Re: standardised test profile - RENAL FUNCTION TESTS

I have several concerns relating to the proposed order set for renal
function testing.

Firstly, the profile should be called ‘kidney function profile’ rather
than ‘renal function profile’. Patients carry their request forms to
phlebotomy appointments and should be helped to understand the tests that
are being done on them. ‘Kidney’ an English word, is more intuitively
understood than ‘renal’ a Latin word.

The authors have interpreted their remit as being to define a ‘urea and
electrolyte profile’ rather than a kidney function test profile (in
fairness, it would appear that the remit actually appended this work as
such). By definition, then, such a profile must include urea. My following
comments relate to the definition and composition of a kidney function test
profile rather than a urea and electrolyte profile, which latter
consideration would be a pointless exercise.

It is widely accepted that urea is an extremely poor marker of kidney
function, being influenced by a range of extra-renal factors. Many
laboratories, including our own, have dropped urea from their kidney
function test profile. In terms of directly measured components, our own
profile now consists of sodium, potassium and creatinine only, with urea
still being available when specifically requested. Indeed, such practice
has now been adopted across Kent with significant cost-benefit to the NHS
and no apparent substantiated clinical dissatisfaction with the service. In
my opinion it would be a retrograde step to suggest that a national profile
should include urea. The authors provide no good rationale to support such
an inclusion. They suggest that understanding the combined and sometimes
counteractive influences of variations in endogenous urea production and
tubular reabsorption of urea ‘can provide clinical insights into the causes
of perturbations of serum …urea and thus it is appropriate that this
analyte should be retained within the collective’. This makes no sense. The
aim is to understand the patient’s renal function, not their serum urea
concentration. Whilst it is always interesting to hypothesise on the
possible causes of relative discrepancies between urea and creatinine
concentrations this is not a justification for measuring both analytes on
each occasion.

I am extremely concerned at the suggestion that eGFR should ‘never form
part of the [sic] U&E profile’. One of the justifications for this
statement is that this would generate a large proportion of inappropriate
estimates, particularly in the acutely ill. I presume that this refers to
the setting of acute kidney injury (acute renal failure) in which it is
true that eGFR may be unreliable due to the delay in equilibration between
biological pools. However, it is only unreliable because the creatinine
concentration from which it is derived is also an inaccurate reflection of
the current state of renal function. Is it proposed that we abandon
creatinine measurement in this setting? It must be noted that in nearly all
of the situations in which eGFR is considered less reliable, it is so
because the underlying creatinine estimation is also unreliable. In my
experience, clinical users find eGFR reporting useful irrespective of
whether the patient is in hospital or the community. Further, In terms of
acutely ill people generally, it must be noted that serum urea
concentration is an even worse marker of kidney function.

The authors further allude to unnecessary angst being generated amongst
older people as a result of automatic eGFR reporting. I accept that this is
a controversial area, but there is no good evidence to suggest that the
decline in GFR that occurs, on average, as a result of ageing, is the
result of anything other than pathology. There is also no evidence to
suggest that the secondary complications of kidney disease occur at a
different level of GFR in older people than younger people. An analogy to
this approach would be to use higher thresholds for glucose
intolerance/diabetes mellitus in older people, which few would advocate.

It should be noted that the Renal NSF part 2, which applies to England,
stated unequivocally that “local health organisations can work with
pathology services and networks to develop protocols for measuring kidney
function by serum creatinine concentration together with a formula-based
estimation of GFR, calculated and reported automatically by all clinical
biochemistry laboratories”. Further, the Department of Health recommended
the introduction of routine eGFR reporting on the 1st April 2006, to
coincide with the Quality and Outcomes Framework for renal disease coming
into effect. A request for a kidney function test is a request for
information that will give the physician a better understanding of the
patient’s renal function. It is widely accepted both nationally and
internationally that eGFR, calculated using the MDRD formula, is a better
indicator of kidney function than creatinine alone. It is therefore
imperative that eGFR should be included within a national kidney function
test profile. One would hope that a recommendation emanating from the
Association for Clinical Biochemistry will not fly in the face of national
recommendations.


Edmund Lamb

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