THE ENTITY of lower nephron nephrosis is now well established, even though the name, coined by Lucké,1 is a new one. It is a syndrome of severe oliguria or anuria following an initial shocklike picture and producing renal insufficiency, which in a large proportion of cases progresses to death in uremia. In many, but not all, cases an additional causative factor is trauma to muscles or red blood cells which allows hemoglobin or myoglobin or their derivatives to circulate in the plasma and be excreted in the urine. Since these compounds are less soluble in acid than in neutral or alkaline solutions, they tend to precipitate as casts in the lower nephron where concentration and acidification take place and may block the tubular lumens in this region or damage the tubular cells.2 The kidneys in these cases are edematous, the cortex being pale and swollen in contrast
HOFFMAN WS, MARSHALL D. MANAGEMENT OF LOWER NEPHRON NEPHROSIS: Report of Six Cases. Arch Intern Med (Chic). 1949;83(3):249–270. doi:10.1001/archinte.1949.00220320003001
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