Thirty – six out of these 50 cases showed red blood corpuscles in the urine. The amount of blood did not appear to indicate the severity of the attack. One of our most serious cases had very little; other clinically mild cases showed much blood. The determination of the presence of red blood corpuscles was made microscopically on the centrifugalized deposit of a fresh specimen.
Twenty – two men had albumin in the urine, and the urines of the remainder – 28 – failed to give the nitric acid or boiling test for albumin.
A few red blood cells, a few casts and endothelial cells in a low specific gravity urine would hardly be sufficient to give a definite and appreciable chemical test, and here we would like to urge the importance of examining microscopically the centrifugalized deposit of urine, since in the absence of this definite examination it would be possible to miss many slight atypical or convalescent cases. Renal tubule cells and cells from the renal pelvis, in all stages in degeneration, were found in 9 cases out of the 50. Leucocytes, more in number than could be accounted for by the blood in the urine, were present in 3 cases.
Of the series of negative cases taken concurrently with those of war nephritis, none showed either casts, or more than a very few endothelial cells. Five had albuminuria; I, who was possibly suffering from a renal calculus, showed renal pelvis, cells; 5 had blood in the urine; 4 showed excess oxalates, and 7 had leucocytes. Of these 44 cases 7 had definite inflammation of the urinary tract, without, however, the endothelial cells found in the nephritis cases.
No cultural results were obtained aerobically or anaerobically – either from the urines or from two cases whose venous blood was examined.
Blood films were made and differentially counted in 15 cases with the following results: Small mononuclears ranged from 16 to 30 per cent., with an average of 22.2 per cent,; large mononuclears from 8 to 18 per cent., with an average of 13.3 per cent.; finely granular polymorphonuclear leucocytes ranged from 47 to 69 per cent., with an average of 62.1 per cent.; and eosinophiles were from 1 to 5 per cent., with an average of 2.4 per cent. “Mast” cells were not counted differentially, but were present frequently.
No myelocytes changed was noted in the red cells and no parasites were observed. The blood counts individually were typical of the so – called protozoal blood count with large mononuclear increase, and in addition to this most of the cases showed a slight eosinophile increase. Citron6 in his cases records an eosinophilia up to 10 per cent.
Two specimens of the cerebro – spinal fluid from cases of uraemia were examined. One was apparently a normal fluid, the other showed excess of small mononuclear cells and contained 0.022 per cent. of urea. Aerobic and anaerobic cultures failed to isolate any pathogenic organism. Only one case of war nephritis has died out of this series of 50. At the postmortem the kidney was found apparently normal and not appreciable enlarged – it certainly was not the enlarged and oedematous kidney of ordinary acute nephritis, and showed no intense engorgement such as is found in early scarlatinal nephritis.
No macroscopic changes were evident. Parts of one kidney were fixed in formalin 10 per cent. and mounted in paraffin. Sections were cut of these and were specially stained and examined for micro – organisms and for protozoa. None, however, were observed. Sections stained with haematoxylin and eosin showed the following points of interest. The nephritis was irregular in distribution; parts of the kidney seemed absolutely normal – one field, for example, showed healthy kidney tissue, and yet the filed next to it showed definite evidence of disease. The nephritis is both tubular and glomerular.
Many of the glomeruli were almost entirely destroyed or swollen and degenerate and filled with endothelial plugs. The cells lining Bowmans capsule showed almost equal destruction, as did the cells of the convoluted and straight tubules. Some of these latter were found filled with casts. Between the glomeruli and among the tubules were patches of interstitial haemorrhage. The smaller arterioles in the affected parts of the kidney showed endarteritis. The nephritis was, in other words, focal and not diffuse. This has also been observed by Pick.4
Of the total number of our clinical cases (250 in all) there were seven deaths. A post – mortem examination was made on each of these, although, with the exception of the case described above, on microscopical investigation of material was possible, in the absence at the time of laboratory facilities. The most striking feature was the small departure from normal in the naked eye appearance of the kidneys.
Four cases had suffered from severe intercurrent purulent bronchitis with consequent circulatory embarrassment. No case showed evidence of chronic renal disease. Patchy pallor of the cortex was noticed in two cases. Moderate enlargement was seen in one case.: the others showed no macroscopic changes except for slight blurring of the cortical structure in one case. These patients had died between the fourth and seventh day of illness.
ETIOLOGY.
It is proposed shortly to consider the various hypothesis that have been advanced on the etiology of war nephritis and to discuss the validity of each.
Damp, cold, and exposure have been suggested by many writers as predisposing causes or even as the immediate causative agents of nephritis, Hirsch, at the Austro – German Medical Congress at Warsaw,3 Pick.4 and other lay special stress on this exposure theory. During the Franco – Prussian War, in which a German authority states that there was much nephritis, it is interesting to note that the chief fighting took place in wet weather.
But against this we have the incidence in the American Civil War, 1861-63, when the cases were most frequent in the summer months. Again, Rose Bradford,5 notes that cases were few in the British Expeditionary Force until March and April, 1915, and that their incidence in the summer of that year was especially high. Taken together, all these conflicting observations do not favor the supposition that damp, cold, and exposure are essential epidemiological factors.
Forced marches have been suggested as a possible cause by Th. Rumpel.6 Certainly prolonged fatigue may produce albuminuria; but this is only transitory, and there is no evidence that this passing albuminuria predisposes to disease at a later date. As a predisposition to renal disease it is as unlikely a factor as a surfeit of green apples is a factor in the cause of mucous colitis. Typical war nephritis occurs among people who have been subject to no excessive muscular fatigue – e.g., hospital nurses and orderlies and patients convalescing from some other disease and from injury.
Streptococcal tonsillitis was suggested by Citron7 as a cause. We find no incidence of this, nor does Abercrombie in his paper8 give any support to this hypothesis. A few of our cases, but a few only, had a streptococcal infection – viz., impetigo; but the majority did not show this.
Singer9 considers that dysentery is a predisposing factor, and also that protective innoculation against enteric fever may lead to a stirring up of other organisms which had hitherto been quiescent. No other writer has, as far as we can learn, considered dysentery to be a factor in the epidemiology of war nephritis, nor do our own cases lend any support to this view. Again, there is nothing in the suggestion that innoculation or vaccination predisposes a man to nephritis. Troops at home are not affected with nephritis, although they are vaccinated and innoculated against enteric.
Lead arsenic, and zinc have been accused of being the causative agents of this condition. Thy can be ruled out at once. The cases do not develop any of the well known symptoms caused by these poisons, and Mackenzie Wallis10 has been able to show by ultra – filtration that the urines of cases of war nephritis do not contain salts of the heavy metals.
Thornley claims11 to have isolated a small Gram – negative diplococcus from the blood of cases of war nephritis. As far as we can discover, this work has not been confirmed, and our own blood cultures showed to such micro – organisms. Mackenzie Wallis10 considers that there are powerfully toxic agents in the urines of cases, and that the organism may be ultra – microscopic. He has not succeeded in producing the typical disease in animals.
That the affection originates in the lung tissue has been suggested by Dunn,12 who described changes in the lungs similar to those seen in cases of irritant gas poisoning. It is possible that the pathological changes noted by this observe were the result of the purulent bronchitis, so often a complication, to which attention has been drawn already. It seems rather to be an intercurrent affection than to have any causative influence on this disease. Exposure to irritant gas could be absolutely excluded in the majority of our own cases.
