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Post-traumatic renal insufficiency is important as a cause of illness and death in initially surviving combat casualties and may be seen in civilian medical practice after accidents or extensive surgery. Hypotension appears to be a primary etiologic factor although delay in therapy, inadequate blood replacement, increase in plasma hemoglobin and other pigments, and the severity of the wound may contribute to the extent of renal damage and to the hypotension itself. Impairment of renal function following trauma may be reflected in different patients by sensitive clearance tesfts only, by azotemia and decreased urinary concentrating ability, by transient oliguria or by marked oliguria of varying duration. This suggests a wide variability in the extent of functional and parenchymal renal injury. With few exceptions, only the oliguric patients develop sufficient electrolyte abnormality or clinical uremia to require special care. In the latter instances rapidly progressive potassium intoxication necessitates prompt evacuation to a treatment center and, in the patients reported here, was the major cause of death prior to the use of hemodialysis. In addition to potassium intoxication, evidence that accelerated tissue catabolism characterizes post-traumatic renal insufficiency is found in (1) rapidly developing clinical uremia with corresponding rates of NPN accumulation, (2) early signs and marked degree of weight loss and emaciation, and (3) edema formation on less than conventional fluid intake allowances. The contrast with acute renal failure of non-traumatic origin has been repeatedly emphasized. Frequently occurring extensive and progressive infection, impaired wound healing and a marked bleeding tendency in some patients complicate the clinical course and intensify the therapeutic challenge.