A CASE REPORT OF BILATERAL RENAL CORTICAL NECROSIS

Abstract

A 29 year-old gravida 1, par 1 was completely asymptomatic until 36 weeks' gestation. On Oct. 2, 1969, she was admitted to the department of Obstetrics and Gynecology of our hospital because of severe abdominal pain and profuse genital bleeding.
Urgent operation by Cesarian section was done with delivery of a dead male fetus. Histerectomy was followed for severe postpartum bleeding. On the next day (Oct. 3, 1969), she was transferred to our department due to postoperative anuria. Blood pressure was 140/90mmHg. and blood examinations were as follows: RBC 279×10⁴, Ht. 27.1%, WBC 12900, serum Na 133mEq/L., K 6.8mEq/L., CL 87mEq/L., Ca 9.0mg/dl., T. P. 5.3g/dl., Alb. 2.6g/dl., Ureanitrogen 41mg/dl., Creatinine 4.1mg/dl. and CO₂ 25mEq/L.
Open biopsy on the right kidney performed 28 hours after the onset of genital bleeding revealed a remarkably decreased renal blood flow. Histologically, renal cortex including interstitial cells was almost necrotized. Hyaline-like thrombi filled the capillary loops of glomeruli as well as the interlobular arteries. The characteristic pathological findings were that the thrombi in the interlobular arteries did not pack the lumen completely leavning some spaces.
Moreover, these vessels were frequently dilated and there were, in places, diapedesis of red cells into the media. VanGieson's elastica stain showed that their internal elastic laminae were elongated, frayed and fragmented. Renal cortical necrosis was diagnosed.
Repeated hemodialysis was performed on the fouth, tenth and seventeenth day of anuria. On twentieth day after the onset of anuria, she passed out urine of about 240ml per day.
The clinical course was showed in Fig. 1.
Hemodialysis gradually improved the patient's conditions to such an extent that she could sit up. On the 54th hospital day, aortography was performed. Main renal artery was clearly outlined with no obstruction. Succeeding interlobar arteries were slightly twisted and their shadows abruptly interrupted in their peripheries. Only a few opacified interlobular arteries were also twisted and showed a lack in smoothness in their internal walls. Nephrogram was not obtained.
On Nov. 26, 1969 (56th hospital day), the patient died suddenly probably of cardiac arrest due to pulmonary edema. The autopsy carried out three hours after death revealed: The right kidney weighed 110gr., the left 126gr.; the cortex (two milimetres thick) was yellowisch-white, whereas the medulla was bluish red with normal papillae.
Histologically, normal architecture of the cortex was completely lost except in a very thin subcapsular area and in juxta-medullary zone. The greater part of the cortex was shrunken and transformed into dense connective tissue. The smaller, interlobular arteries were destructed and almost absent. Walls of only a few remained interlobular arteries were consisted from degenerative cells and their lumens were either empty or occasionally containing few red cells. The larger arcuate arteries were almost intact, while the smaller segments of them were filled with organized occlusive thrombi, some of which showed recanalization. Thrombi revealed various features from containing cells to organizing. The larger renal arteries, main renal artery and interlobar arteries were distinctly free from pathological changes.
We discussed on the pathogenesis of bilateral cortical necrosis in our own case from the point of renal morphological findings obtained by open biopsy, autopsy and renal angiography, comparing with the reports in the literatures.
Based on the above mentioned arterial changes, especialy the destructive changes in the walls of interlobular arteries, it may be assumed that primarily the necrosis occurred in the vessels prior to the occurance of necrosis in the surrounding tissues.