ACB South West and Wessex Region
Scientific Meeting
Hot
Topics in Renal Disease
ASSOCIATION
FOR CLINICAL BIOCHEMISTRY SOUTH WEST
AND WESSEX REGION SCIENTIFIC
MEETING
Tuesday
4th July 2006 Postgraduate Centre Salisbury District Hospital
HOT
TOPICS IN RENAL DISEASE
Meeting
Report
Charlotte
Dawson, Bristol Royal Infirmary
The
impact of the 2005 National Service Framework (NSF) for renal disease
is about to be experienced in clinical biochemistry laboratories across
the country. It was timely therefore that SW and Wessex ACB members and
a number of colleagues from other regions should meet in Salisbury on
a hot July day to discuss ‘Hot Topics in Renal Disease'.
Estimated
glomerular filtration rate (eGFR): ‘If the plughole can't be stretched,
can the flow be stemmed?'
The
morning was devoted to issues around eGFR and was rounded off by a lively
debate between the audience and a panel comprising the morning's three
speakers. Dr Juan Mason, consultant nephrologist at Salisbury District
Hospital, started with a brief overview of the NSF and in particular the
NSF Part 2 published in 2005 which requires that laboratories generate
an eGFR report alongside every creatinine request. Monitoring changes
in GFR delineates progression of kidney disease and is a strong predictor
of onset of kidney failure and risk of complications of kidney disease,
but its routine use has historically been the preserve of the nephrologist.
Reporting eGFR and translating it to a chronic kidney disease (CKD) stage
will enable the non-specialist to diagnose early CKD so that measures
to reduce the risk of complications and progression of CKD can be initiated,
and specialist referral made in an appropriate and timely fashion. It
is important to recognise however that the decline in GFR associated with
progression to endstage renal failure is a continuum with no true divisions
between CKD stages, and that evidence of a decline in GFR in an individual
is of greater clinical significance than the absolute eGFR value. eGFR
uses the abbreviated MDRD study equation which requires data about a patient's
age, sex, serum creatinine and ethnicity. It has been selected over other
formulae for its simplicity and higher correlation with radioactive iothalamate
standard clearance, a gold standard GFR measure, especially in those patients
with early kidney disease being targeted by the new NSF guidelines and
managed away from specialist care.
However
our second speaker, Mr Finlay MacKenzie from UKNEQAS, reminded us that
we are notoriously bad at measuring creatinine. The wide inter-laboratory
variation in bias and precision of creatinine methods produces significant
differences in GFR values, particularly in the near reference range ie
in patients with CKD stages 1 & 2 being targeted by the NSF. He advocates
applying one's laboratory creatinine results to SAUSAGE (Seeking Agreement
Using a Slope Adjusted GFR Estimate), SAUSAGES (Successfully Adopting
UKNEQAS for Slope Adjusted GFR Estimates) and culinary variations thereof
to produce a method-specific slope-adjusted eGFR value to enable more
meaningful eGFR reporting across laboratories.
Finally,
Dr Neil Dalton from Guy's Hospital in London, re-iterated the superiority
of GFR over serum creatinine for facilitating clinical interpretation
of renal function and for correct drug dosing in CKD. He highlighted the
limitations of existing methods of measuring GFR, stressing the challenges
we still face in detecting early kidney disease. He concluded by emphasising
the need to educate healthcare professionals in the limitations of eGFR,
and suggested that with every eGFR report we quote a range of possible
values rather than a single figure.
From
the panel discussion it was clear that the audience too had concerns about
implementing the NSF guidelines, both for the reasons given in the preceding
lectures and because of the inevitable costs – GPs will be rewarded for
requesting creatinine / eGFR and relevant additional tests on at risk
patients, but no extra funding will be available to laboratories to provide
these tests or to specialist nephrology services to cope with the predicted
increase in referral rate. Over lunch we were invited to mull over a poster
prepared by Roberta Goodall and Roy Fisher summarising the results of
a survey they conducted across the region on creatinine methods and current
implementation of eGFR reporting. They found that the NSF recommendations
were generally not being adhered to at present.
Cardiovascular
disease, bone disease and tubular disease
In
the afternoon there was a shift in emphasis towards other laboratory tests
associated with kidney disease. Dr John O'Connor from Royal Devon &
Exeter Hospital provided a fascinating hypothesis for why troponins are
raised in CKD. He dispelled the common misconception that it is due to
reduced renal clearance in a population at risk of cardiovascular disease.
Instead he provided evidence for an anti-apoptotic role for erythropoietin
(EPO) which is lost in CKD because of reduced EPO synthesis. As a result,
cardiac myocytes are susceptible to apoptosis and subsequently release
troponin T without an actual ischaemic event. He suggested that all patients
on renal replacement therapy should be screened for their baseline troponin
so that any rise in troponin from this baseline can be interpreted as
caused by a true ischaemic event. Dr Jo Taylor, consultant nephrologist
at Dorset County Hospital followed with an informative tour of bone disease
in renal failure, its management, and targets for calcium, phosphate and
PTH levels in CKD stages 3-5. The day was concluded with an entertaining
presentation of case histories of paediatric renal tubular dysfunction
by Dr Richard Coward, consultant paediatric nephrologist at Bristol Children's
Hospital.
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