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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