was 2.44 mmol/l. He had no alarming symptoms,
both Chostvek's and Trousseau's signs were negative and there
was no clinical evidence of tetany. An electrocardiogram was
essentially normal, with no prolongation of the QT or QTc interval.
In light of the severe hypocalcaemia he was initially treated
with i.v. 30 ml 10% calcium gluconate, was dialysed against
a high calcium dialysate (calcium concentration 1.75 mmol/l),
and 4 h later his repeated adjusted serum calcium level was
2.57 mmol/l.
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Fig. 1. Gadolinium-enhanced magnetic resonance angiogram demonstrating right renal artery stenosis (arrowed).
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The next morning, his adjusted calcium was 2.11 mmol/l, phosphate
was 1.92 mmol/l and serum parathyroid hormone was 20 pmol/l.
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Discussion
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Although the patient on admission had not been treated with
vitamin D analogues, the decrease in his adjusted calcium level
(0.79 mmol/l) was so dramatic that it could not be attributed
to solely 1,25-dihydroxycholecalciferol deficiency. The patient
had initially been dialysed with a dialysate ionised calcium
concentration of 1.25 mmol/l, which would have maintained his
adjusted serum calcium in the normal range. The striking feature
was that the patient had no symptoms of severe hypocalcaemia
or evidence of tetany.
The intravenous administration of gadolinium (as gadodiamide) can cause pseudohypocalcaemia (spurious hypocalcaemia). Two of the four commercially available (gadodiamide, Omniscan® and gadoversetamide, OptiMARK®) intravenously administered gadolinium-based contrast agents used in magnetic resonance imaging (MRI) may undergo dechelation (both in vivo and in vitro) and interfere with o-cresolphthalein based colorimetric methods of measuring total serum calcium [1–4]. These compounds have been hypothesized to dechelate in the presence of o-cresolphthalein, releasing Gd3+ ions, which subsequently form a dimeric gadolinium–o-cresolphthalein complex (2Gd–2OCP). The formation of the 2Gd–2OCP complex reduces the ultra violet absorbance of o-cresolphthalein, hence altering the results for serum calcium if tested by this method [3]. A decrease in serum calcium has only been demonstrated with o-cresolphthalein-based colorimetric methods. This effect on colorimetric analysis is not seen with dimeglumine gadopentetate (Magnevist®) or gadoteridol (ProHance®). Alteration is not seen in the serum calcium level as measured by atomic emission spectroscopy with the addition of gadodiamide. However, this method is more expensive and less convenient in daily practice. This recently described cause of pseudohypocalcaemia is enhanced in both duration and severity in patients with renal insufficiency [2,4] because of delayed excretion of the gadolinium chelate and may be seen more often with the increased use of MRI to investigate such patients. Fortunately there were no adverse effects from supplemental calcium administration in our patient, who remains well on an outpatient haemodialysis program.
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Teaching point
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Gadolinium-based contrast agents used in MRI may cause pseudohypocalcaemia.
With increasing use of contrast-enhanced MR angiography it is
likely that this effect will be seen with increasing frequency.
Moreover a clinically significant high calcium level may be
incorrectly overlooked due the falsely lowered value. Awareness
of this effect is important to avoid inappropriate and potentially
harmful treatment as occurred in our case.
Conflict of interest statement. None declared.
[see related Letter by Decupere et al. (doi:10.1093/ndt/gfh902)]
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References
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- Doorenbos CJ, Ozyilmaz A, van Wijnen M. Severe pseudohypocalcemia after gadolinium-enhanced magnetic resonance angiography. N Engl J Med 2003; 349: 817–818[Free Full Text]
- Emerson J, Kost G. Spurious hypocalcemia after Omniscan- or OptiMARK-enhanced magnetic resonance imaging: an algorithm for minimizing a false-positive laboratory value. Arch Pathol Lab Med 2004; 128: 1151–1156[Medline]
- Lin J, Idee JM, Port M et al. Interference of magnetic resonance imaging contrast agents with the serum calcium measurement technique using colorimetric reagents. J Pharm Biomed Anal 1999; 21: 931–943[CrossRef][Web of Science][Medline]
- Prince MR, Erel HE, Lent RW et al. Gadodiamide administration causes spurious hypocalcemia. Radiology 2003; 227: 639–646[Abstract/Free Full Text]
Received for publication: 21.12.04
Accepted in revised form: 22. 3.05
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Introduction
Case report