Tsunemichi Suzuki

IMMUNE COMPLEX‐MEDIATED GLOMERULONEPHRITIS AND INTERSTITIAL PNEUMONIA SIMULATING GOODPASTURE'S SYNDROME

An autopsy case of what was clinically considered to be Goodpastures syndrome was Investigated. The lung had hemorrhagic interstitial pneumonia, showing granular patterns of IgG and C3 along the alveoli by the immunofluo‐rescent method and electron‐dense subepithelial deposits by electron microscopy. The kidney had crescentic and segmental necrotizing glomerulonephritis associated with membranous nephropathy. Uneven, continuous patterns of immunofluorescent IgG and C3 along the GBM were noted. Electron microscopy showed numerous subepithelial deposits, and immunoelectron microscopy revealed that IgG was not present in the GBM itself but present in the subepithelial deposits. Anti‐GBM antibody activity was not detected in the serum or the kidney eluate. It was suggested that renal and pulmonary lesions occurred through the same mechanism and in association with immune deposits. We propose that there is a disease having immune complex‐mediated renal and pulmonary lesions which clinically resembles the conventional Goodpastures syndrome.

Congenital mesoblastic nephroma

For more than a decade congenital mesoblastic nephroma of infancy has been recognized as an entity different from Wilms tumor in its clinical and histopathologic features. However, this tumor is sometimes confused with Wilms tumor and consequently, inadvertent and vigorous therapy compatible with that for Wilms tumor is given. we reviewed the literature and analyzed 90 cases of congenital mesoblastic nephroma in the English and Japanese literature. The importance of early and accurate histopathologic diagnosis of the resected specimen to avoid inappropriate post-operative therapy is emphasized, and the peculiar features of congenital mesoblastic nephroma are characterized.

AN ADULT CASE OF PRIMARY PULMONARY HYPERTENSION; AS COMPARED WITH AN ADULT CASE OF PATENT DUCTUS BOTALLI AND EXPERIMENTAL VASOPRESSIN PULMONARY THROMBOARTERIOPATHY OF THE RABBIT

According to SPENCER, the first case of a “ primary arterial disorder confined to the lung” had been repoIted by MONCKEBERG in 1907. Since then, reported cases of “ primary pulmonary hypertension ” as well as “ secondary ” due to a fore-going cardiovascular anomaly have increased in number. Although the peculiar arterial changes called as the “ plexiform ”, “angiomatoid”, “ glomoid ” or “ glomerulus-like ” structures or the “ arteriovenous shunts ”, etc, have been reported by several authors, the essential changes of the pulmonary arteries in these disorders are now believed to be thrombosclerotic in nature. On the other hand, DUGUID’S fascinating thrombosclerotic concept on coronary sclerosis have been followed by many experimental studies on arterial thrombosclerosis of the lung. Recently, we have had a chance to study almost simultaneously a case of this disorder and a case of “ secondary pulmonary hypertension ”, each of which was a woman of 38 years. Furthermore, YAJIMA observed experimental systemic pulmonary thrombosis of the rabbit induced by YANO with Vasopressin. This report is the result of observations on thrombosclerotic lesions of the lnug found in these materials.

An Autopsy Case of Parainfectious Encephalomyelitis

The case was that of a 31-year-old house wife who was admitted to our First Hospital. In early April, 1960, she had numbness below the waist and also pain in the back, associated with a fever . She was, however, able to walk at that time. Soon later she developed sensory paralysis and paresis of both legs, resulting in abasia. In the middle of May, 1960, she was admitted to a hospital in Noda City, and a diagnosis of viral myelitis was made through the examination of her spinal fluid. She received corticosteroid for the following week, and her symptoms were much improved. She was then discharged from the hospital on June 28, 1960. In late July, 1960, she developed herpes zoster on the right shoulder and the left side of the chest, associated with a fever of 38°C and abasia. During her second hospitalization the same treatment as before had been given with some improvement of her symptoms. In the middle of September, 1960, she suddenly developed severe pain over the waist, and it recurred once a week during the following two months. Since January 1, 1961, she had noticed progressive hyposthesia and rectovesical disturbance. She was, then, unable to rise from her bed owing to marked general weakness, On February 4, 1961, she was admitted to the medical clinic of our First Hospital. Upon admission, no psychological finding nor opticaI symptom was recognized. The upper half of her body was free of any paralysis in sensation or motion. Both legs showed flaccid paralysis. No abnormality was demonstrated with her abdominal and Achilles tendon reflexes. Pathological reflexes were present. Laboratory examination revealed negative serology test for syphilis and neutrophilia in her entire clinical course. The polio-neutralizing antibody titer was lower than 8. Lumbar puncture yielded water-clear fluid with a pressure of 120mmH20, a cell count of 11/3 and a protein of 2 fractions. Her family and past histories were non-contributory.

AN AuTOPSY CASE OF “FAMILIAL CARDIOMEGALY”

An autopsy case of a 27 year old male with gigantic heart of unknown etiology and with evidence of familial occurrence, which might be classified to “familial cardiomegaly” (EVANS) was reported.