Hemolysis and acute kidney failure

Abstract

Deposits of iron and hemosiderosis in the kidney have been observed in diseases with intravascular hemolysis, including paroxysmal nocturnal hemoglobinuria, and valvular heart diseases and prosthetic heart valve implants. However, the decrease in kidney function associated with hemolysis caused by cardiac valvular disease or prostheses is less well recognized. We present a case of intravascular hemolysis after repair and banding of the mitral valve that resulted in massive renal tubular deposition of hemosiderin with decreased kidney function. We discuss the pathophysiologic process of both acute and chronic tubular injury from heme and heme proteins, including injury to organelles resulting in autophagic vacuoles containing damaged organelles, such as mitochondria. We conclude that tubular injury resulting from heme proteins should be considered as a cause of decreased kidney function in all patients with a cardiac valvular disease or prosthesis.

Figure 1

(A) Hematoxylin and eosin and (B) periodic acid–Schiff sections show brown pigment deposits in the proximal tubular epithelial cells accompanied by tubular degeneration and necrosis. (C) Prussian blue iron stain shows hemosiderin deposits in the tubular epithelial cells (A-C: original magnification, ×20).

Figure 2

Electron microscopy of tubular epithelial cells shows groups of dark granules likely made up of heme proteins (white arrows) and autophagolytic lysosomal vacuoles (black arrows) containing mitochondria (original magnification, A: ×3,400; B: ×17,500). An apoptotic cell shedding into the tubular lumen also can be seen.