心臓血管奇形,古いLöhlein型巣状腎炎そして限局性膜性増殖性糸球体腎炎

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  • 内田 俊和
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 佐々木 正典
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 申 連〓
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 三浦 継夫
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 五味 芳保
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 安藤 あつ子
    日本大学医学部病理学第一,第二講座,同内科学第二講座
  • 竹内 正
    日本大学医学部病理学第一,第二講座,同内科学第二講座

書誌事項

タイトル別名
  • Cardiovascular anomalies, old Löhlein type nephritis and segmental membrano-proliferative glomerulonephritsaensuing
  • シンゾウ ケッカン キケイ フルイ Lohleinガタ スジョウ ジンエン ソ
  • —An interpretation of relationship between these lesions at one autopsy case—
  • ―相互の病変の病理発生を検討する―

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抄録

With hand of an autopsy case (NA-5728), 28 years old male, an interpretation is given of the relationship between cardiocascular anomalies, sclerotic Lohlein nephritis and terminal membrano-proliferative glomerulonephritis in pathogenetic view. The cardiovascular anomalies are consisting of aorto-pulmonary window, VSD and a left side pulmonary artery delivered from the aorta, not from the pulmonary artery. There was also an endocarditis, still active locally, at the aortic valve which delivered emboli to give a splenic infarction and Lohlein focal nephritis. The cardiovascular anomalies of this type caused secondry pulmonary hypertension to form a plexiform lesion of the pulmonary artery and also severe hypoxgenemia. The serum level of Na ranged at 142 mE/l.It has been proven that 3 times positive blood cultures for viridans steeptococci were given at the age of 6 years old, though negative blood culture intensively done at terminal seriod. Serum com-plement level at the terminal was proven to be normal in which severe nephrotic syndrome was ensuing. <BR>As to the pathogenesis of renal lesions; sclerotic focal nephritis and membrano-proliferative glom erulonephritis it would be suggested that some alteration of immunological background occure in the past history. First positive viridans in culture turned negative in the later part of history. There are also causative processes of hemodynamic alteration involving hypoxia attributable to nephritic lesions. In case of congestive heart failure membranous nephritis was described to occur. Hypernatremia developed at the terminal period, though blood pressure ranged at the level 104/70 mmHg. <BR>Summerizing these congestive heart failure would play some role for triggering the membrano-proliferative glomerulonephritis at the end coinciding alteration of immunological state.

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