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KMID : 0381219700020080023
Journal of RIMSK
1970 Volume.2 No. 8 p.23 ~ p.27
PATHOLOGIC PHYSIOLOGY OF ACUTE RENAL FAILURE


Abstract
A review on pathlogic physiology of acute renal failure is made by comparing functional derangements and structural alterations. Functional alterations are divided into oliguric and diuretic phases, and morphologic alterations in each phase are discussed to explain morphologic basis for functional alterations.
The oliguric phase is eminenced by marked reduction or total absence of the urinary output and loss of proximal contvoluted tubular functions, such as loss of concentrating power of urea and creatinine, loss of ability to conserve electrolytes, and loss of ability to extract PAH from the blood. The basis for the reduction of urinary output is considered to be due to reduction of renal blood flow resulting into lowered glomerular filtration, and other possibilities, such as backflow of filtered urine through damaged tubules, tubular obstruction by heme casts, or increased intra-renal pressure, are also considered but unlikely. The tubular functional changes are explained on the basis of morphologic alterations of entire length of the tubule especially proximal convoluted .segments, and two types of tubular lesions, nephrotoxic and tubulorrehxic, are discussed.
The recovery from acute renal failure is initiated as diuresis. However, the complete restoration of the tubular functions wil take several weeks to months. The time interval is required for the maturation of regenerated tubular epithelial cells to restore damaged tubular cells. Even after full clinical recovery, renal function may remain below the lower limits of the normal in some cases, and this is explained on the basis of permanent loss of some nephrons especially in cases of tubulorrhexic type of damage. The initiation of diuresis is considered to be due to the relatively rapid recovery of renal blood flow to glomeruli resulting into normal or sometimes increased filtration, in the face of continuous impairment of tubular water absorption due to persistent tubular
damage.
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