At the start of this meeting there were not sufficient participants present for the meeting to be quorate. However, further participants arrived such that a quorum of 10 participants was achieved by the start of discussion of the first ‘scoring’ case (case T243).
Comments and suggestions on the management of the scheme were invited. None were received.
Cases in circulations T and U were discussed.
This was submitted for education and interest only, so will not be used for scoring purposes.
The majority diagnosis was of fibrillary glomerulonephritis, with others suggesting immunotactoid glomerulopathy or ‘non-amyloid structured immunoglobulin deposits’ in the absence of a scale on the EM images. However, the immune complex deposits appeared to be exclusively subepithelial, and had it not been for their fibrillar architecture the case would have been typical membranous glomerulonephritis. Indeed, a minority view amongst participants was that this was membranous glomerulonephritis with ‘structured’ deposits. The submitting pathologist was present; he indicated that he had considered fibrillary glomerulonephritis but had finally concluded that it should be classified as membranous glomerulonephritis because the distribution of deposits was not that of fibrillary glomerulonephritis. Those present at the meeting concurred with this view, despite it being in disagreement with the majority diagnosis.
Responses for this case will be deleted before personal scores are generated.
All participants had agreed that this was a case of granulomatous interstitial nephritis; the various diagnostic categories were divided only on the basis of the suggested cause (or its absence). The submitting pathologist had indicated a strong suspicion that this was due to sarcoidosis, but even with clinical correlation this was not proven.
It was agreed that all diagnoses proffered should be merged under ‘Granulomatous interstitial nephritis’.
The consensus diagnosis was of hereditary nephropathy of Alport type, on the basis of EM appearances, clearly of autosomal type as the patient is female. After some discussion it was agreed that all diagnoses which indicated an inherited nephropathy should be considered correct for scoring purposes, except for the suggestion of Fabry’s disease.
There was a brief discussion of the frequent suggestion that
immunohistochemistry for type IV collagen alpha chains was needed – even though
relatively few laboratories in the
This was a straightforward case of IgA nephropathy or Henoch Schönlein purpura, depending on whether or not one included the clinical information about the rash in the diagnostic process. Either were regarded as correct; all other diagnoses were regarded as incorrect for scoring purposes.
This was a case of lupus nephritis, presenting in a 15 year old male.
Participants present pointed out that at previous EQA meetings it has been indicated that whenever a diagnosis of lupus nephritis is made in the EQA scheme, there should be an indication of class. Consequently only diagnoses mentioning lupus class IV would be merged and regarded as fully correct. Lupus nephritis with no indication of class would justify half marks, as would ‘MPGn pattern, could be lupus’. Other diagnoses would be regarded as incorrect.
This was a typical case of post-infective acute diffuse proliferative glomerulonephritis. However, responses had revealed that the information provided was misleading; it was unclear whether the phrase ‘All immunology negative’ referred to serology or immunohistochemistry. It was unfortunate that the case was submitted with only a H&E section for examination. In view of the submitting pathologist’s diagnosis of post-infective glomerulonephritis it seemed likely that ‘all immunology negative’ had referred to the soluble immunology rather than to immunohistochemistry. Many participants had clearly assumed the opposite.
In view of this misleading clinical information it was agreed that the case would not be used for personal scoring.
This was a straightforward case of IgA nephropathy.
One participant had given ‘IgA nephropathy AND membranous nephropathy’ as a single diagnosis line, not as a differential. It was agreed that the case showed no evidence of membranous nephropathy, so this should be accorded half marks.
The clinical information provided with this case hinted strongly at the presence of a plasma cell dyscrasia, but the consensus diagnosis (and that of the submitting pathologist) was of membranous glomerulonephritis.
It was agreed that the interstitial nephritis present was a consequence of the membranous nephropathy, so an unqualified diagnosis of ‘interstitial nephritis’ was incorrect, but ‘membranous glomerulonephritis and interstitial nephritis’ would be regarded as correct.
All the other diagnoses proffered indicated the presence of some other disease process (myeloma, lupus, macroglobulinaemia, Sjogren’s, secondary membranous) in addition to the membranous glomerulonephritis. Participants at the meeting agreed that these additional diagnoses could not be supported on the basis of the material circulated, so these diagnostic categories should be awarded half marks.
All had agreed that this was a case of myeloma cast nephropathy, and all diagnostic categories should be merged under that heading for scoring.
Many had noted the presence of a few neutrophils in some tubules and raised the need to exclude urinary tract infection, but this was not regarded by the meeting as an essential component of the diagnosis.
This case clearly illustrated diabetic changes, with a fairly severe tubulointerstitial nephritis which was not readily attributable to the presence of diabetes. The information provided also indicated the presence of IgA in the glomeruli, but this generated numerous complaints that its significance could not be evaluated in the absence of images of the IF panel and without electron microscopy. Many participants had suggested concurrent IgA nephropathy on this basis, though it was notable that the submitting pathologist had not.
Numerous participants also indicated the need to exclude urinary tract infection, on the basis of neutrophils within some tubules.
In view of this multiplicity of diagnoses and the absence of material essential to evaluate the significance of the glomerular IgA positivity it was agreed that this case could not be used for scoring purposes.
This was a case of granulomatous interstitial nephritis, which could reasonably be attributed to the stated presence of sarcoidosis. All diagnostic categories would therefore be merged under this heading with the exception of ‘cast nephropathy’, which was regarded as incorrect.
Numerous participants had noted the need to exclude an infective process even in the face of a clinical diagnosis of sarcoidosis.
The meeting agreed that, in this context, the somewhat cryptic abbreviation ‘BHL’ probably meant ‘bilateral hilar lymphadenopathy’.
This was a case of amyloidosis, demonstrated by the presence
of a positive Congo Red. In view of the clinical information this is presumably
amyloid of
There was a brief discussion of the extent to which participants
investigate the type of amyloid, bearing in mind that such cases should be referred
to the national Amyloidosis Centre, which will result in sophisticated immunohistochemical
studies including tests for rarer inherited forms of amyloidosis. Only a minority
of participants present use immunohistochemistry to determine amyloid type locally.
One participant recommended anti-SAA as a way to resolve cases where a negative
Congo red was suspected to be a method failure, but others suggested that performing
EM on all cases was a surer way to avoid missing the diagnosis. The majority
of those present are still using a simple permanganate
bleach as a way to distinguish
Professor Furness reported that an increasing number of participants were choosing to pay the £30 ‘excess charge’ rather than submitting a case for circulation when requested. It was agreed that this charge should be doubled. Porfessor Furness pointed out that this was not unreasonable as the subscription fee had not altered for many years.