Would anyone have ideas on how to explain a creatinine result of
1478uM (ref 50-115) with a urea of 5.6 which changed in about six hours
to creat=124, with urea still =5.6?
The patient, a 19 year old male, was transferred from another
hospital for specialist spinal care. Approximately 24 hours earlier he
had been involved in a road traffic accident in which two people had been
killed. He was an unrestrained back seat passenger and sustained severe
injuries including complete cord transection (T12/L1), chest injury,
haemothorax, ruptured diaphragm, and small haematoma. On presentation to
our hospital his blood pressure was 120/80, heart rate 92/min. He was
haemodynamically stable.
He had pre-op blood tests performed which threw up an unusual result.
Na=138mM, K=5.2, Cl=98, TCO2=26, Urea=5.6 (2.5-7.5), Creatinine=1478uM
(50-115).
Amy=132 (110-330); pH=7.40, Pco2=5.2, Po2=7.1 (11-14).
The creatinine was repeated in dilution and the result confirmed.
[creatinine was measured on the Beckman Synchron CX7 using a kinetic
Jaffe method]
About six hours later, just before the planned operation, the
renal profile was repeated:
Na=135, K=4.1, Cl=100, TCO2=26, Urea=5.6, Creat=124.
CK was measured retrospectively on these two samples and showed levels of
3670 IU/L and 4010 respectively.
The only ‘treatment' given between these samples was 1L N saline IV.
Post-op results: Urea=6.4, Creat=138; CK=839.
I also approached the lab in the ‘other' hospital to see if they had any
results prior to the transfer. Unfortunately creatinine had not been
measured.
Results included CK=2850, urea=5.9, Na=139, K=4.6.
Possible explanations include:
a) Pre-analytical:
Wrong patient - the sample was taken on call (when such error less
likely), but anyway we still have the internal ‘discrepency' between urea
and creatinine.
b) Analytical:
Interference with Jaffe reaction - the level seems very severe for
this and also some well-known interferents are less likely in the face of
normal pH and anion gap. It was not possible to test with an enzymatic
assay.
c) Physiological / Pathological:
Any degree of renal failure should presumably give an elevated urea.
The muscle damage could give a sharp rise in creatinine but would one
expect it this high? And what cleared it so fast?
If a patient with severe muscle damage had a ureteric blockage which
was then cleared it might lead to a rapid rise in creatinine and a rapid
fall. But would urea not also rise a bit? Also his treatment gives no
direct support for this theory.
We have seen this type of difference (though not quite to the same
degree) in a chronic renal failure patient, but her levels were
consistent over weeks and were probably due to peritoneal dialysis.
Has anyone on the list seen a case like this. Can anyone offer any
suggestions.
All thoughts welcome.
--
Dr Peadar McGing,
Principal Biochemist,
Biochemistry Dept, Mater Hospital, Dublin 7, Ireland.
Tel: (+353 1)8032080; Fax: (+353 1)8034781.
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