Abstracts Hemoglobinemia and Hemoglobinuria

HEMOGLOBINEMIA AND HEMOGLOBINURIA JOSEPH F. ROSS, M.D. HEMOGLOBIN PRECIPITATION IN RENAL TUBULES. A STUDY OP ITS CAUSES AND Eppacrs. Yuile, C. L. , Gold, M. A., and Hinds, E. G.: J. Exper. Med. 82.’ 361-74, 1945. Yuile and his collaborators report a continuation of their well conceived and carefully controlled studies of the mechanism of hemoglobin excretion and its effects on the kidney. They point out that in their experience injections of large amounts of purified solutions of hemoglobin do not produce hemoglobin casts or tubular blockage in normal rabbits, regardless of whether the urine is acid or alkaline, an observation confirmed by several other investigators. However, injection of hemoglobin solutions into rabbits with pre-existing tubular damage (produced by clamping the renal artery for a period of i to 2.5 minutes or by injecting sodium tertrate solution) resulted in definite impairment of kidney function. In rabbits with alkaline urine this renal dysfunction was transient and did not result in death. In animals with acid urine extreme renal failure, uremia, and death occurred. Hemoglobin casts were few in number and soon disappeared from the tubules in the animals with alkaline urine, but were numerous, persistent and ‘indicative of tubular blockage’ ‘ in the acidunic rabbits. It was of interest that in instances of extreme pre-existing tubular damage (produced by sodium tantrate) hemoglobin casts were not found, even in animals with very acid urine. In such instances hemoglobin probably was not excreted by the kidney and thus did not enter the tubular lumina. The authors conclude that the ultimate outcome in any given instance of hemoglobinunia is dcpendent upon a fine balance between the degree of renal injury and the level of hemoglobinunia, as well as upon the pH of the urine. ‘ RENAL DAMAGE FROM FERROHEME PIGMENTS MYOGLOBIN, HEMOGLOBIN, HEMATIN. Coreoran, A. C. , and Page, I. H..Texas Reports on Biol. & Med. 3? 52.8-44, 1945. In an attempt to elucidate the etiology of the renal failure occurring in cases of crush injury and transfusion reaction, investigations were made of renal function following injections of myoglobin, metmyoglobin, hemoglobin and hematin into aciduric dogs. Renal function was evaluated from studies of the clearances of diodrast and inulin, and of the tubular secretory capacity for diodnast. Unfortunately the hemoglobin solutions used were simply solutions of lysed dog red blood cells and undoubtedly contained possible toxic substances other than hemoglobin. Solutions of purified pigments would have been more desirable. Control studies on dogs with alkaline urine are not reported. Renal function was impaired in all experiments, regardless of whether hemoglobin, myoglobin or metmyoglobin was injected, and consisted in an immediate decrease in the tubular secretory capacity followed by a reduction in the renal plasma flow and in the glomerular filtration rate. Impaired function in some instances was greater 48 hours after the injection than during the period of myoglobinunia and persisted in mild degree for the two week period of the study. The renal injury was not severe enough to produce uremia or death, and anatomical studies are not reported. Hematin was extremely’ toxic when injected intravenously and produced death from shock” when given in a dose of 31.6 mg. per Kg. It apparently produced intense effenent anteniolan vasoconstniction in the kidney, glomerular damage, and a marked decrease in renal plasma flow and tubular secretion. Uremia developed in an animal which received the injection of a smaller dose. The authors attribute the renal injury to (i) obstruction of the tubules by pigment (although they did not demonstrate such obstruction), (i) ingestion of the pigment by tubular cells with resulting impairment of tubular secretory activity (no evidence was presented that ingestion of pigment interferes with tubular function), and ( ) “cytotoxic distal tubular activity of intratubularly liberated hematin.” 2.57 For personal use only. on September 23, 2017. by guest www.bloodjournal.org From