-----Original Message-----Ed
From: Clinical biochemistry discussion list [mailto:[log in to unmask]]On Behalf Of Eric Kilpatrick
Sent: 10 May 2007 17:27
To: [log in to unmask]
Subject: Re: Standardised test profiles - ACB Scientific Committee
This is a very important exercise and, like Robert Hill, I am disappointed by the lack of feedback on an issue which is likely to affect our daily working lives. Remember, it is possible that if these test profiles are agreed that they may end up forming the basis for lab reimbursement which, in turn, may mean we will not be reimbursed for any additional tests we do other than for those in a particular profile, even- I suspect- if clinically justified.
Can I be deliberately provocative just to stimulate some debate from others?
Having brought the subject of money up (as you did yourself when you mention about saving Kent NHS money by reducing urea requests) in some respects I wish the focus would move away from this and more towards what the patient needs from us. What test profile do we need to most efficiently deal with a particular patient presentation? Does the inconvenience of repeat sampling for urea in low eGFR patients outweigh not doing them routinely? When I look at TPN patient results I seem to act on the urea result far more often than I do the sodium. Not evidence based really, but if you are ditching urea, what is your clinical reason for sticking with sodium routinely on every sample? Not that I'm advocating a minimalist approach. On the contrary, in the acute situation bicarb even seems more useful to me than the sodium.
There must be plenty of other opinions out there, or else the mailbase is dead!
Kindest regards
Eric
> Date: Thu, 10 May 2007 15:38:03 +0100
> From: [log in to unmask]
> Subject: Re: Standardised test profiles - ACB Scientific Committee
> To: [log in to unmask]
>
> 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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