CHAPTER XIV
Nephritis
John P. Merrill, M.D.
An evaluation of nephritis occurring in the military duringWorld War II must necessarily be considered in the light of our knowledge of thedisease in general, since there appears to be little difference in its variousaspects between military and civilian experience. In this discussion, we shallconcern ourselves principally with glomerulonephritis.
GLOMERULONEPHRITIS
Etiology-The present evidence for the etiology ofglomerulonephritis implicates an immune response in which the glomeruli areprimarily involved by inflammatory change. The disease can be producedexperimentally in rats by the injection of rabbit serum from animals who havebeen previously immunized to a homogenate of rat kidney.1Other hyperimmune reactions involving small vessels generally may alsoaffect the glomeruli by inflammatory change. Such changes have been produced byhypersensitivity to the sulfonamides.2 Thedisease in man appears to be closely associated with an antecedent infection byso-called nephritogenic strains of the hemolytic streptococcus. The lag periodbetween infection with the streptococcus and the onset of nephritis probablyrepresents development of an immune process, similar to that found in theexperimental animal. Interpretation of animal and human data suggests that insome fashion renal tissue and streptococcal protein combine to form an antigen,the immunologic reaction to which produces the inflammatory changes.3This protein has been tagged by tracer substances and actually found to belocalized in the glomeruli. In this way, an autoantibody is produced and mayhelp to explain the continuing progress of the disease in some clinicalsituations long after the initial infection has subsided.
Clinical aspects.-In man, glomerulonephritis alsoappears to be preceded by infection with the Group A hemolytic streptococcus.This correlation, however, is not a perfect one since frequently a history ofprevious
1Farr, L. E., and Smadel, J. E.: Experimentally Induced Nephritis in Rats, Functional and Clinical Studies. J. Clin. Invest. 15: 449, 1936.
2Rich, A. R.: The Role of Hypersensitivity in Periarteritis Nodosa, as Indicated by 7 Cases Developing During Serum Sickness and Sulfonamide Therapy. Bull. Johns Hopkins Hosp. 71: 123-140, March 1942.
3Lange, K., Craig, F., Oberman, J., Slobody, L., Ogur, G., and LoCasto, F.: Changes in Serum Complement During the Course and Treatment of Glomerulonephritis. A.M.A. Arch. Int. Med. 88: 433-445, October 1951.
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streptococcal infection cannot be obtained; in addition,well-documented cases of nephritis have followed infection with othermicro-organisms, such as the pneumococcus. Undoubtedly, however, the hemolyticstreptococcus is the prime offender, and the analogy with rheumatic fever andprevious streptococcal infection is an interesting one. Probably both representhyperimmune responses to previous infection with the streptococcus. There are,however, striking differences as shown in table 75.4 Whereas rheumatic feverrather consistently occurs in about 3 percent of hemolytic streptococcalinfections, the rate for nephritis is extremely variable (table 76).5 A surveyof the literature indicates that the percentage of nephritis following scarletfever varies from 0 to 18 percent. Furthermore, nephritis may occur inpseudoepidemics. These variations in incidence suggest to one author that thestreptococcus may vary in its nephritogenic properties. In the United States,type 12, and to a lesser extent type 4 of Group A, streptococci have beenusually associated with this complication.
The latent period following streptococcal infection as wellas the drop in serum complement during the acute phase again suggest thepossibility of hypersensitivity to this organism or to a product thereof. Otherforms
TABLE 75.-Biological differences betweenglomerulonephritis and rheumatic fever
Biological feature | Glomerulonephritis | Rheumatic fever |
Geographic distribution | Uniform | Most common in northern latitudes |
Age | Any age | Rare in infancy |
Familial factors | Family contacts | Familial tendency |
Sex incidence | Males predominate, 2 to 1 | Equal |
Second attacks | Rare | Common |
Average latent period between infection and first attack | 10 days | 18 days |
Latent period between infection and second attack | Shortened as compared to latent period in first attack. | Usually same as latent period in first attack |
Relation of degree of ASL1 increase to incidence of attacks | No known relation | Incidence of attacks proportional to ASL1 increase |
Time of ASL1 increase in relation to onset relapse | After | Before |
Serum complement | Decreased | Increased |
Type of initiating Group A hemolytic streptococcus | 4, 12, 25, and untyped (12 predominates) | Any type |
1Antistreptolysin titer.
Source: Modified from Earle, D. P., Jr., and Seegal, D.: Natural History of Glomerulonephritis. J. Chron. Dis. 5: 3-13, 1957.
4Earle, D. P., Jr., and Seegal, D.: Natural History of Glomerulonephritis. J. Chron. Dis. 5: 3-13, 1957.
5Rammelkamp, C. H., and Weaver, R. S.: Acute Glomerulonephritis; Significance of the Variations in Incidence of Disease. J. Clin. Invest. 32: 345-358, April 1953.
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TABLE 76.-Variations in incidence of nephritis following scarletfever observed in four hospitals
| Author | Year |
| Nephritis (percent) |
Granud | 1890 | 668 | 7.2 |
| 1913 | 1,338 | 2.2 |
| 1937 | 259 | 3.5 |
| 1938 | 208 | 1.4 |
| 1939 | 1,298 | 2.6 |
| 1946 | 338 | 1.5 |
Hunter | 1904 | 114 | 2.6 |
| 1905 | 135 | .7 |
| 1906 | 179 | 1.6 |
| 1907 | 220 | 5.0 |
Joe and Williamson | 1920 | --- | 1.4 |
| 1921 | --- | 2.7 |
| 1922 | --- | 1.3 |
| 1923 | --- | 2.1 |
| 1924 | --- | 4.6 |
| 1925 | --- | 4.9 |
Peters and Cullum | 1910-14 | 2,771 | 1.9 |
| 1915-19 | 1,329 | 1.9 |
| 1920-24 | 2,496 | 2.5 |
| 1925-29 | 3,148 | .9 |
| 1930-34 | 2,427 | .4 |
| 1935-36 | 1,350 | 3.2 |
Source: Rammelkamp, C. H., and Weaver, R. S.: AcuteGlomerulonephritis; Significance of the Variations in Incidence of Disease. J.Clin. Invest. 32: 345-358, April 1953.
of hypersensitivity in man may also cause glomerulonephritis.These include disseminated lupus erythematosus, polyarteritis from unknowncauses, and variants of these phenomena due to hypersensitivity to penicillin,to the sulfonamides, and to other drugs.
The clinical course of acute glomerulonephritis (figs. 40 and41) is also extremely variable. It may be manifested only by hematuria andproteinuria which may go entirely unnoticed. At the other end of the spectrum,the disease may occur suddenly and with severity. Oliguria, marked hematuria,hypertension, edema, and convulsions may all be present. In some cases, theinitial attack may be followed by progressive diminution in renal function andby death from uremia or hypertensive cardiovascular disease. In others, thepatient may enter a so-called latent phase with minimal proteinuria andhematuria, which may persist without other manifestations. Chronicglomerulonephritis does follow well-documented attacks of acute disease, butmany cases of chronic glomerulonephritis give no history of such an acuteattack. In these cases, which undoubtedly have been smoldering for months oryears before brought to the physician's attention, the
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pathology is somewhat different. Indeed, Ellis6 believesthat the history and pathology in these instances are distinct enough to suggestthat the disease itself may be different. It is entirely possible, however, thatthe underlying etiologic factors are the same but that the resultant differencesin clinical picture and pathology may reflect failure to note the earlyinflammatory response and the difference in the degree and rate of change.Glomerulonephritis-latent, subacute, or chronic-may be characterized byexacerbations. These may follow reinfection with the hemolytic streptococcus butmay also be related to other infections, to trauma, or to stress.
Pathophysiology of glomerulonephritis-Thevariability inthe clinical course is paralleled by variability in the pathophysiology of theacute disease. Mild inflammatory change in the glomeruli may be reflected onlyby proteinuria and slight hematuria. In the more severe cases, the rate ofglomerular filtration is decreased out of proportion to diminution in tubular
6Ellis, A.: Natural History of Bright's Disease:Clinical Histological and Experimental Observations (Croonian Lectures). Lancet1: 1, January 1942.
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function. The proteinuria is thought to be the result ofincreased permeability of the glomerular capillaries, but since there may begeneralized edema some authors have suggested that the disease may actuallyrepresent generalized capillary changes. The evidence for this idea is not good,however, and it is possible to explain the generalized edema by retention ofsodium secondary to diminution in rate of filtration with continued ingestion ofsalt and water. This explanation may also account for the hypertension, thehypervolemia, and the congestive failure that occur in some of these patients.With marked inflammatory change, decrease in rate of filtration leads tooliguria, and although tubular function remains good the urine may be of highspecific gravity. Some degree of hypertension occurs in 50 percent ofhospitalized patients with acute glomerulonephritis, and this in part may beexplained by hypervolemia. In addition, however, in many instances it mustrepresent "true renal hypertension." Patients with severe disease maymanifest striking anemia. This has been shown in part7to be due todecreased survival of circulating red cells. With the onset of uremia,
7Emerson, C. P.: Pathogenesis of Anemia in Acute Glomerulonephritis; Estimations of Blood Production and Blood Destruction inCase Receiving Massive Transfusions. Blood 3: 363-372, April 1948.
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it undoubtedly represents both decreased survival of theerythrocytes and depression of the bone marrow.8 Congestive heart failure isdue to both hypervolemia and hypertension. In some instances, Aschoff bodieshave been found in the myocardium of patients with acute glomerulonephritis, butit is questionable whether primary myocardial involvement is a significantfactor in the heart failure. The nephrotic syndrome may be a strikingmanifestation of any stage of glomerulonephritis.
Treatment.-Treatment of the acute phase ofglomerulonephritis is relatively nonspecific. Although the use of penicillinfollowing streptococcal infections appears to decrease the incidence ofsubsequent nephritis,9 there is little evidence that penicillinmodifies the course once the full-blown disease has appeared. Bed rest duringthe acute phase appears to be the treatment of choice, as long as evidence ofactivity is manifested by fever, marked hematuria, tachycardia, or elevation ofthe sedimentation rate. In the presence of oliguria and edema, the diet shouldbe low in sodium. If oliguria is severe and prolonged and marked retention ofnitrogen occurs, the patient should be treated like any other patient with acuterenal failure. Congestive heart failure may be prevented by the drasticlimitation of salt and water, but, once this complication has ensued, digitalismay be indicated. The anemia of acute glomerulonephritis does not requiretreatment unless it becomes severe (hematocrit below 25). Under suchcircumstances, treatment should be by infusion of small amounts of freshlydrawn, packed red blood cells. Rest in bed should be continued until allevidence of activity of the disease has subsided. Once the temperature andsedimentation rate have returned to normal, however, there is little evidencethat bed rest per se over a period of more than 6 weeks modifies the course ofthe disease.
Although the adrenal corticosteroids have achieved strikingtherapeutic results in the treatment of the nephrotic stage ofglomerulonephritis, their use in the treatment of acute nephritis has beendisappointing.10 The treatment of chronicglomerulonephritis is beyond the scopeof this chapter. There is little that can be done for the underlying diseaseexcept to prevent exacerbations. Treatment of the renal failure accompanyingchronic glomerulonephritis is a complex problem and must be carefullyindividualized.11
INCIDENCE
The data on the incidence of nephritis during World War IIare difficult to collect. Most of the reports include nephritis under the broadcategory of
8Scheitlin, W., and Merrill, J. P.: Pathogenesis of Anemiain Chronic Rental Failure. [Unpublished data.]
9Rammelkamp, C. H., Jr.: Prevention of Acute Nephritis. Ann.Int. Med. 43: 511-517, September 1955.
10(1) Thorn, G. W., Merrill, J. P., Smith, S.III, Roche, M., and Frawley, T. J.: Clinical Studies With ACTH and Cortisone in Renal Disease. Arch.Int. Med.86: 319-354, September 1950. (2) Burnett, C. H., Greer, M. A., Burrows, B. A., Sisson, J. H., Reiman, A. S., Weinstein, L. A., and Colburn, C. G.: The Effect of Cortisone on the Course of AcuteGlomerulonephritis. New England J. Med. 243: 1028-1032, 1950.
11Merrill, John P.: The Treatment of Renal Failure:Therapeutic Principles in the Management of Acute and Chronic Uremia. NewYork: Grune & Stratton, Inc., 1955.
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cardiovascular renal disease. Of those for which theinformation is broken down, few give any information beyond the number of casesadmitted. Preliminary data are available, however, from the Medical StatisticsDivision, Office of The Surgeon General, U.S. Army. These are shown for theyears 1942-45 as the number of admissions per year per 1,000 average troopstrength for the various theaters (table 77).
Approximately 6,100 admissions for nephritis were reportedduring the 4 war years. Of 4,800 admissions for nephritis that were specifiedas acute or chronic during the 4-year period, 35 percent were labeled acute,giving a ratio for chronic nephritis to acute nephritis of approximately 2 to 1.Data indicating the extent to which nephritis appeared as a secondary diagnosisare available for 1944 and 1945 only. For these 2 years combined, the totalincidence (cases admitted for nephritis plus cases admitted for another causewith nephritis as a secondary diagnosis) in the entire Army exceeded theadmissions for nephritis by about 50 percent.
TABLE 77.-Admissions for nephritis in the U.S.Army, by area or theater and year, 1942-45
[Preliminary data based on sample tabulations of individual medical records]
[Rate expressed as number of admissions per year per 1,000 average strength]
Area of theater | 1942-45 | 1942 | 1943 | 1944 |
|
Continental United States | 0.27 | 0.26 | 0.24 | 0.25 | 0.35 |
Overseas: |
|
|
|
|
|
| Europe | 0.24 | 0.16 | 0.22 | 0.13 | 0.34 |
| Mediterranean1 | .23 | .22 | .22 | .25 | .20 |
| Middle East | .29 | .33 | .32 | .43 | 0 |
| China-Burma-India | .15 | .34 | .63 | .17 | .09 |
| Southwest Pacific | .15 | .37 | .17 | .11 | .15 |
| Central and South Pacific | .11 | .16 | .18 | .11 | .06 |
| North America2 | .25 | .35 | .31 | .15 | .15 |
| Latin America | .20 | .26 | .17 | .21 | .14 |
|
| 0.20 | 0.24 | 0.23 | 0.15 | 0.23 |
|
| 0.24 | 0.26 | 0.24 | 0.20 | 0.28 |
1Includes North Africa.
2Includes Alaska and Iceland.
3Includesadmissions on transports.
The data in table 77 are somewhat difficult to interpretsince the admission rates were for all types of nephritis and not limited toacute glomerulonephritis. In 1944-45, for example, nearly 45 percent of theadmissions for nephritis were diagnosed as chronic glomerulonephritis and 25percent as acute glomerulonephritis. Approximately 30 percent were unclassified.Thus, although it appears that admission rates were con-
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sistently lower in the Pacific theaters than in the continental United Statesand in Europe, a fact which is contrary to the criteria listed in table 75, itis not certain that this comparison is valid for acute glomerulonephritis.12It is probable also that diagnostic facilities and medical admissions forurinary abnormalities differed in the continental United States and in thePacific theaters.
Table 78 compares the incidence of rheumatic fever, scarlet fever, andstreptococcal sore throat. The data here are based on sample tabulations ofindividual medical records. Incidence data (new admissions plus secondary cases)for rheumatic fever and nephritis are not available for 1942-43. However,the extent to which incidence exceeded admissions in the U.S. Army, worldwide,in 1944-45 (for rheumatic fever, incidence exceeded new admissions by about 10percent; for nephritis, incidence exceeded new admissions by approximately 50percent), may be used as a rough approximation to incidence. These data suggest,although they do not conclusively prove, that the incidence of both rheumaticfever and nephritis was lower in the Southwest Pacific Area and theChina-Burma-Indiatheater than in the continental United States and Europe. The interpretationhere is open to the same criticisms raised in the preceding paragraphs. The datain table 78 also suggest that the increase or decrease in the yearly incidenceof rheumatic fever and nephritis in the continental United States and Europevaried independently in each disease. The variation, however, appeared to be inthe same direction in the China-Burma-India theater. The relationship betweenthe incidence of rheumatic fever and scarlet fever, in terms of variation ofyearly rates, appeared to be roughly the same in the continental United States.Variations in incidence in scarlet fever bore no apparent relationship tothat of nephritis. Thus, the table gives some hint that incidence of rheumaticfever and scarlet fever in the continental United States may follow roughlythe same trend, but there is little correlation in other areas. This discrepancypoints up again the observation that there are nephritogenic strains of Group Astreptococci and that apparently the epidemic streptococci of World War II wereless capable of producing nephritis and rheumatic fever and erythema (scarletfever). It should be noted, however, that before the end of 1944 scarletfever was a poor index of the presence of streptococcal disease generally.
The relative rarity of nephritis is borne out by an examination of extractsfrom the medical service reports of various general hospitals in the
12In contrast are the epidemics of acute glomerulonephritis atthe U.S. Naval Training Center, Bainbridge, Md., early in World War II and again during the winter of 1951-52. The data unfortunately are available only forthe latter outbreak (Annual Report, Commission on Acute Respiratory Disease,Armed Forces Epidemiological Board, 1952-53). During this time, cases of glomerulonephritis outnumbered those of rheumatic fever by 2 to 1. It wasfound that nearly half the cases of exudative pharyngitis at Bainbridge weredue to Group A, type 12 streptococci, and there was a close association betweeninfections due to this type of streptococcus and the subsequent developmentof acute nephritis. During a control study involving approximately 400patients, 15 cases of acute nephritis occurred following type 12 streptococcalinfections, but no cases were observed after infections with types 3, 6, or 19.-J.P. M.
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[Preliminary data based on sample tabulations of individualmedical records]
[Rate expressed as number per year per 1,000 average strength]
Year and area | Rheumatic fever2 | Scarlet fever | Streptococcal sore throat | Nephritis2 |
| |
|
|
|
|
Continental United States | 0.58 | 1.08 | (3) | 0.26 |
Europe | .33 | .41 | (3) | .16 |
Southwest Pacific | .46 | 1.26 | (3) | .37 |
China-Burma-India | .23 | 1.26 | (3) | .34 |
| |
|
|
|
|
Continental United States | 1.29 | 2.43 | (3) | .24 |
Europe | .31 | .44 | (3) | .22 |
Southwest Pacific | .26 | .17 | (3) | .17 |
China-Burma-India | .48 | .40 | (3) | .63 |
| |
|
|
|
|
Continental United States | 1.12 | 1.93 | .82 | .25 |
Europe | .43 | .65 | .31 | .13 |
Southwest Pacific | .36 | .03 | .34 | .11 |
China-Burma-India | .26 | .06 | .62 | .17 |
| |
|
|
|
|
Continental United States | .50 | .98 | 3.58 | .35 |
Europe | .50 | .59 | 1.13 | .34 |
Southwest Pacific | .38 | .01 | .94 | .15 |
China-Burma-India | .20 | .09 | 1.15 | .09 |
1Rates shown for rheumatic fever and nephritis are in termsof new admissions and for which the diagnosis indicated was the primary cause ofadmission; whereas, for scarlet fever and streptococcal sore throat the ratesare incidence rates (include secondary cases as well as new admissions).
2Incidence data are available only for 1944 and 1945. Duringthis period, for the Army as a whole, the incidence of rheumatic fever exceededthe new admissions by about 10 percent, and the incidence of nephritis exceededthe new admissions by approximately 50 percent.
3Data are not available.
Zone of Interior and from oversea theaters. In general, thediagnosis of glomerulonephritis accounted for 5 percent or less of alladmissions. Of those patients in whom a diagnosis of renal disease was made,renal and ureteral calculi were the most frequent cases. Usually, the incidenceof chronic glomerulonephritis exceeded that of acute glomerulonephritis.Occasionally, glomerulonephritis was seen following bacterial endocarditis,sensitivity to sulfonamides, and disseminated lupus erythematosus. The pathologyand clinical course did not appear to differ significantly from cases seen incivilian installations. The preponderance of diagnoses of chronic glo-
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merulonephritis over acute may reflect a disease that was notpresent upon induction, or more probably the progression of a disease whoseonly manifestation, proteinuria, was missed on the examination of the urine atinduction. This fact points up again the insidious onset of this form of adisease which has led some observers to believe it to be of different etiology.
The incidence of renal disease in Army Air Forcesinstallations was comparable. In one Army Air Forces regional hospital of 500beds, 117 cases of renal disease in men aged from 18 to 38 were reported over a12-month period. The majority of these were renal calculi and congenitalanomalies of the kidney with and without evidence of infection. Of theremainder, 35 were cases of acute pyelonephritis, of mixed idiopathicalbuminuria, and only 2 of acute glomerulonephritis.
Prognosis.-Deaths from nephritis from all theatersand areas per year per 100,000 average troop strength are shown in table 79.Although these overall figures are not broken down with regard to the acute andthe chronic forms, extracts of reports from various general hospitals indicateagain as in civilian life that deaths from chronic nephritis greatly exceededthose from the acute phase. About one-half of the number of patients admittedfor nephritis in World War II received separation for disability. Although dataon separations due to nephritis are not yet available, the cited figure may beregarded as a close approximation to the number of cases receiving separationdue to disability from nephritis.
TABLE 79.-Deaths from nephritis in U.S. Army, by area and year, 1942-45
[Rate expressed as number of deaths per yearper 100,000 average strength]
Area |
| 1942 | 1943 | 1944 | 1945 |
Continental United States | 0.9 | 1.0 | 1.2 | 0.8 | 0.4 |
Overseas | 1.1 | 1.2 | 1.1 | 1.1 | 1.1 |
|
| 1.0 | 1.1 | 1.1 | 0.9 | 0.8 |
TYPES
Field nephritis.-Two types of nephritis of particularinterest to the military deserve special mention. Trench nephritis, also calledfield or war nephritis, was reported in World War I and was suggested as aspecial entity. It was said to be characterized by frequent presence ofbronchitis and dyspnea, by sudden onset of uremic manifestations, and by anextraordinarily low mortality. It is of interest that this represented about 5percent of medical diseases admitted and was strikingly more frequent than acutenephritis in a general civilian hospital. The author of one report13noted
13Fitz, R.: Trench Nephritis at a British General Hospital in France. Mil. Surgeon 45: 80-98, July 1919.
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that it occurred most commonly among relatively old soldiers.This author did believe that acute nephritis, of which "trench nephritis"appeared to be a variant, was more common in France than in the United States.In no case, it was said, was there evidence for believing that the diseaseshowed any chronic progressive tendency and recovery was the rule.
In World War II, field or war nephritis again receivedconsiderable attention. In several reports,14 it is represented as ofincreased incidence in the German Army, and it is mentioned as "quite aproblem in the German Army in Italy during the winter of 1944-45."Although German concepts at that time favored a virus etiology, there was noevidence to support this view. Many authors noted massive edema without some ofthe other features of the nephrotic syndrome, notably proteinuria. Thismay perhaps have been due to the poor state of nutrition in the troops. Twolater reports from Holland15 stressed the increased incidence of acuteglomerulonephritis with a tendency to appear in epidemic form, in which thedisease characteristically occurred in older patients and was manifestedby massive edema. The similarity of these "epidemics" to "trenchnephritis or war nephritis" was noted.
Since at least one epidemic occurred among politicalprisoners, it is possible that here, too, poor nutrition played a role. Asurvey of extracts of reports from the various general hospitals in the overseatheaters bore out the impression that acute hemorrhagic nephritis was morefrequent among prisoners of war. The fact that substandard nutrition may havehad something to do with this is suggested by a report from a generalhospital in the Zone of Interior, in which it is noted that asymptomaticsubacute and chronic glomerulonephritis was discovered in a considerablenumber of prisoners returned from both Japanese and German camps.16 Therepeated emphasis on its occurrence in soldiers in whom the elasticity oftissues may have been poorer than in soldiers in the younger age group mayagain explain the massive edema. German medical officers stressed the factthat a history of recently antecedent nasopharyngitis due to hemolyticstreptococcal infection was rare, and these officers considered that suddenchilling or wetting played an important role as a precipitating etiologicfactor in field nephritis. Most American medical officers did not considerthis disease a separate entity but rather a modification by environment anddietary circumstances of the ordinary type of acute glomerulonephritis. It maybe noted that typical field nephritis did not occur in any appreciable
14(1) Essential Technical Medical Data, Mediterranean Theater of Operations, U.S. Army, for May 1945, dated 1 June 1945. (2) Semiannual Report, Chief Consultant in Medicine, Office of the Chief Surgeon, European Theater of Operations, U.S. Army, 1 Jan.-30 June 1945, Exhibit D, Report on Acute Nephritis in Prisoners-of-War; Exhibit E, Report on Survey of Edema of Undetermined Etiology ("Trench Nephritis").
15(1) Klein, F.: Acute Glomerulonephritis. Acta med. scandinav. 129: 156-163, 1947. (2) Formijne, P.: On an Epidemic of Acute Glomerulonephritis in Amsterdam. Acta med. scandinav. 129: 509-512, 1948.
16Annual Report, Schick General Hospital, 1945.
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amount in American troops who were in contact with theGermans in the northern Apennines during the winter of 1944-45.
Nephritis in scrub typhus.-A second type of nephritis ofsome interest was that seen with scrub typhus. Albuminuria, diminished renalfunction, and even azotemia were not uncommon in epidemic typhus.17Theautopsied cases of scrub typhus showed evidence of interstitial nephritis invarying degrees. The kidneys were usually swollen and congested18 withcharacteristic focal interstitial lesions and occasionally evidence of severevascular damage and glomerular injury. The glomeruli were not uniformlyaffected, however, but some definitely showed increased cellularity and ischemia.Occasionally, clinical manifestations were those of acute glomerulitis withnumerous granular casts and erythrocytes. An occasional death in uremia isreported in this disease, but where mentioned it seems to be as much due todehydration and hypotension with generalized vascular collapse as to renaldisease per se.
SUMMARY
In general, experience with glomerulonephritis inthe Army did not differ from that in civilian life.
The incidence of acute glomerulonephritis in World War IIwas rather low and was exceeded by a number of other renal diseases, ofwhich congenital defects and renal calculi predominated.
The diagnosis of chronic glomerulonephritis was somewhatmore frequent than the diagnosis of acute glomerulonephritis, emphasizing theinsidious nature of the former.
So-called trench or field nephritis, although thought by someto differ in etiology and clinical manifestations, was probably acuteglomerulonephritis possibly modified by the poor nutritional status of many ofthe patients in whom it was seen.
Interstitial nephritis with some of the manifestations ofacute glomerulonephritis was seen occasionally in scrub typhus, but was rarelythe primary cause of death.
17Yeomans, A., and others: Azotemia in Typhus Fever. Ann. Int. Med. 23: 711-753, November 1945.
18Settle, E. B., Pinkerton, H., and Corbett,A. J.: Pathologic Study of Tsutsugamushi Disease (Scrub Typhus) WithNotes on Clinicopathologic Correlation. J. Lab. & Clin. Med. 30: 639-661,August 1945.
