BACKGROUND: Focusing on glomerular thrombotic microangiopathy (TMA), we detected urinary podocytes to evaluate podocyte damage following glomerular endothelial cell injury. METHODS: We analyzed the relationship between urinary podocytes as biomarkers for podocyte injuries and clinical manifestations in five patients of anti-cancer-drug-induced glomerular TMA. RESULTS: Cancer in all five patients was advanced, including 4 cases of renal cell carcinoma treated with tyrosine kinase inhibitor, and one with intrahepatic bile duct carcinoma treated with gemcitabine. Urinary podocytes were detected in 2 cases that rapidly developed acute kidney injury (AKI) and nephrotic syndrome, while they were not detected in 3 cases of slowly progressive chronic renal failure. One case with AKI, presenting sequential manifestations of urinary podocytes, showed the decrease and disappearance of urinary podocytes in accordance with the cessation of the anti-cancer drug, followed by improvement in renal function and in clinical symptoms such as hypertension. CONCLUSIONS: These findings indicate that severe endothelial cell dysfunction during the acute phase of glomerular TMA leads to podocyte loss.
BACKGROUND: Focusing on glomerular thrombotic microangiopathy (TMA), we detected urinary podocytes to evaluate podocyte damage following glomerular endothelial cell injury. METHODS: We analyzed the relationship between urinary podocytes as biomarkers for podocyte injuries and clinical manifestations in five patients of anti-cancer-drug-induced glomerular TMA. RESULTS:Cancer in all five patients was advanced, including 4 cases of renal cell carcinoma treated with tyrosine kinase inhibitor, and one with intrahepatic bile duct carcinoma treated with gemcitabine. Urinary podocytes were detected in 2 cases that rapidly developed acute kidney injury (AKI) and nephrotic syndrome, while they were not detected in 3 cases of slowly progressive chronic renal failure. One case with AKI, presenting sequential manifestations of urinary podocytes, showed the decrease and disappearance of urinary podocytes in accordance with the cessation of the anti-cancer drug, followed by improvement in renal function and in clinical symptoms such as hypertension. CONCLUSIONS: These findings indicate that severe endothelial cell dysfunction during the acute phase of glomerular TMA leads to podocyte loss.