急性腎不全の予後に関する臨床的検討 第2報 : 急性腎不全救命例における腎機能遠隔予後について

Abstract

In order to clarify the etiology and pathogenesis of acute renal failure, numerous studies have been carried out without definitive conclusion. On the other hand, mechanism and natural history on the recovery of renal function following acute renal failure has not been discussed sufficiently especially on the long-term prognosis of renal function. The author investigated on the recovery of renal function following acute renal failure due to tubular necrosis in 25 out of 26 survived cases experienced during the last 10 years at the Yokohama City University Hospital. In the most cases, BUN and serum creatinine stabilized to normal levels within 4-5 weeks after the onset of the renal shutdown with exception of 2 cases whose BUN and serum creatinine did not recover to normal levels. Chronic renal failure ensued in lout of these 2 cases. Renal function tests including phenolsulfonphthalein excretion test, clearance studies namely glomerular filtration rate and renal plasma flow recovered rapidly during first 3 months after the onset of renal shutdown followed by slow improvement up to 12 months. No more improvement was found thereafter. On the contrary, renal concentrating ability improved gradually up to 2 years. The author speculated that these rapid recovery of renal function during first 3 months was owing to release of vasoconstriction of the renal cortical vessels and slow improvement of renal function thereafter was owing to the functional maturation of the tubular epithelial cells. In 8 out of 17 cases, glomerular filtration rate recovered to normal level (over 90 ml/min.) after 1 year. In 8 cases, glomerular filtration rate remained below normal and 1 case glomerular filtration rate was severely depressed. Renal biopsy was carried out in 20 cases in the diuretic phase. Histopathologically, slight tubular degeneration and interstitial cell infiltrations were found in about half of the cases. However, there was no histological difference between the cases whose renal function recovered to normal and the cases whose renal function was subnormal. The pathogenesis of this permanent renal function disturbance in acute renal failure was studied in experimental canine models induced by administration of mercury chloride and/or by clamping the renal pedicles. Three days after administration of mercury chloride and/or clamping of the renal pedicles, BUN ranged 30.5 ± 12.1 mg/dl and 73.1 ± 14.8 mg/dl respectively. Recovery of renal function in the mercury chloride administered group was more delayed than that of the ischemic group. However, renal histology revealed almost complete recovery in both groups. From these experiments, the author could not obtain definitive conclusion concerning the reason why permanent disturbance of renal function ensued after acute renal shutdown.