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Chapter XIV

Contents

CHAPTER XIV

Nephritis

John P. Merrill, M.D.

An evaluation of nephritis occurring in the military during World War II must necessarily be considered in the light of our knowledge of the disease in general, since there appears to be little difference in its various aspects between military and civilian experience. In this discussion, we shall concern ourselves principally with glomerulonephritis.

GLOMERULONEPHRITIS

Etiology-The present evidence for the etiology of glomerulonephritis implicates an immune response in which the glomeruli are primarily involved by inflammatory change. The disease can be produced experimentally in rats by the injection of rabbit serum from animals who have been previously immunized to a homogenate of rat kidney.1 Other hyperimmune reactions involving small vessels generally may also affect the glomeruli by inflammatory change. Such changes have been produced by hypersensitivity to the sulfonamides.2 The disease in man appears to be closely associated with an antecedent infection by so-called nephritogenic strains of the hemolytic streptococcus. The lag period between infection with the streptococcus and the onset of nephritis probably represents development of an immune process, similar to that found in the experimental animal. Interpretation of animal and human data suggests that in some fashion renal tissue and streptococcal protein combine to form an antigen, the immunologic reaction to which produces the inflammatory changes.3 This protein has been tagged by tracer substances and actually found to be localized in the glomeruli. In this way, an autoantibody is produced and may help to explain the continuing progress of the disease in some clinical situations long after the initial infection has subsided.

Clinical aspects.-In man, glomerulonephritis also appears to be preceded by infection with the Group A hemolytic streptococcus. This correlation, however, is not a perfect one since frequently a history of previous

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.


386

streptococcal infection cannot be obtained; in addition, well-documented cases of nephritis have followed infection with other micro-organisms, such as the pneumococcus. Undoubtedly, however, the hemolytic streptococcus is the prime offender, and the analogy with rheumatic fever and previous streptococcal infection is an interesting one. Probably both represent hyperimmune responses to previous infection with the streptococcus. There are, however, striking differences as shown in table 75.4 Whereas rheumatic fever rather consistently occurs in about 3 percent of hemolytic streptococcal infections, the rate for nephritis is extremely variable (table 76).5 A survey of the literature indicates that the percentage of nephritis following scarlet fever varies from 0 to 18 percent. Furthermore, nephritis may occur in pseudoepidemics. These variations in incidence suggest to one author that the streptococcus may vary in its nephritogenic properties. In the United States, type 12, and to a lesser extent type 4 of Group A, streptococci have been usually associated with this complication.

The latent period following streptococcal infection as well as the drop in serum complement during the acute phase again suggest the possibility of hypersensitivity to this organism or to a product thereof. Other forms

TABLE 75.-Biological differences between glomerulonephritis 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.


387

TABLE 76.-Variations in incidence of nephritis following scarlet fever observed in four hospitals

Author

Year


Number of cases of scarlet fever

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.: Acute Glomerulonephritis; 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 unknown causes, 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 and 41) is also extremely variable. It may be manifested only by hematuria and proteinuria 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, the initial attack may be followed by progressive diminution in renal function and by death from uremia or hypertensive cardiovascular disease. In others, the patient may enter a so-called latent phase with minimal proteinuria and hematuria, which may persist without other manifestations. Chronic glomerulonephritis does follow well-documented attacks of acute disease, but many cases of chronic glomerulonephritis give no history of such an acute attack. In these cases, which undoubtedly have been smoldering for months or years before brought to the physician's attention, the


388

FIGURE 40.-Photomicrograph, acute glomerulonephritis. Note epithelial crescent, erythrocytes in Bowman's space, and slightly increased cellularity of the tuft. There is protein precipitate in the tubules with some cells and cell debris, There are also interstitial edema and increased cellularity of the interstitial tissue. [Description, courtesy Dr. G. J. Dammin.]

pathology is somewhat different. Indeed, Ellis6 believes that the history and pathology in these instances are distinct enough to suggest that the disease itself may be different. It is entirely possible, however, that the underlying etiologic factors are the same but that the resultant differences in clinical picture and pathology may reflect failure to note the early inflammatory response and the difference in the degree and rate of change. Glomerulonephritis-latent, subacute, or chronic-may be characterized by exacerbations. These may follow reinfection with the hemolytic streptococcus but may also be related to other infections, to trauma, or to stress.

Pathophysiology of glomerulonephritis-The variability in the clinical course is paralleled by variability in the pathophysiology of the acute disease. Mild inflammatory change in the glomeruli may be reflected only by proteinuria and slight hematuria. In the more severe cases, the rate of glomerular 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). Lancet 1: 1, January 1942.


389

FIGURE 41.-Photomicrograph, acute glomerulonephritis. Note epithelial proliferation of the glomerular tuft, the interstitial edema, and protein precipitate in the tubules. [Description, courtesy Dr. G. J. Dammin.]

function. The proteinuria is thought to be the result of increased permeability of the glomerular capillaries, but since there may be generalized edema some authors have suggested that the disease may actually represent generalized capillary changes. The evidence for this idea is not good, however, and it is possible to explain the generalized edema by retention of sodium secondary to diminution in rate of filtration with continued ingestion of salt and water. This explanation may also account for the hypertension, the hypervolemia, and the congestive failure that occur in some of these patients. With marked inflammatory change, decrease in rate of filtration leads to oliguria, and although tubular function remains good the urine may be of high specific gravity. Some degree of hypertension occurs in 50 percent of hospitalized patients with acute glomerulonephritis, and this in part may be explained by hypervolemia. In addition, however, in many instances it must represent "true renal hypertension." Patients with severe disease may manifest striking anemia. This has been shown in part7 to be due to decreased 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 in Case Receiving Massive Transfusions. Blood 3: 363-372, April 1948.


390

it undoubtedly represents both decreased survival of the erythrocytes and depression of the bone marrow.8 Congestive heart failure is due to both hypervolemia and hypertension. In some instances, Aschoff bodies have been found in the myocardium of patients with acute glomerulonephritis, but it is questionable whether primary myocardial involvement is a significant factor in the heart failure. The nephrotic syndrome may be a striking manifestation of any stage of glomerulonephritis.

Treatment.-Treatment of the acute phase of glomerulonephritis is relatively nonspecific. Although the use of penicillin following streptococcal infections appears to decrease the incidence of subsequent nephritis,9 there is little evidence that penicillin modifies the course once the full-blown disease has appeared. Bed rest during the acute phase appears to be the treatment of choice, as long as evidence of activity is manifested by fever, marked hematuria, tachycardia, or elevation of the sedimentation rate. In the presence of oliguria and edema, the diet should be low in sodium. If oliguria is severe and prolonged and marked retention of nitrogen occurs, the patient should be treated like any other patient with acute renal failure. Congestive heart failure may be prevented by the drastic limitation of salt and water, but, once this complication has ensued, digitalis may be indicated. The anemia of acute glomerulonephritis does not require treatment unless it becomes severe (hematocrit below 25). Under such circumstances, treatment should be by infusion of small amounts of freshly drawn, packed red blood cells. Rest in bed should be continued until all evidence of activity of the disease has subsided. Once the temperature and sedimentation rate have returned to normal, however, there is little evidence that bed rest per se over a period of more than 6 weeks modifies the course of the disease.

Although the adrenal corticosteroids have achieved striking therapeutic results in the treatment of the nephrotic stage of glomerulonephritis, their use in the treatment of acute nephritis has been disappointing.10 The treatment of chronic glomerulonephritis is beyond the scope of this chapter. There is little that can be done for the underlying disease except to prevent exacerbations. Treatment of the renal failure accompanying chronic glomerulonephritis is a complex problem and must be carefully individualized.11

INCIDENCE

The data on the incidence of nephritis during World War II are difficult to collect. Most of the reports include nephritis under the broad category of

8Scheitlin, W., and Merrill, J. P.: Pathogenesis of Anemia in 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 Acute Glomerulonephritis. 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. New York: Grune & Stratton, Inc., 1955.


391

cardiovascular renal disease. Of those for which the information is broken down, few give any information beyond the number of cases admitted. Preliminary data are available, however, from the Medical Statistics Division, Office of The Surgeon General, U.S. Army. These are shown for the years 1942-45 as the number of admissions per year per 1,000 average troop strength for the various theaters (table 77).

Approximately 6,100 admissions for nephritis were reported during the 4 war years. Of 4,800 admissions for nephritis that were specified as 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 diagnosis are available for 1944 and 1945 only. For these 2 years combined, the total incidence (cases admitted for nephritis plus cases admitted for another cause with nephritis as a secondary diagnosis) in the entire Army exceeded the admissions 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


1945

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


Total overseas3

0.20

0.24

0.23

0.15

0.23


Total Army

0.24

0.26

0.24

0.20

0.28


1Includes North Africa. 
2Includes Alaska and Iceland. 
3Includes admissions on transports.

The data in table 77 are somewhat difficult to interpret since the admission rates were for all types of nephritis and not limited to acute glomerulonephritis. In 1944-45, for example, nearly 45 percent of the admissions for nephritis were diagnosed as chronic glomerulonephritis and 25 percent as acute glomerulonephritis. Approximately 30 percent were unclassified. Thus, although it appears that admission rates were con-


392

sistently lower in the Pacific theaters than in the continental United States and in Europe, a fact which is contrary to the criteria listed in table 75, it is not certain that this comparison is valid for acute glomerulonephritis.12 It is probable also that diagnostic facilities and medical admissions for urinary abnormalities differed in the continental United States and in the Pacific theaters.

Table 78 compares the incidence of rheumatic fever, scarlet fever, and streptococcal sore throat. The data here are based on sample tabulations of individual 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 10 percent; for nephritis, incidence exceeded new admissions by approximately 50 percent), may be used as a rough approximation to incidence. These data suggest, although they do not conclusively prove, that the incidence of both rheumatic fever and nephritis was lower in the Southwest Pacific Area and the China-Burma-India theater than in the continental United States and Europe. The interpretation here is open to the same criticisms raised in the preceding paragraphs. The data in table 78 also suggest that the increase or decrease in the yearly incidence of rheumatic fever and nephritis in the continental United States and Europe varied independently in each disease. The variation, however, appeared to be in the same direction in the China-Burma-India theater. The relationship between the incidence of rheumatic fever and scarlet fever, in terms of variation of yearly rates, appeared to be roughly the same in the continental United States. Variations in incidence in scarlet fever bore no apparent relationship to that of nephritis. Thus, the table gives some hint that incidence of rheumatic fever and scarlet fever in the continental United States may follow roughly the same trend, but there is little correlation in other areas. This discrepancy points up again the observation that there are nephritogenic strains of Group A streptococci and that apparently the epidemic streptococci of World War II were less capable of producing nephritis and rheumatic fever and erythema (scarlet fever). It should be noted, however, that before the end of 1944 scarlet fever was a poor index of the presence of streptococcal disease generally.

The relative rarity of nephritis is borne out by an examination of extracts from the medical service reports of various general hospitals in the

12In contrast are the epidemics of acute glomerulonephritis at the 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 for the 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 was found that nearly half the cases of exudative pharyngitis at Bainbridge were due to Group A, type 12 streptococci, and there was a close association between infections due to this type of streptococcus and the subsequent development of acute nephritis. During a control study involving approximately 400 patients, 15 cases of acute nephritis occurred following type 12 streptococcal infections, but no cases were observed after infections with types 3, 6, or 19.-J. P. M.


393

TABLE 78.-Morbidity rates1 of rheumatic fever, nephritis, and certain streptococcal infections among U.S. Army personnel stationed in selected areas, by year, 1942-45

[Preliminary data based on sample tabulations of individual medical records]
[Rate expressed as number per year per 1,000 average strength]

Year and area

Rheumatic fever2

Scarlet fever

Streptococcal sore throat

Nephritis2


1942

 

 

 

 

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


1943

 

 

 

 

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


1944

 

 

 

 

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


1945

 

 

 

 

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 terms of new admissions and for which the diagnosis indicated was the primary cause of admission; whereas, for scarlet fever and streptococcal sore throat the rates are incidence rates (include secondary cases as well as new admissions).
2Incidence data are available only for 1944 and 1945. During this period, for the Army as a whole, the incidence of rheumatic fever exceeded the new admissions by about 10 percent, and the incidence of nephritis exceeded the new admissions by approximately 50 percent.
3Data are not available.

Zone of Interior and from oversea theaters. In general, the diagnosis of glomerulonephritis accounted for 5 percent or less of all admissions. Of those patients in whom a diagnosis of renal disease was made, renal and ureteral calculi were the most frequent cases. Usually, the incidence of chronic glomerulonephritis exceeded that of acute glomerulonephritis. Occasionally, glomerulonephritis was seen following bacterial endocarditis, sensitivity to sulfonamides, and disseminated lupus erythematosus. The pathology and clinical course did not appear to differ significantly from cases seen in civilian installations. The preponderance of diagnoses of chronic glo-


394

merulonephritis over acute may reflect a disease that was not present upon induction, or more probably the progression of a disease whose only manifestation, proteinuria, was missed on the examination of the urine at induction. This fact points up again the insidious onset of this form of a disease which has led some observers to believe it to be of different etiology.

The incidence of renal disease in Army Air Forces installations was comparable. In one Army Air Forces regional hospital of 500 beds, 117 cases of renal disease in men aged from 18 to 38 were reported over a 12-month period. The majority of these were renal calculi and congenital anomalies of the kidney with and without evidence of infection. Of the remainder, 35 were cases of acute pyelonephritis, of mixed idiopathic albuminuria, and only 2 of acute glomerulonephritis.

Prognosis.-Deaths from nephritis from all theaters and 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 and the chronic forms, extracts of reports from various general hospitals indicate again as in civilian life that deaths from chronic nephritis greatly exceeded those from the acute phase. About one-half of the number of patients admitted for nephritis in World War II received separation for disability. Although data on separations due to nephritis are not yet available, the cited figure may be regarded as a close approximation to the number of cases receiving separation due 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 year per 100,000 average strength]

Area


1942-45

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


Total Army

1.0

1.1

1.1

0.9

0.8


TYPES

Field nephritis.-Two types of nephritis of particular interest to the military deserve special mention. Trench nephritis, also called field or war nephritis, was reported in World War I and was suggested as a special entity. It was said to be characterized by frequent presence of bronchitis and dyspnea, by sudden onset of uremic manifestations, and by an extraordinarily low mortality. It is of interest that this represented about 5 percent of medical diseases admitted and was strikingly more frequent than acute nephritis in a general civilian hospital. The author of one report13 noted

13Fitz, R.: Trench Nephritis at a British General Hospital in France. Mil. Surgeon 45: 80-98, July 1919.


395

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 disease showed any chronic progressive tendency and recovery was the rule.

In World War II, field or war nephritis again received considerable attention. In several reports,14 it is represented as of increased incidence in the German Army, and it is mentioned as "quite a problem in the German Army in Italy during the winter of 1944-45." Although German concepts at that time favored a virus etiology, there was no evidence to support this view. Many authors noted massive edema without some of the other features of the nephrotic syndrome, notably proteinuria. This may perhaps have been due to the poor state of nutrition in the troops. Two later reports from Holland15 stressed the increased incidence of acute glomerulonephritis with a tendency to appear in epidemic form, in which the disease characteristically occurred in older patients and was manifested by massive edema. The similarity of these "epidemics" to "trench nephritis or war nephritis" was noted.

Since at least one epidemic occurred among political prisoners, it is possible that here, too, poor nutrition played a role. A survey of extracts of reports from the various general hospitals in the oversea theaters bore out the impression that acute hemorrhagic nephritis was more frequent among prisoners of war. The fact that substandard nutrition may have had something to do with this is suggested by a report from a general hospital in the Zone of Interior, in which it is noted that asymptomatic subacute and chronic glomerulonephritis was discovered in a considerable number of prisoners returned from both Japanese and German camps.16 The repeated emphasis on its occurrence in soldiers in whom the elasticity of tissues may have been poorer than in soldiers in the younger age group may again explain the massive edema. German medical officers stressed the fact that a history of recently antecedent nasopharyngitis due to hemolytic streptococcal infection was rare, and these officers considered that sudden chilling or wetting played an important role as a precipitating etiologic factor in field nephritis. Most American medical officers did not consider this disease a separate entity but rather a modification by environment and dietary circumstances of the ordinary type of acute glomerulonephritis. It may be 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.


396

amount in American troops who were in contact with the Germans in the northern Apennines during the winter of 1944-45.

Nephritis in scrub typhus.-A second type of nephritis of some interest was that seen with scrub typhus. Albuminuria, diminished renal function, and even azotemia were not uncommon in epidemic typhus.17 The autopsied cases of scrub typhus showed evidence of interstitial nephritis in varying degrees. The kidneys were usually swollen and congested18 with characteristic focal interstitial lesions and occasionally evidence of severe vascular damage and glomerular injury. The glomeruli were not uniformly affected, however, but some definitely showed increased cellularity and ischemia. Occasionally, clinical manifestations were those of acute glomerulitis with numerous granular casts and erythrocytes. An occasional death in uremia is reported in this disease, but where mentioned it seems to be as much due to dehydration and hypotension with generalized vascular collapse as to renal disease per se.

SUMMARY

In general, experience with glomerulonephritis in the Army did not differ from that in civilian life.

The incidence of acute glomerulonephritis in World War II was rather low and was exceeded by a number of other renal diseases, of which congenital defects and renal calculi predominated.

The diagnosis of chronic glomerulonephritis was somewhat more frequent than the diagnosis of acute glomerulonephritis, emphasizing the insidious nature of the former.

So-called trench or field nephritis, although thought by some to differ in etiology and clinical manifestations, was probably acute glomerulonephritis possibly modified by the poor nutritional status of many of the patients in whom it was seen.

Interstitial nephritis with some of the manifestations of acute glomerulonephritis was seen occasionally in scrub typhus, but was rarely the 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) With Notes on Clinicopathologic Correlation. J. Lab. & Clin. Med. 30: 639-661, August 1945.

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