ACUTE renal insufficiency, including the syndrome of lower nephron nephrosis, is characterized not only by retention of nitrogenous end-products but also by profound disturbance in fluid and electrolyte metabolism. Thorough understanding of the underlying pathophysiology is essential for the correct management of these patients. Bywaters1 renewed interest in the syndrome of acute renal insufficiency with his description of azotemia following crushing injuries. The pathologic changes, the pathogenesis, and the clinical picture have been summarized recently by Burch and Ray,2 Muirhead,3 Strauss,4 and Lucké.5
Since the maintenance of fluid and electrolyte equilibrium during the critical oliguric and early diuretic phase of lower nephron syndrome appears distinctly to influence the fatality rate, an effort has been made to study the nature of disturbances in these equilibria. Complete metabolic studies of sodium, potassium, chloride, nitrogen, and water balance were made in 5 cases of severe acute renal insufficiency for periods of 6 to 23