Cavh in Myorenal Syndrome

Abstract

Rhabdomyolysis describes the damage of striated muscle cell membranes which leads to fluid and electrolyte imbalances and to liberation of muscle components. The causes leading to rhabdomyolysis are numerous. The renal tubular overload with myoglobin can induce acute renal failure. The acute myoglobinuric renal failure in patients with crush- syndrome has been known since the first description by Bywaters and Beall (1941). This description gave rise to numerous reports on cases of acute renal insufficiency after traumatic or nontraumatic rhabdomyolysis. In about 8-20% of patients with rhabdomyolysis an acute myoglobinuric renal failure is observed. Myoglobinemia, toxic muscle cell membrane components, and alteration of renal perfusion lead to acute tubular necrosis. Circulatory collapse and shock represent additional factors in the pathogenesis of the acute renal failure (Bogaerts et al., 1982; Colombo et al., 1985; Grossmann et al., 1974; Hamilton et al, 1971; Hamilton et al., 1972; Kathrein et al., 1983; Koffler et al., 1976; Rowland and Penn, 1972; Sidorara et al., 1985). The usual therapy consists of adjustment of volume depletion and balancing of acid-base-electrolyte metabolism.