Mending the Valve, Burdening the Kidney: A Case of Renal Hemosiderosis With Mitral Valve Repair.

Renal hemosiderosis, marked by the buildup of hemosiderin in the renal cortex due to chronic intravascular hemolysis, can lead to acute kidney injury. Iron deposited may exacerbate renal damage through processes like lipid peroxidation and free radical formation, impacting cellular function and precipitating renal disease. Although seen commonly with chronic intravascular hemolysis in the setting of sickle cell anemia, thalassemia, and in the setting of prosthetic cardiac valves. While acute renal failure following prosthetic cardiac valve placement is relatively uncommon, some cases of renal injury in the setting of mechanical hemolysis have been reported, in the postsurgical period, typically within 2 weeks. In this case report, we present a 67-year-old male patient, following mitral valve repair, who developed anemia within 2 weeks of the repair. Evaluation with echocardiography did not initially show findings of worsening mitral regurgitation, however, his anemia and kidney function worsened over the next 6 months. Further evaluation, during that time showed worsening mitral valve regurgitation in repeated echocardiography, with renal hemosiderosis confirmed via kidney biopsy, revealing glomerulosclerosis with hemosiderin deposits. Due to persisting anemia and worsening kidney function, the patient is being planned for a mitral valve replacement. The potential recovery of renal function remains uncertain. Despite the common occurrence of intravascular hemolysis following prosthetic valve placement or valve repair, only a few cases of acute renal failure have been reported. In these cases, severe hemolytic anemia developed shortly after surgery, within 2 weeks, with increased levels of creatinine, even reported as high as 8.2 mg/dL and renal biopsy revealed acute tubular injury and widespread tubular hemosiderosis, resembling the findings in the index case. Diagnosis depends on the evaluation of anemia, showing signs of hemolysis, with echocardiology findings of worsening valvular abnormalities, and kidney biopsy findings showing hemosiderin deposits. Treatment strategies encompass the management of anemia alongside considerations for either mitral valve replacement or repair. This case underscores the importance of considering the possibility of renal hemosiderosis, associated with mitral valve repair. The delay in diagnosis observed in this case is not uncommon, and timely recognition becomes pertinent to prevent irreversible renal injury and improve long-term outcomes.