Hemoglobinuric Nephrosis in Traumatic Shock

Rethinking Ischemic Acute Kidney Injury as Nephrotoxicity

“…Second, well-established findings demonstrating the presence of hemoglobin within renal tubules following ischemia appear to have been largely forgotten in much of the recent research into the complex etiology of ischemic AKI. 12–14 This new evidence provides a novel explanation for these findings, including the presence of hemoglobin in the distal tubules and urine of patients with ischemic AKI, even in those without elevated levels of circulating hemoglobin in the blood. 12 In a 1975 article on ischemic kidney injury in the Journal of the American Medical Association , Berman notes that “few syndromes have had as many names and periodic rediscoveries as acute tubular necrosis,” the parade of names illustrating the changing concepts of pathogenesis of ischemic AKI.…”

“… 12–14 This new evidence provides a novel explanation for these findings, including the presence of hemoglobin in the distal tubules and urine of patients with ischemic AKI, even in those without elevated levels of circulating hemoglobin in the blood. 12 In a 1975 article on ischemic kidney injury in the Journal of the American Medical Association , Berman notes that “few syndromes have had as many names and periodic rediscoveries as acute tubular necrosis,” the parade of names illustrating the changing concepts of pathogenesis of ischemic AKI. 15 Based on the evidence presented by McLarnon that red blood cell trapping mediates toxic injury to the outer medulla following kidney ischemia, it may be worth resurrecting the name “hemoglobinuric nephrosis,” at least in concept, to explain the pathogenesis of outer-medullary tubular injury in ischemic AKI.…”

Extravasation of Blood and Blood Toxicity Drives Tubular Injury from RBC Trapping in Ischemic AKI

“… 37–40 , 44 This is consistent with the typical gross appearance of the AKI kidney, in which the cortex is pale and cortical vessels are collapsed, while the outer-medulla appears dark red and the outer-medullary vessels are dilated. 3 , 4 , 8 , 25 , 45–47 While initially it was thought that the dusky red color of the outer-medulla represented medullary hyperemia, it has since become evident that the continued inflow of blood into the medulla during periods of kidney ischemia results in intense RBC congestion (RBC trapping) in the outer-medullary vasculature due to the failure of these medullary vessels to drain. 14 , 25 Why then, if cortical ischemia is severe and the medullary circulation continues to be perfused (at least initially as RBC trapping develops), is ischemic/hypoxic kidney injury largely restricted to the OM?…”

Centennial Changes in Surgical Care and Research

“…25 Consequently, the use of saline infusions and blood transfusions became common in the treatment of injured patients in World War II, but the volume of fluid required was still unappreciated, as indicated by the high occurrence rate of renal failure in patients with severe mechanical and thermal injuries (18.6% in 427 unselected autopsied battle casualties dying in Army hospitals in Italy in World War II). 26 Sulfonamides and other antimicrobials were synthesized and developed between the two world wars, and penicillin, discovered in 1928, finally became available in the early years of World War II. 27 These agents strikingly decreased wound infections and other infections in combat casualties in World War II.…”