Report of the Participants’ Meeting held at 13:20 – 14:20 pm on Wednesday 9th January 2008
in Room 11, Examination Schools, Oxford, as a companion meeting to the Pathological Society Meeting at the same time.
The meeting opened at 1.20 pm, with over 20 participants present.
Professor Furness reminded participants of the purpose of the meeting, being review of Circulations Z and A and also the responsibility of the meeting to act as a Steering Committee to consider scheme management and to discuss any problems in the running of the scheme.
Case 278 generated complaints of inadequate material from over half the respondents. Subsequent information from the submitting pathologist indicated that he too regarded the renal biopsy as inadequate, but he had submitted the specimen because of the unexplained fibro-inflammatory process in the fragments of retroperitoneal fat that were also included. A large proportion of participants had indeed noted and commented on this extra-renal process, some raising a suspicion of a connective tissue neoplasm; but the participants meeting agreed unanimously that the case should not be used for personal assessment.
Subsequent clinical information suggested that the inflammatory process was probably related to previous operative intervention in the form of an aorto-femoral bypass.
Case 279 was a case of crescentic glomerulonephritis. The clinical information indicated that this was due to anti-glomerular basement membrane antibodies. Almost everybody made a diagnosis which included mention of anti-GBM disease or Goodpasture syndrome. A small minority made a diagnosis of crescentic glomerulonephritis without any mention of the underlying cause. The participants’ meeting considered this. In view of the clinical information provided, and also bearing in mind the impressive uniformity of the changes between glomeruli, the meeting agreed that a failure to suggest anti-GBM disease as the underlying cause was a significant omission and that ‘crescentic glomerulonephritis NOS’ should be awarded only half marks.
Case 280 was a complex case where diagnoses proffered included tubulo-interstitial nephritis, athero-embolus and myeloma cast nephropathy, with all possible combinations of these three. Other minority diagnoses included light chain deposition disease and pyelonephritis. The meeting agreed that the morphological evidence for myeloma cast nephropathy was relatively slender, and the diagnosis was based largely on the clinical information indicating that light chains were present in the urine. It was agreed that cast nephropathy could cause a ‘tubulo-interstitial nephritis’ (to use the term loosely), though in this case the evidence of TIN appeared to be out of proportion to the evidence of cast nephropathy.
After discussion, the participants meeting agreed that this combination of multiple diagnoses and possible diagnoses was too complex to permit use of the case for personal scoring.
Case 281. This was a nephrectomy specimen from a 42 year old with progressive deterioration in renal function and poorly controlled hypertension. The meeting agreed that the underlying process was almost certainly reflux nephropathy/chronic pyelonephritis. There were a few foci of acute inflammatory cell infiltration, including neutrophils in tubules, suggesting an element of active ascending infection (acute pyelonephritis). There were also a few rather poorly formed granulomas. The meeting felt that the granulomas were probably secondary to the chronic pyelonephritis, but that it was reasonable to raise the possibility of sarcoidosis for clinical consideration.
The meeting agreed that “granulomatous pyelonephritis” and “granulomatous tubulo-interstitial nephritis” are two different diagnoses, the former being a reasonable descriptive term to be applied to this case, the latter describing a diffuse process, therefore not appropriate to this case. However, Professor Furness indicated that many of the responses received had been complex and discursive, indicating a degree of confusion between these two categories. It was agreed that the case could not be used for personal scoring.
Case 282. This was a case of lupus nephritis. In the past participants have repeatedly been reminded that if a diagnosis of lupus is suggested then the relevant class should also be offered. As a result, the meeting agreed that “necrotising glomerulonephritis ?lupus” should be awarded half marks because a formal class was not offered. Similarly “lupus class Vd” should be awarded half marks, on the grounds that even if use of the old WHO classification is accepted, the biopsy actually showed remarkably little evidence of spike formation on the silver stain so under WHO or ISN/RPS classifications, this would be lupus class IV.
Case 283. This was a case of amyloidosis, subsequently confirmed to be of AL type. All participants made the same diagnosis.
Professor Furness pointed out that a relatively high proportion of cases in this circulation were being deemed by the meeting to be not suitable for personal scoring, and that this would cause this whole circulation to be of questionable value for personal scoring purposes. The meeting agreed nevertheless to proceed as above.
Case 284 was a biopsy where the only debate was whether this should be described as Henoch-Schönlein purpura (in view of the rash on the legs) or whether a diagnosis of IgA nephropathy was more appropriate. The meeting agreed that for scoring purposes these two diagnoses should be merged and both regarded as correct. Subsequent information indicated that clinicopathological correlation justified a diagnosis of Henoch-Schönlein purpura.
Case 285. This was a case of crescentic pauci-immune glomerulonephritis, with clinical information strongly suggesting that it should be regarded as Wegener’s granulomatosis. Subsequent information indicated that the patient was MPO-ANCA positive. A participant pointed out that this is not the type of ANCA normally associated with Wegener’s granulomatosis, but the meeting agreed that that diagnosis as Wegener’s was nevertheless appropriate because it is defined on a clinical rather than a serological basis, and also because some of the renal inflammation had a granulomatous element.
The meeting agreed that all diagnoses indicating either Wegener’s or a “pauci-immune” glomerulonephritis should be regarded as correct. The diagnosis “necrotising glomerulonephritis” was regarded as insufficiently precise, because so many different processes can cause glomerular necrosis. This diagnosis was therefore to be awarded half marks.
Case 286. This biopsy was stated in the clinical information to be from a patient with known lupus nephritis, so the problem was clearly one of appropriate classification. The meeting agreed that this was unequivocally class IV (whether under ISN/RPS or WHO classifications). The meeting noted the difficulty that participants had in deciding whether or not significant chronic damage was present (classification as A or A/C) and agreed to merge all diagnoses of lupus class IV for scoring purposes. The meeting agreed that classification as Class III was wrong.
Case 287. The meeting agreed that the morphological diagnosis in this biopsy was of a thrombotic microangiopathy. The association of this condition with Gemcitabine treatment had been noted by many participants.
The other diagnoses proffered were regarded as incorrect for personal scoring purposes.
Several participants had noted the presence of crystals within the biopsy, but the meeting agreed that these were insufficiently extensive to represent an explanation for acute renal failure. A few oxalate crystals can be seen in many cases of advanced renal damage. It was also pointed out that if the adenocarcinoma of the pancreas had resulted in exocrine pancreatic insufficiency and malabsorption, this can precipitate oxalate deposition in the kidney.
Case 288. This was a case of amyloidosis, subsequently confirmed to be of AL type. All participants proffered the correct diagnosis.
Case 289. This was a case of IgA nephropathy and all participants proffered the correct diagnosis.
Professor Furness explained a problem with provision of cases for the EQA scheme. For the first time, a shortage of cases had delayed the start of Circulations B and C. As a result these circulations would run into the start of the summer holiday period in July, with consequent disruption for participants towards the end of the circulations.
No clear solution to this problem was identified beyond considering increasing the penalties against those who are asked for cases but do not supply them.
The possibility of supplying associated material in electronic form over the internet was raised by a participant. The meeting agreed that at present cases should continue to be circulated in the form of at least one glass slide (H&E) per case, but that other investigations might be made available in electronic form, perhaps over the internet, rather than as digital photographic prints. Professor Furness indicated that one case in the newly started pair of circulations (B and C), submitted as an ‘education only’ case, was provided with such internet-based material. It would therefore be timely to review how this method of delivery of images was viewed by participants at the next participants’ meeting (in July 2008).
Participants were invited to comment on the management of the scheme and suggest improvements, but no further comments were received.
The meeting closed at 2.20pm.
Professor P. N. Furness, EQA Scheme Organiser 11th January 2008