UK National Renal Pathology EQA Scheme

 

Report of Participants’ Meeting held on Thursday 6th July 2006
during the Centenary Meeting of the Pathological Society in Manchester.

 

To cover cases in circulations V and W

 

The meeting opened at 3pm.

Scheme Management Issues

Professor Furness highlighted the following problems:

In the most recent circulation there have been more problems than usual with participants failing to pass on the slides to the next participant in the circulation.  The spare sets of sections have all been used, but some participants have still not been able to examine the slides on time.  Participants were reminded of the importance of keeping to the circulation schedule, in accordance with the reminder letters which are issued by the scheme secretary.

Some participants are still failing to provide suitable EQA cases on request, despite the recent increase in the “penalty” charge on the subscription for those who fail to provide a case.  This may necessitate a further increase in the penalty charge next year if the situation does not improve.

There have been some problems in the most recent circulations relating to the quality of the material circulated.  Professor Furness stated his intention that in the future the pathologist supplying each case will be identified on the circulation sheets, so anyone providing grossly inadequate material would be identifiable to all participants.

It has become clear that in some centres colleagues are discussing EQA cases with each other and submitting identical or near identical responses.  The question of such “collusion” was discussed in depth when histopathology EQA schemes were established in the 1990’s, and at that time it was agreed that such collaboration was not acceptable practice in relation to EQA cases.  It was recognised that seeking further opinions from colleagues is good practice in routine work, but this would render any personal scoring system meaningless. 

The issue was discussed by participants present at the meeting, and the possibility was raised of department registering as a single “departmental participant”, submitting one response on behalf of all pathologists in that department.  This has the disadvantage that individual pathologists, who may have to accept responsibility for reporting renal biopsies when colleagues are absent, have no personal feedback on their EQA performance. 

After a vote the overwhelming majority was in favour of retaining the original position, that collaboration between pathologists in EQA responses is not acceptable.  All participants are reminded of this position.  The summary of the EQA scheme procedures provided on the scheme website will be modified to make this clear.

Professor Furness reported that CPA Accreditation of the scheme has now lapsed, in accordance with the questionnaire circulated by post.  The response rate to that questionnaire was over 60% and only one participant indicated a desire to maintain CPA Accreditation.  The scheme remains under the oversight of the RCPath Steering Committee, the Histopathology Panel of the Joint Working Group on Quality Assurance and its own participants through the participants meetings.

The question of undertaking EQA using “virtual slides” was discussed briefly.  It would be possible to achieve this at present without increasing participant subscription fees, but the consensus of the meeting was that the circulation of glass slides remains preferable.  Virtual slides will not be pursued at present.

The scheme accounts have developed a small surplus, and as virtual slides will not be used Professor Furness proposed a reduction in the standard participant’s subscription fee to £60.00 in the next year.  This will represent a one-off reduction, not a permanent change, but the accounts will be reviewed after that reduction has had an effect.

Professor Furness reminded participants that although trainees can participate in the EQA Scheme they should notify the scheme secretary of their status, as anyone who does not undertake primary responsibility for reporting renal biopsies should not be involved in the ranking system for the evaluation of persistent sub-standard performance.  A recent incident had revealed a trainee who had been participating in full in the scoring system and whose performance may have masked sub-standard performance in others. 

Professor Furness apologised for the fact that the timing of the Pathological Society meeting meant that some of those present at the meeting may not yet have had an opportunity to submit responses to one of the circulations to be discussed.  Anyone in that situation was invited either to leave the room for the duration of the discussion on that circulation, or voluntarily withhold responses on this occasion.  An attendance sheet was circulated on which participants were invited to indicate if this option applied to them, to facilitate checking by the EQA scheme secretary.

Participants were invited to raise any further points concerning the running of the scheme.  No further points were raised.

 

Case Discussion

Circulation V:

Case V254:  A 50 year old male with nephrotic syndrome. 

The meeting agreed that this was a case of light chain nephropathy, and that for personal scoring “light chain nephropathy” and “monoclonal immunoglobulin deposition disease” would be merged and regarded as correct. 

The single participant who responded with “cryoglobulinaemia (and light chain nephropathy)” as a single diagnosis would be awarded half marks. 

After some discussion, the diagnosis “not diagnostic (reaction to light chain deposits?)” was regarded as wrong, despite the mention of light chains, because the material circulated was regarded by the meeting as unequivocally diagnostic. 

The other proffered diagnoses were regarded as incorrect.

 

Case V255:  A 60 year old woman with signs and symptoms of vasculitis, a history of SLE/Sjögren’s syndrome and “full house” immunofluorescence.

The meeting agreed that this was lupus nephritis.  In accordance with agreement at previous Participants’ Meetings identification of a class was regarded as necessary to obtain full marks.  Diagnoses which mentioned lupus but did not offer a class were accorded half marks. 

Numerous participants had indicated that cryoglobulins should be excluded, but cryoglobulinaemia without mention of lupus was regarded by the meeting as incorrect, at least partly on the basis of the intraluminal deposits being positive for all classes of immunoglobulin and complement. 

Those who mentioned lupus in combination with a comment about this being a mesangiocapillary pattern were regarded as correct, since the mesangiocapillary pattern would equate to a diagnosis of class IV. 

 

Case V256:  A 62 year old female with acute renal failure.

The meeting regarded this as a case of tubulo-interstitial nephritis, in accordance with the submitting pathologist’s original report.  It was agreed that all diagnoses including this term as a definite diagnosis should be merged and regarded as correct.  “Acute pyelonephritis (consider TIN)” would be accorded half marks and acute pyelonephritis without mention of tubulo-interstitial nephritis was regarded as incorrect.

 

Case V257: A 57 year old male with a history of diabetes.

This was clearly a case of diabetic nephropathy. 

After some discussion the meeting agreed that the single participant who made a diagnosis of “diabetic retinopathy” had probably meant to write diabetic nephropathy, but the error should nevertheless be penalised by awarding half marks. 

FSGS was regarded as incorrect. 

Professor Furness pointed out that the verbal description of C1q immunostaining could be confusing to some participants.  Immunoperoxidase for C1q is invariably much stronger than immunofluorescence, and a description based on immunoperoxidase could therefore be misleading to participants accustomed to immunofluorescence.  Despite this, the meeting decided that a diagnosis of C1q nephropathy should be regarded as incorrect, in part because the electron microscopy was incompatible with that diagnosis.

 

Case V258:  A 24 year old woman, with heavy proteinuria presenting six months after an uneventful pregnancy.

This was a case of linear dense deposit disease.  All other proffered diagnoses were regarded as incorrect.

A few participants had questioned the provision of information about C9 rather than C3.  Professor Furness confirmed that the information provided was unequivocally “C9”.  One participant present confirmed that some laboratories routinely use C9 rather than C3. 

 

Case V259:  A 54 year old male presented with creatinine of 300.  ?Myeloma.

This case was correctly identified by the majority of participants as representing myeloma cast nephropathy.  However, the majority of participants had expressed the view that the material circulated was inadequate for EQA.  The meeting agreed that the correct diagnosis had been made largely on the basis of the clinical information provided rather than examination of the microscope slides circulated.  The comment “significant immune deposits present within glomeruli” was also regarded as unclear and potentially misleading.  It was agreed that despite the presence of a consensus diagnosis this case should be deleted for the purposes of personal scoring.

 

Circulation W

Case W260:  A 73 year old man with renal failure.

The meeting agreed that this was a case of amyloidosis, the diagnosis having been confirmed by the National Amyloidosis Centre.  Cast nephropathy was regarded as incorrect.  Participants who suggested “amyloidosis and cast nephropathy” would be accorded half marks, as the material circulated was not regarded as providing adequate evidence for a diagnosis of cast nephropathy. 

 

Case W261:  A 48 year old woman with nephrotic syndrome.

The consensus diagnosis of participants was of primary FSGS, though the meeting agreed that several of the glomerular abnormalities could be interpreted as “glomerular tip” lesions.  However, almost 40% of participants had returned a diagnosis of minimal change nephropathy.  This raised the possibility that some of the material circulated had not included the representative lesions.  The pathologist who had submitted this case was present at the participants’ meeting, and stated that he had deliberately included the case as an “early” example of primary FSGS and had personally checked every slide provided to ensure that glomerular abnormalities were present.  The meeting accepted this, concluding that a diagnosis of minimal change nephropathy was incorrect in this case.

Following the standard operating procedures of the EQA scheme, it was agreed that with such a large proportion of participants having returned an incorrect diagnosis, this case could not be used for personal scoring.

It was, however, agreed that the case had considerable educational value, and those 40% of participants who had missed the diagnosis should review their criteria for the diagnosis of minimal change nephropathy.  Representative images, as shown at the participants meeting, will be available on the EQA Scheme website (www.pathology.plus.com/renaleqa/) under “Recent Circulations”.

 

Case W262:  A 52 year old woman with acute renal failure.

The meeting agreed that this was a case of tubulo-interstitial nephritis, though with unusually large numbers of neutrophils within tubules raising a concern about the possibility of ascending bacterial infection.

The diagnoses proffered represented a spectrum of opinion; from pure tubulo-interstitial nephritis with no mention of infection, to acute pyelonephritis with no mention of tubulo-interstitial nephritis.  It was pointed out that this biopsy also showed considerable evidence of chronic damage, and “interstitial nephritis” might be used by some participants to refer merely to the lymphocytic infiltration associated with such old scarring.

After lengthy discussion it was agreed by the participants present that this case could not be used for personal scoring, but that an educational message to participants was indicated in that “interstitial nephritis” as an unqualified term is so vague as to be almost meaningless.  The phrase should be qualified in some way to explain whether this is regarded as an immunologically mediated process or merely passive lymphocytic infiltration associated with renal scarring. ‘Acute tubulointerstitial nephritis’, indicating the former, is preferable where applicable.

 

Case 263:  A 54 year old male with proteinuria.

The meeting agreed that this was a case of mesangiocapillary glomerulonephritis, type I. 

One participant had attributed this pattern to “solvent nephropathy”.  While seeing no great justification for this the meeting agreed that the participant should not be penalised. 

Mesangiocapillary glomerulonephritis type II (dense deposit disease) was regarded as incorrect despite the availability of only a description of the electron micrographs, on the basis of other features, notably the immunohistochemistry, being incompatible with that diagnosis.

The meeting agreed that the diagnosis of mesangiocapillary glomerulonephritis demanded further investigation as to an underlying cause, and that lupus nephritis seemed quite likely.  Nevertheless, a confident unqualified diagnosis of SLE class IV was regarded as over-interpretation of the results justifying half marks.  The single proffered diagnosis of “proliferative glomerulonephritis probably lupus IV G” was regarded as somewhat vague, justifying half marks.

The subsequent clinical information identifying a serum paraprotein but no cryoglobulin was noted.  The lupus serology of the patient remains unknown.

 

Case W264:  An 81 year old male with proteinuria of 24g per 24 hours.

This was regarded as a case of focal segmental glomerulosclerosis.  It was agreed that all “variants” of FSGS should be merged and regarded as correct.

A problem was raised by the simultaneous presence of cholesterol emboli, which had not been identified by the submitting pathologist and which the meeting agreed had not been present in all sections.  Cholesterol emboli can on rare occasions produce glomerular crescents and can produce segmental glomerular scarring, but it was agreed that cholesterol embolisation alone could not account for such heavy proteinuria.  On this basis an unqualified diagnosis of “cholesterol emboli” was incorrect.  Other proffered diagnoses were also regarded as incorrect since nothing other than primary FSGS (of some form) could account for the morphology and the heavy proteinuria.

 

Case W265:  A 62 year old woman with fever, myalgia, blood and protein in the urine, ANCA positive, immunohistochemistry negative.

This was clearly a case of vasculitis, affecting glomeruli and small muscular arteries.

Professor Furness explained the wide range of terms which had been used by participants in this case, most of which had been merged under the headings “microscopic polyangiitis” or “pauci-immune vasculitis”.  It was agreed that both these terms could be regarded as correct, since the important thing was to identify the presence of a microscopic vasculitis.

There was some discussion at the meeting as to how to deal with the other proffered diagnoses.  It was agreed that “polyarteritis nodosa” without qualification by the term “microscopic” would be regarded as incorrect.  It was recognised that this was potentially a controversial decision, but the meeting agreed that without such qualification “polyarteritis nodosa” should be used to refer to an exclusively large vessel vasculitis, which was clearly not the case in the present example.

The diagnosis “granulomatous vasculitis – “Churg-Strauss” generated some discussion, as many felt that this was an excessively precise, interpretation, not justified by the material circulated.  A vote was evenly split between regarding this as incorrect and awarding half marks.  It was therefore agreed that this diagnosis would be awarded 30%.

___________

 

 

At the end of the meeting the quality of some of the circulated material was again discussed.  It was agreed that participants should be reminded that where a diagnosis rests heavily on electron microscopy, then images of the electron microscopy must be circulated, not just a description.  Professor Furness confirmed that he is able, if necessary, to replicate images for circulation.

 

This report, with the case analyses and the images discussed at the Participants’ Meeting, will be made available on the Scheme Website (www.pathology.plus.com/renaleqa/ )

 

The meeting closed at 4.30pm.