35

CLINICO-PATHOLOGICAL CONFERENCE-No. 21

Polyarteritis or glomerulonephritis ?

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FIG. i.-Chest X-ray on December 5, 1952 (afterhaemoptysis). Faint opacity in right mid-zone;this cleared within three days.

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FIG. 2.-Chest X-ray on January 6, 1953 (ward unitfilm; also after haemoptysis). There is evidence ofextensive consolidation of the right lower zone. Thisalso cleared within a few days.

Clinical History (Dr. J. F. Goodwin)The patient was a man aged 24 years, a rivet

heater by trade. In 1948 he was treated forpneumonia with sulphonamides. In 1949, afterdischarge from the Army, he developed upperabdominal pain and nausea, unrelated to food,but relieved by alkalies. He remained well untilSeptember 1952, when he developed increasingdyspnoea on exertion and a cough, followed inOctober by repeated small haemoptyses. A chestX-ray at this time was normal, but a further filmtaken two weeks later showed shadowing in themid-zones of both lungs (Figs. i and 2). He wastreated with bed rest and penicillin for two weeks.The haemoptyses ceased but he noticed increasingpallor and dyspnoea and developed urinary fre-quency and nocturia. On December 14 he wasadmitted to Hammersmith Hospital.On Examination. A pale, anxious young man

with pyrexia of 99 to o00°.

Cardiovascular System. Heart normal. B.P.I25/60. Jugular venous pressure i cm. above thesternal angle.

Optic Fundi. Scattered hard white exudatessurrounded by fine red stippling. Small haemor-rhages. No papilloedema.

Respiratory System. Crepitations at the base ofthe right lung.

Gastro-intestinal System. Abdomen normal.No splenomegaly. Rectal examination normal.

CentralandPeripheral Nervous Systems. Normal.No skin lesions, petechiae, icterus or lympha-

denopathy.

*Held at the Postgraduate Medical School of London(Hammersmith Hospital) on May 27, 1953. The re-port was assembled by Dr. Bernard Lennox. Thesections were prepared under the direction of Mr. J.Griffin and the photomicrographs are by Mr. E. V.Willmott.

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36 POSTGRADUATE MEDICAL JOURNAL January I954

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FIG. 3.-Electrocardiogram on admission to hospital. Tendency to low voltage, flat T waves anddepression of ST segment compatible with severe anaemia.

InvestigationsBlood: Hb., 511 g., 35 per cent. R.B.C., 2.1

million. M.C.V., 8i c.i. M.C.H.C., 30 percent. Reticulocytes, 5.9 per cent. W.B.C., 7,000;normal differential count; no eosinophilia. E.S.R.,37 mm. in one hour (corrected for anaemia, i mm.in one hour). Platelets, 296,000 per c.mm.Bleeding time, 24 min. Clotting time, 4 min.Plasma proteins, 6.5 g./Ioo ml. A/G ratio, 1.5.Blood urea, 25 mg. per cent. Serum bilirubin,0.5 mg. per cent. Blood cultures, sterile. DirectCoombe's test, negative. W.R., negative. Electro-lytes, normal. Agglutinations, negative.

Electrocardiogram (Fig. 3). Low voltage com-plexes and flat T waves consistent with severeanaemia.

Urine: Albumin ++. R.B.C. --+. W.B.C.+ +. Occasional hyaline cast. Sterile on culture.No acid-fast bacilli in 24-hour collection.Bone marrow biopsy: Signs of iron deficiency

anemia. No L.E. cells.X-ray of chest: Considerable resolution of

shadows previously seen.

ProgressThe patient remained febrile and had several

epistaxes. Red blood cells became more numerousin the urine and the urinary output began to fallwhile the blood urea rose (247 mg. per cent. on

December 24, I952). He developed signs of col-lapse of the lower lobe of the left lung, which wasconfirmed by X-ray, and was thought to be due toan infarct. Several superficial vein thromboses oc-curred on the arms, but a biopsy of the skin overone of these did not show any vascular lesion.There were still no neurological signs and nohypertension, and the fundi remained unchanged.TreatmentRepeated blood transfusions were given and the

haemoglobin rose to 84 per cent. The patient wasgiven a protein-free diet consisting of 400 g.carbohydrate and Ioo g. fat, with vitamins added,through a nasal drip. Parenteral penicillin therapyand oral cortisone, Ioo mg. per day for io days,followed by 50 mg. per day for 3I days, wasadministered.

Further ProgressHe improved on this therapy and the fundal

changes regressed slightly. His serum electrolytesremained normal except for reduction in bicar-bonate and sodium. On January 24, I953 theywere: Na, 135 mEq./l.; K, 4.8 mEq./l.; Cl,Ioo mEq./l.; CO,, 15 mEq./l. The bloodpressure rose transiently to 70/oo00 but fell to135/85. The blood urea rose to 412 mg. per cent.and by February 6, I953, he was anuric and drowsy

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January 1954 Clinical Section 37

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FIG. 4.-Electrocardiogram three days before death showing augmented T waves due tohyperkalaemia (serum potassium 7 mEq./l.).

with hissing respirations. The electrocardiogram(Fig. 4) showed augmented T waves characteristicof hyperkalaemia. Electrolytes: Na, 132 mEq./l.;K, 7 mEq./l.; Cl, 8I mEq./l; CO2, I7 mEq./l.Blood urea: 536 mg. per cent.He died in coma on February 9, I953.Clinical diagnosis: Polyarteritis nodosa.

Uraemia.

Pathology (Dr. G. A. K. Missen)The significant macroscopic findings at autopsy,

which was performed 2I hours after death, wereconfined to the lungs and kidneys, but the appear-ances of the latter were not conclusive. However,the histological appearances were those of poly-arteritis nodosa of the microscopic type (Davson,Ball and Platt, I948; Wainwright and Davson,I950).The body was that of a young man, 5 ft. I in.

tall and weighing io st. 3 lb. The serous cavitiesshowed no inflammation or excess fluid. Thekidneys (245 g. and 240 g.) were increased in size,their cut faces being tense and bulging and showedno focal lesions. The cortices were swollen and ofa dull greyish-pink in colour. The pattern of thecortex and its demarcation from medulla appearednormal, though after fixation the glomeruli werevisible to the naked eye as opaque, whitish dots.Medullae appeared normal. Capsules strippedeasily to reveal uniform, dull-pink surfaces (Fig.

5). The bladder contained 750 ml. of turbidbrown urine.The lungs (right, 880 g., left, 580 g.) were con-

gested and relatively airless especially in theirdependent parts. Five small organizing infarcts

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FIG. 5.-The kidneys.

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3X POSTGRADUATE MEDICAL JOURNAL January 1954

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FIG. 6.-The infarcts in the right lung.

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FIG. 7.-Low power view of kidney to show absence ofnormal glomeruli. H. & E. x 36.

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FIG. 8.-A glomerulus. Severe glomerulitis of somestanding with slight crescent formation. Theafferent arteriole shows moderate fibrinoid necrosis.H. & E. x I60.

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FIG. 9.--Aute arteritis in the sinus renalis. H. & E.x x60.

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January 1954 Clinical Section 39

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FIGS. o and i i.-Lesions of arteries in the lungs, withlocalized destruction of the elastic tissue, stronglysuggestive of healed arteritis. Elastic Van Gieson:X 90.

were found in the right lung; one in the anteriorfringe of the middle lobe and the remainder at thebase of the lower lobe in or near its inferiorfringe (Fig. 6).The heart (320 g.) was normal except for a

single petechial haemorrhage beneath the visceralpericardium. The liver (I,940 g.) showed a palecut surface with an exaggerated pattern. Ante-mortem thrombus was found in the prostaticvenous plexus and deep veins of the (left) calf.No micro-aneurysms or other infarcts were found.

HistologyKidneys. No normal glomeruli were seen

though they were present in normal numbers(Fig. 7). Many tufts were obliterated by partialor complete fibrosis. Others showed adhesions tothe capsule, the epithelium of which was hyper-trophic. Epithelial crescents were seen. In a fewglomeruli a part of the tuft was preserved. Theseappearances suggested the end-result of a general-ized necrotizing glomerulitis.The convuluted tubules were dilated and the

distal epithelium flattened. Plentiful casts wereseen in the collecting tubules. The interstitial

tissue was oedematous and infiltrated with plasmacells and lymphocytes, especially around theglomeruli.

Despite examination of sections at many differ-ent levels, the only abnormality of the renal vesselsto be found was fibrinoid necrosis of a fewglomerular afferent arterioles (Fig. 8). Acutearteritis of three small vessels was found in thesinus renalis (Fig. 9) as well as veins containingorganizing thrombus. The larger arteries in thissite were normal.

Lungs. Sections of the hilar regions showed con-gestion, haemorrhage, some oedema and manysiderophages. Sections of the right middle lobeconfirmed the presence of an organizing infarct.Within this area were a number of arteries con-taining organized thrombus and showing destruc-tion, confined to a sector of their circumference,either of intima and elastica only or else of allcoats (Figs. o and I ).

Liver. Showed periportal and a little centrilo-bular fatty infiltration.

Spleen (130 g.) showed no arterial or otherlesions.No vascular or other relevant lesions were found

in any of the following organs or tissues: Heart,voluntary muscles, pituitary, adrenal, thyroid,parathyroid, pancreas, testis, epididymis, sper-matic cord, small intestine, vertebral bone marrowand cerebral cortex.

SummaryPolyarteritis nodosa of microscopic type leading

to pulmonary infarction and diffuse necrotizingglomerulitis with ultimate renal failure.

TABLE IFREQUENCY OF LESIONS OCCURRING IN POLYARTERITISNODOSA (MODIFIED FROM HARRIS, LYNCH AND O'HARE,

1939)Percent.

Renal lesion . .. .. . ..87Pyrexia .. .. .. .. .. 80Leucocytosis* . .. .. .. .. 70Hypertension .. .. .. 64Abdominal pain . .. .. .. 57Anaemia . .. .. .. .. 50Oedemat .. .. . . .50Peripheral neuritis .. .. 20Fits .. .. .. .. . . I 5

*Eosinophilia, 20 per cent.tDue to renal or cardiac failure or to myositis.Skin lesions, cardiac involvement, pulmonary and

ocular changes also occur.

DiscussionDR. GOODWIN: Whether we accept this case as

one of periarteritis nodosa or not it may be helpfulto review the disease very briefly in terms of theclinical picture produced by the various patho-

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40 POSTGRADUATE MEDICAL JOURNAL January 1954

logical lesions. Periarteritis nodosa is, I think,somewhat of a misnomer, because the lesion, as Iunderstand it, is initially a pan-arteritis withfibrinoid necrosis which involves the inner coatsfirst and then spreads outwards, the periarteritisbeing a secondary phenomenon. The lesion pro-duces thrombosis in the vessel, and by weakeningof the wall produces nodular aneurysms. Thelesions may be scattered along the course ofarterioles and arteries anywhere in the body, so thata pleomorphic clinical picture can occur. Kuss-maul and Maier defined periarteritis nodosa as aclinical and pathological entity in I866, and in1878 Meyer added the diagnostic triad of chloroticmarasmus, polymyositis and polyneuritis, andgastro-intestinal symptoms. This triad did notinclude a renal element, although a type of Bright'sdisease with febrile features had been described.Christeler in 1926 added nephritis to the triad.Harris, Lynch and O'Hare (1939) analyzed thesymptoms and signs in order of frequency in 101published cases with 87 autopsies (Table i). Itwill be seen that this patient suffered from five ofthe nine listed complaints: Severe anaemia,pyrexia, abdominal pain, renal insufficiency andslight oedema; but it is interesting to note thathypertension was not a feature. In addition, hepresented with fleeting pulmonary infiltrationssimilar to those described by Elkeles and Glynn(I944) who considered them to be due to areas ofinfarction or atelectasis. The present case alsohad fundal changes consisting of small, hard, whiteexudates adjacent to arteries, and small haemor-rhages. Sampson and Herson (1949) describedretinal detachment, haemorrhages and exudates,occlusion of the central retinal artery and hyper-tensive retinopathy. Lesions of the outer eye(conjunctivitis and iridocyclitis) may also occur.Skin lesions are sometimes a feature of the diseaseand consist of purpuric eruptions, variants oferythema nodosum or subcutaneous nodules.Coronary occlusion, pericarditis and even endo-carditis may occur (Miller and Daley, 1946), butclinical evidence of cardiac disease was equivocalin this patient.

Davson, Ball and Platt (1948) classified the renallesions and pointed out that in addition to pro-ducing an acute arteritis with infarcts the diseasecould occur in a microscopic form, the appearancesbeing those of malignant nephrosclerosis orglomerulo-nephritis.A clinical diagnosis of periarteritis nodosa is

usually possible if the condition is kept in mind inpatients with obscure fever and vascular and renallesions. In an excellent paper Miller and Daley(1946) suggested that the disease could be roughlydivided into various types: (i) Pyrexia of unknownorigin; (2) Atypical abdominal symptoms with or

without hypertension; (3) A primary renal diseasewith atypical features, and (4) A disease showingpolyneuritic or polymyositic features.As regards prognosis, Grant (I939) found that

about 50 per cent. of cases recovered, and it seemsthat if the lesions do not involve important viscera,recovery may well be possible and, in fact prob-ably often occurs. The cause of periarteritis issupposed to be some sort of anaphylactic hyper-sensitivity; I do not know of any better sugges-tions having been made. The responsible antigenis usually bacterial in origin (Miller and Daley,I946), but drugs such as sulphonamides, thiouracil,iodine and deoxycorticosterone acetate have beensuspected. This patient had no drugs other thansulphonamides and alkalies, the former many yearsago.

Finally, treatment. Schick and his associates(1950) treated six cases with cortisone or ACTH ofwhom four recovered and two died of renalfailure.* When the kidneys are involved par-ticularly severely the prognosis is extremely bad,which is, in fact, what Dr. Milne said when hekindly saw the case in consultation.

PROF. DIBLE: I am not at all happy, you know,about the diagnosis of polyarteritis nodosa in thiscase. If the name means anything, it is difficultto see any polyarteritis. The one outstandinglesion was the glomerular lesion and that was acapillaritis, not an arteritis. That might be aquibble but the fact remains that every glomerulusin that kidney showed the most extensive changesand it was only by extremely thorough searchingthat any lesions could be found in any other partsof the body which might be interpreted as beingexamples of polyarteritis. Whether polyarteritisand glomerulo-nephritis are distinct diseases ornot, on the basis of what we have seen and heardthis morning I am beginning to wonder. But ifwe are to regard them as distinct diseases I feelthat the evidence here is that the lesion is nephriticand not an arterial or arteriolar condition.

PROF. MCMICHAEL: That is a challenge to thepathologists, surely.

DR. DONIACH: Can we call Dr. Milne a path-ologist for this purpose?DR. MILNE: I am not going into the morass of

pathological argument, but from the clinical pointof view this disease could never have beenglomerulo-nephritis. First of all there is absolutelyno history of any phase typical of acute Type Inephritis. He was an intelligent man and we wentinto that history very carefully. There was no

*Since the Conference took place Simpson, Hallf.andMorgan (Brit. med. J., ii, 659, 1953) have reportedrecovery of a patient with polyarteritis nodosa followingtreatment with ACTH.

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January 1954 Clinical Section 41

history of an oedematous state typical of Type IInephritis. That is negative evidence. The positiveevidence was, first, the presence of transientpulmonary infiltrations which are very typical ofthe pulmonary infiltrations of polyarteritis nodosa.Second, the severe anaemia and the fever whichresisted antibiotic treatment. Third, and evenmore typical, are the retinal lesions. I do not knowwhether these are specific retinal lesions of poly-arteritis nodosa (and I do not very much care),but I do know that they are not secondary to theusual causes of retinal lesions in glomerulo-nephritis. Retinal lesions in glomerulo-nephritisare secondary either to severe hypertension whichmay cause exudate, haemorrhage and papilloedema,or to capillary damage due to severe uraemiawhich does seem to lead to a haemorrhagictendency. Now this man had neither of thosewhen he had severe retinal lesions, he had nohypertension, he had no evidence of past hyper-tension and he had no uraemia at that time; theblood urea was low. I have seen the samephenomenon in cases of phaeochromocytoma, butin them, of course, there is a paroxysmal hyper-tension to account for it. Another thing in favourof polyarteritis nodosa is the extreme rapidity ofprogress of the renal lesion to severe fatal uraemiadespite the fact that there was not the viciouscircle of Bright's disease so well described byClifford Wilson. He states that in the develop-ment of uraemia in Bright's disease the rapidity ofprogress is dependent on the diastolic pressure.Cases with a high diastolic pressure progressrapidly to severe uraemia and death. This manprogressed terribly quickly despite a normal oronly very slightly raised diastolic blood pressure.That was very suggestive of a primary arteriallesion and I think the pathologists have demon-strated this-or, to be strict, a panarteriolitis orpancapillaritis in the kidneys. That to me istypical of the microscopic variety of polyarteritisnodosa.

PROF. MCMICHAEL: Well, that is very emphaticand I must say I support it. I think that there areare some obviously queer border lands betweensevere arterial damage and glomerulitis. Experi-mentally many years ago Wilson and Byronshowed that in experimental malignant hyper-tension there was an associated glomerulitis. Ivery well remember a case of a boy who presentedwith a picture which we took clinically to be anacute nephritis which turned out to be a kind ofjuxta-glomerular arteritis at post-mortem. So Ithink we are here on a border-land betweennephritis-or capillaritis, if it is to be called that-and arteritis. I wonder if we ought not to drop theterm 'nodosa' because there were, in fact, nonodules either macroscopically or microscopically.

It might help if we merely called them arteritisrather than periarteritis nodosa. There was verylittle periarteritis here.DR. LENNOX: May I just interject something

which I think is relevant to everything that hasbeen said so far? I think the views of Pearl Zeekon the matter of polyarteritis have been neglectedrather more than they deserve. She maintainsthat there are two different diseases mixed up inpolyarteritis. One is the typical textbook ' poly-arteritis nodosa' with hypertension in which thelesions are confined to the arteries and in whichthe 'nodosa' is often justifiable because you seemacroscopically visible aneurysms. That is adisease which may be simply a variant of malig-nant hypertension. The other is a sensitivitydisease in which the lesions are never macroscopicand in which not only the arteries are involved butalso the lungs and sometimes the veins. Now thiswould fit in perfectly. It is not a ' nodosa' type,i.e., there are no lesions of larger arteries. Ad-mittedly we have no evidence of the sensitivityphenomenon, but that is a difficulty in any attemptto explain the glomerulitis in this case and it maybe that there is some sensitization we have missed.We have got venous lesions and lung lesions andthere was no hypertension. It is in these atypicalcases of polyarteritis without hypertension andwith venous and pulmonary lesions that we getjust such a confusing border-line picture as thepresent case. Perhaps all these so-called micro-scopic arteritides, non-nodose polyarteritides, fallinto this second group.

DR. HARRISON: I do not think we should takeZeek's sub-division too literally. When she pub-lished that paper I dug out all our polyarteritiscases and tried to divide them according to Zeek,and they just will not divide. I am sorry, but thedata spoils this beautiful theory. However, I doagree with Dr. Lennox, there is an enormous vari-ability in polyarteritis and it probably does em-brace'a lotmore than one standard case. I think Dr.Missen has made out a very good case on thestrength of these lung arteries. I think we have totake the polyarteritis very seriously in any arterythat has got half its wall bitten clean away.

PROF. DIBLE: Yes, but it is so usual to findthese in the spleen. Would not you agree thatthat is the organ where you find them most fre-quently? I was a little surprised to find there werenot any splenic lesions.

DR. HARRISON: I agree that it is unusual, butcan we exclude the diagnosis on that alone?

PROFESSOR MCMICHAEL: There are somequestions I would like to ask. First, what is thecause of the anaemia? Clearly it was not related tosevere uraemia. The blood urea was only 25 mg.when his Hb. was only 5 g. Second, was the

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42 POSTGRADUATE MEDICAL JOURNAL January 1954necrosis of half of the glomerulus similar to thelesion seen in subacute endocarditis? And third,what do you really think was the pathology ofthese transient lung lesions? You did say somehaemorrhage was found in the lungs but nofibrinous oedema. I wonder what they really are.Is there any information on that?DR. GOODWIN: We were very puzzled by the

anaemia clinically and we could not really explainit at all, but we did wonder how much blood he hadactually lost. We did not see how the amount hehad lost from his alleged haemoptyses would besufficient to produce that degree of anaemia andwe did wonder whether he was losing it via hisgastro-intestinal tract. We never got any positiveoccult blood in the stools and we did not forobvious reasons do barium meals or enema oranything of that sort.DR. DONIACH: I do not think we can say

positively what the central lung lesions were a fewmonths before he died. In a negative way the factthat we found no evidence of fibrosis in the hilarsections would suggest some transient congestionor oedema.

DR. BAYLISS: It could not have been haemor-rhage with aspiration of blood? He had quite fre-quent haemoptyses, had he not? And if he hadaspirated blood back down a segment he couldhave got changes which would have looked likethat.

DR. DONIACH: It could have resolved com-pletely-yes, that cannot be ruled out.

PROF. McMICHAEL: I think the radiologistmight have something to say.

DR. STEINER: The interesting feature here wasthat the patient came to the Chest Clinic withhaemoptysis. He was watched there for threeweeks with these fleeting shadows and that iswhat we quite often see. Such shadows are notnecessarily either tuberculous lesions or the resultsof haemorrhage into the lung. We have seen afew shadows due to atypical pneumonias whichlook like this, and the physicians at that timethought, after they had excluded tubercle, thatthey were due to atypical pneumonia. I was notaware at the time of these fleeting shadows inpolyarteritis nodosa, but at the same time DrSherlock had a patient in her ward who presentedwith a very similar picture with haemoptyses andwith multiple fleeting shadows in the lung whichcleared within a week completely. I think at the

time the haemoptyses were thought to be due tooozing from a retropharyngeal vein.DR. DONIACH: We sent a copy of the kidney

section to Dr. Davson to get his opinion on it.At the time we sent it we had not the otherevidence of arteritis-the lung lesions and thepelvic lesions had not been seen. He wrote backand said that the kidney would do for a micro-scopic type of polyarteritis, but in the absence offinding any other vessels affected he could notmake a definite statement. He said that thenephropathologist in this sort of case gets morehelp from the clinical story than from looking atsections.

DR. FRASER: I would like to ask Dr. Milnewhether in the earliest phase in such a case as thisyou would expect to see albuminuria.

DR. MILNE: I should say it entirely depends onthe distribution of the lesion. If the glomeruli areinvolved obviously albuminuria will occur and Ithink we saw from Dr. Goodwin's Table that therenal lesions are, if not the commonest, very highup in the list and therefore the great majority ofcases have albuminuria; but many of course cometo autopsy without any renal lesions whatsoever.DR FRASER: I was meaning in this microscopic

type where it seems to me it was implied youalways have renal lesions. You do not think thatis so?

DR. MILNE. I would not like to be dogmatic.This type has been described recently by Davsonwho is particularly interested in the kidney and Itake it it is conceivable that such types might occurwithout involving the kidney, but as far as I knowthis has not been described.DR. LENNOX: There has been at least one

article describing microscopic arteritis limited tothe appendix. I take it you would assume that inthose cases there would be no albuminuria!

BIBLIOGRAPHYDAVSON, T., BALL, J., and PLATT R. (I948), Quart. J. Med.,

17, 175-ELEKELES, A., and GLYNN, L. E. (I944), Brit. J. Radiol., 17,

368.GRANT, R. T. (I939), Clin. Sci., 4, 245.HARRIS, A. W., LYNCH, G. W., and O'HARE, J. P. (1939),

Arch. intern. Med., 63, I63.MILLER, H. G., and DALEY, R. (1946), Quart. J. Med., 15, 255.SAMPSON, R. S., and HERSON, R. N. (x949), Ibid., I8, I23.SCHICK, R. M., BAGGENSTOSS, A. H., FULLER, B. F., and

POLLEY, Hi. F. (950S), Proc. Mayo Clin., 25, 492.WAINWRIGHT, J., and DAVSON, T. (1950), J. Path. Bact.,

62, I89.

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