Serum TCII levels were determined in 57 patients with acute and chronic renal failure. They were divided into 3 groups, group I was malarial patients with acute renal failure, group II and III were patients with acute renal failure and chronic renal failure from other underlying causes, respectively. All patients in group I had serum TCII over 2000 pg/ml while these values were within the normal limits in the other 2 groups. These findings indicated that elevated serum TCII occurred only in malarial patients with acute renal failure. The clearance and urinary excretion of TCII in malarial patients were found to be lower and increased to the normal levels after recovery from azotemia, indicating that the failure of excretion of TCII by the kidneys may be responsible for elevated serum TCII levels. The pathophysiological changes in the kidneys in malarial patients may reduce the amount of filtered TCII-B12 through the glomeruli and decrease TCII-B12 uptake by the renal tubules resulting in the decreased TCII degradation by tubular cells. Therefore, the intravascular TCII survival is prolonged with elevated serum TCII levels in these patients.