UK National Renal Pathology EQA Scheme

Report of Participants’ Meeting held at 11.00 am, July 1st 2003

as a Satellite Meeting to the Bristol Pathology 2003 Meeting

Circulations K and L

The original breakdown of proffered diagnoses, before amendment as described below, is available on the scheme website at http://www.le.ac.uk/pa/pnf1/eqa/ along with all the images displayed during the case discussion at the Participants’ Meeting.

My apologies for not supplying CPD certificates to those who attended the meeting.  If you attended the meeting and would like to receive a CPD certificate, please email Karen Iliffe, Scheme Secretary, on ki9@le.ac.uk

Discussion of cases in Circulation K

K194

The agreed diagnosis was dense deposit disease, largely on the basis of the electron microscopy.  In view of recent evidence that this is pathogenetically distinct from mesangiocapillary glomeruolonephritis type I (there have been suggestions that the old name should be dropped and dense deposit disease used to emphasise the separation) it was agreed that mesangiocapillary glomerulonephritis type I should be regarded as incorrect.  Mesangiocapillary glomerulonephritis without stating the type was regarded as insufficiently specific so should receive half marks.

For once the absence of a H&E raised no objections – perhaps because the diagnosis relies heavily on e.m.

K195

The agreed diagnosis was (primary) focal segmental glomerulosclerosis.  An argument was presented that the diagnosis of ‘glomerular tip lesion’ recognised the presence of a segmental abnormality and would result in a discussion with the clinicians as to the possibility of the prognosis perhaps being less favourable than one might expecting with a diagnosis of minimal change, which was regarded as incorrect.  The ‘tip lesion’ diagnosis was therefore to be accorded half marks.

The mention of the correct diagnosis in the clinical history resulted from this being put in the clinical information when the case was submitted to the EQA scheme.  This was then transcribed accurately by the Scheme Secretary, and not noticed but the Organiser until after the response sheets had been posted.  However, it was pointed out that request forms often arrive with a suggested diagnosis, which sometimes proves to be correct;  so the case was retained for scoring purposes.

K196

The morphology in this case was nodular glomerulosclerosis.  Only a H&E was supplied, making it difficult to exclude amyloid on the basis of morphology  We were told the IF was negative. . Many participants had demanded further studies, especially electron microscopy However, we were told that the patient had been diabetic for 30 years, so several participants suggested that it would be perverse to make any diagnosis other than diabetic nephropathy.  After discussion it was agreed that nodular glomerulosclerosis and diabetic nephropathy should be regarded as correct;  all other diagnoses were wrong.

K197

This was a case of fibrillary glomerulopathy or immunotactoid glomerulopathy.  Many participants had commented that they could not distinguish between the two without higher magnification electron micrographs, and / or a scale on the EM images.  These two diagnoses were therefore meerged for personal scoring.  The other proffered diagnoses were regarded as incorrect.

K198

The diagnosis was membranous glomerulonephritis.  The close proximity of the subepithelial deposits was assumed to explain the apparent linearity of the IgG on IF.  The presence of slight glomerular hypercellularity was accepted as justification for suggesting ‘atypical membranous’ and it was agreed that this should e regarded as correct.

The meeting discussed minority diagnoses ‘Membranous Gn AND Churg-Strauss’ and ‘Membranous Gn AND granulomatous vasculitis’.  The meeting considered the evidence for Churg Strauss syndrome or granulomatous vasculitis to be much too slight to justify proposal as part of the principal diagnosis, and agreed that these ‘combined’ diagnoses should receive half marks.

K199

The meeting agreed that all diagnoses suggesting tubulo-interstitial nephritis should be merged and regarded as correct, irrespective of whether acuteness, granulomas of the link to uveitis were mentioned.  Fanconi syndrome was regarded as incorrect (even though biochemically this may well have been the result), as was cystinosis.

The poor morphology of he section supplied was discussed.  ‘Foam artefact’ was identified, resulting from tissue being squashed between tissue processing sponges before it has been hardened by the fixative.

Discussion of cases in Circulation L

L200

The main diagnosis was of myeloma cast nephropathy, as supported by the information provided about the subsequent clinical course.  Coincidental severe chronic vascular disease was noted.  All responses which mentioned myeloma were to be regarded as ‘correct’ fro personal scoring, even if mentioned only in terms of ‘exclude myeloma’.  (Any participant whose response mentioned myeloma but was coded under diagnostic category 3 or 4 should contact the Organiser).

L201

This case was for education and interest only, as pathologists who do not routinely report renal transplant biopsies could not be expected to detect the presence of acute cellular and vascular rejection (Banff type IIa).  As several pathologists suggested, this was attributable to the withdrawal of immunosuppression, after the graft failed but before graft nephrectomy.

The other diagnosis was of crescentic glomerulonephritis due to recurrent IgA nephropathy, presumably representing recurrence of the original disease.  It was noted that IgA mesangial deposits recur very frequently in renal transplants, but that it is rare for the recurrent deposits to trigger such florid morphological changes and consequent renal impairment.

Responses to this case will be deleted prior to the calculation of personal scores.

L202

This was a case of acute tubular necrosis due to oxalate crystal deposition, subsequently confirmed to be duet to antifreeze (ethylene glycol) ingestion.  Diagnostic categories 1, 2 and 4 were regarded as correct (despite 2 not specifying the type of crystal). Categories 6 and 7 wrongly identified the crystals as urate, and the meeting regarded these diagnoses as incorrect.  The minority diagnosis of ‘Oxalate nephropathy and mesangiocapillary glomerulonephritis’ was awarded half marks, as the meeting could see no grounds for the second diagnosis.  Diagnoses which did not mention the presence of crystals were regarded as incorrect, even if ATN was correctly identified.

L203

The most popular diagnosis was primary focal segmental glomerulosclerosis.  This agreed with the diagnosis of the submitting pathologist and was regarded by the meeting as correct.  It was noted that the submitting pathologist, who presumably had access to a fullest of electron micrographs, had not suggested the possibility of an inherited abnormality of basement membranes.  However, the case had several unusual features, and as the favoured diagnosis was suggested by only 54% of participants it was agreed that this case would not be used for personal scoring.

L204

This was a pauci-immune focal segmental necrotising glomerulonephritis, consistent with a vasculitic process.  It was agreed that ‘focal necrotising glomerulonephritis’ should be regarded as correct, despite the absence of comment on the cause of the necrosis.  However, ‘crescentic glomerulonephritis’ was not sufficiently specific and should receive half marks.

L205

This was an obvious case of amyloidosis (based largely on the information provided, as an amyloid stain was not circulated).  The single divergent diagnosis was a single response stating ‘Waldenstron’s macroglobulinaemia’, but as that response mentioned the presence of amyloid under ‘secondary diagnoses’ it was regarded as correct.

One participant suggested that ‘Amyloidosis’ should only get half marks, as the correct diagnosis was ‘Amyloidosis secondary to Waldenstrom’s macroglobulinaemia’.  The Organiser was grateful that the meeting did not ask him to apply this suggestion, as (a) it would require him to re-enter all the responses for that case and (b) the proportion of participant suggesting the ‘completely correct’ diagnosis would then almost certainly be less than 50%, which would necessitate dropping the case for personal scoring, with exactly the same result of everyone getting exactly the same credit!

Comments and suggestions on the management of the scheme

The Organiser reminded the participants present that they were expected to act as a form of ‘steering committee’ for the scheme, providing advice on the running of the scheme and suggestions for improvements and expansion of the scheme.  No such suggestions were forthcoming. (Any participants not present who may have such comments or suggestions, pleas send them to the Organiser on peter.furness@leicester.ac.uk).

Any other business

None raised.

Meeting closed at 11.55 a.m.

Circulations M and N are both current; they will swap over each half of the participants when the scheme re-starts early in September and will be completed just before Christmas 2003.  A Participants’ Meeting will be arranged as early as possible in 2004 to discuss these circulations.  Does anyone have suggestions for a venue and/or a suitable meeting which this can be linked to?

Peter Furness

Scheme Organiser

2nd July 2003