American journal of diseases of children

ZUELZER, WOLF W.; CHARLES, SEYMOUR; KURNETZ, RUBEN; NEWTON, WILLIAM A.; FALLON, RICHARD

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030008001pmid: 14798944

INTRODUCTION IN INFANTS parenchymal diseases of the kidneys other than those associated with congenital anomalies, pyelonephritis and tumors are regarded as rarities. In this age group glomerulonephritis is uncommon and renal disease of vascular origin is virtually unknown. The experience in our laboratory over the last 10 years indicates, however, that a variety of major injuries to the renal parenchyma, based on vascular disturbances, occur in infants with sufficient frequency to warrant attention. Between 1940 and 1950 there were 40 cases of major renal disease associated with vascular dysfunction seen among 2,058 autopsies performed on infants and children in this department. This group does not include cases of renal infarct or focal embolic glomerulonephritis secondary to bacterial endocarditis. Of the 40 patients, 34 were infants. In the same 10 year period 18 patients with acute or chronic glomerulonephritis were studied at autopsy, and only two of these were under 2

ZUELZER, WOLF W.; KURNETZ, RUBEN; CHARLES, SEYMOUR

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030009002

SYMMETRICAL cortical necrosis of the kidneys has been regarded as uncommon at any age. Until recently only about 100 cases have been published.1 The occurrence of symmetrical cortical necrosis of the kidneys in infants was unknown until 1949, when Campbell and Henderson2 described two instances, one in a 5 month old infant, the other in a 9 week old infant. Originally the disturbance was thought to be a specific complication of pregnancy, but it is now clear that it can occur in either sex at any age. According to the comprehensive review by Duff and Murray,1 the etiology of symmetrical cortical necrosis is varied. Of the cases in which pregnancy was not a factor, the majority seem to have been associated with acute infection, such as diphtheria, scarlet fever, pneumonia or malaria. Poisoning with a variety of substances, shock following trauma, extreme dehydration and purpura have also

ZUELZER, WOLF W.

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030022003

UNDER the term acute glomerular thrombosis we report briefly two cases that have certain similarities to the cases of symmetrical necrosis in that the intrarenal blood flow is interrupted but differ from them in that the site of the circulatory obstruction is clearly in the glomeruli and the mechanism consists in the formation of thrombi in the glomerular capillary loops. The condition, which seems to represent a complication of certain severe bacteremias and appears to depend on the presence of micro-organisms within the glomerular capillaries, has received little attention since Blackman and Rake1 described it under the title "acute pneumococcal nephritis." One of the cases (case 4) reported as symmetrical cortical necrosis in a young infant by Campbell and Henderson2 seems to fall in this category. Since the renal lesion is associated with severe infection, the development of clinical manifestations is often cut short by death of the

ZUELZER, WOLF W.

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030025004

ARTERIOLAR necrosis of the kidneys is a lesion found characteristically in malignant hypertension. To our knowledge this condition has not been previously reported as occurring in infancy. Our case material includes two cases of arteriolar necrosis. One of these, case 14, has been reported elsewhere in detail.1 This was an instance of a peculiar glomerulonephritis in an 8 year old boy who after nephrectomy for an embryoma of one kidney had received intensive radiation therapy over an area that included the remaining kidney. He had died with signs of hypertension and renal failure. The glomeruli were found to be obliterated, and the tubules, dilated and atrophic, and the arterioles throughout showed fibrinoid necrosis and often were surrounded by small hemorrhages. The vascular changes were interpreted as secondary to the combination of hypertension and uremia resulting from the severe generalized glomerular obstruction. The second case in this group concerns an

ZUELZER, WOLF W.; KURNETZ, RUBEN; NEWTON, WILLIAM A.

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030028005

FEW REFERENCES concerning occlusion of the renal arteries by embolism or thrombosis in infants can be found in the recent literature. Gross1 reported two such cases in 1945 and pointed out that arterial embolism and thrombosis in infancy are likely to be commoner than indicated by the number of published cases. Morrison2 in the same year described total ischemic infarction of one kidney in an infant with thrombosis of the abdominal aorta ascribed to a peculiar arteritis. Blockage of a renal artery leads to albuminuria and passage of blood and casts in the urine. Azotemia, oliguria and anuria and uremia will follow if both renal arteries are affected. The diagnosis of arterial occlusion of the kidneys is difficult unless emboli with resultant infarction appear in the extremities. Our material contains, in addition to cases of localized infarcts secondary to bacterial endocarditis, five instances of total renal infarction due

ZUELZER, WOLF W.

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030032006

THE EFFECTS of gradual or incomplete occlusion of the renal arteries or their branches are not as well known as are those of sudden complete blockage of the arterial circulation. Whereas the latter situation leads to acute necrosis and, if enough renal parenchyma is destroyed, to death of the organism, lower degrees of arterial obstruction may permit survival of tissue elements but in time will lead to atrophy and other retrogressive changes. In a recent paper, Christofersen and Hirsch1 have called attention to this sequence of events which may result from a variety of pathological processes associated with gradual occlusion of intrinsic renal arteries. In such a kidney the nephrons decrease in size and ultimately revert to fetal characteristics. The loss of function of the atrophic nephrons leads to progressive renal failure and death in uremia. One may postulate that the nephrons of a kidney in which the blood

ZUELZER, WOLF W.; KURNETZ, RUBEN; FALLON, RICHARD

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030034007

IT WAS pointed out by Barenberg 1 that the physicians of the nineteenth century regarded thrombosis of the renal veins as a common occurrence in young infants. For several decades of the present century, however, little attention was paid to this condition. In 1941 Barenberg and his associates reported five cases discovered among 25 autopsies of infants with epidemic diarrhea of the newborn. More recently Morrison reported briefly the summaries of 18 cases.2 Another series of four cases was reported by Fallon.3 Her series included a patient in whom the diagnosis of bilateral thrombosis of renal veins was made on clinical grounds and who survived, although at the end of a three month follow-up period the blood urea nitrogen level was still elevated. Campbell and Mathews,4 and Sandblom5 each reported what appear to be the only successful cases of surgical removal of the infarcted kidney in

ZUELZER, WOLF W.; KURNETZ, RUBEN

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030045008pmid: 14798951

IN THE preceding article it was pointed out that thrombosis of the renal veins is not necessarily associated with infarction and, on the other hand, that hemorrhage into the renal parenchyma is not invariably accompanied with thrombosis. Apart from hemorrhage into the renal substance occurring as part of a generalized bleeding tendency such as characterizes leukemia, hemophilia or purpura, massive hemorrhage in the renal parenchyma is sometimes observed in the absence of visible structural changes in the veins of the kidney. Our observations suggest, however, that the mechanism in these cases bears a close relationship to that of venous thrombosis. Our case material contains two pertinent instances of massive destruction of kidney substance by hemorrhage, both occurring in young infants. In the first of these, case 34, the patient, a 3 month old girl, had died from pneumococcic meningitis after an illness of two days' duration preceded by diarrhea. The

ZUELZER, WOLF W.; KURNETZ, RUBEN

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030046009

A DISCUSSION of lower nephron nephrosis and presentation of cases is included conveniently in this series of articles although the exact role of vascular factors on its pathogenesis is by no means established. It is generally assumed, however, that circulatory disturbances within the kidney play an important role in the development of the renal lesions.1 Lower nephron nephrosis has become familiar in recent years through the studies of Bywaters2 in England and Lucke1 in this country, who proposed the name which has come into general usage. Originally described during World War I, the condition was rediscovered during World War II when Bywaters explored the nature of renal symptoms observed in victims of crushing injuries. Lower nephron nephrosis has also been reported following nontraumatic ischemia of muscle, heat stroke, burns, transfusion reactions, malarial hematinuria (blackwater fever), sulfonamide intoxication and poisoning with mushrooms and other vegetable and chemical substances.

GRULEE, CLIFFORD G.; CLARK, EARL H.

1951 American journal of diseases of children

doi: 10.1001/archpedi.1951.02040030054010

THE OCCURRENCE of two deaths from an outbreak of thallotoxicosis involving four children who attended the same preschool nursery is herein reported. Although thallium was discovered in 1861 by Crookes,1 its toxicity was not recognized for some years. Initially thallium acetate was used internally to combat night sweats in tuberculous patients,2 and later it was employed for the treatment of ringworm infection of the scalp. In 1931 Lubin introduced thallium acetate in a depilatory cream, under the trade name of koremulu. Numerous cases of poisoning were reported from its use. Most poisonings, however, have occurred as a result of the internal use of thallium acetate as a depilatory in the treatment of ringworm in children. Thallium poisonings in industry also have been recorded. In 1920 thallous sulfate was introduced in Germany as a rodenticide under the trade name of zelio. The German literature3 contains reports of both