Sinai P

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: CONCORD is a global program for worldwide surveillance of cancer survival. A recent analysis of the CONCORD-2 study shows a 9-10% lower survival rates for blacks affected by colon cancer (CC) as compared to whites in the US between 2001 and 2009.

Methods: We aim to investigate the differences in the survival of blacks and whites affected by CC in the National VA Cancer Cube Database in the same time-period. Overall, 30,196 CC cases between 2001 and 2009 were examined.

Results: 66.12% (19,967) of CC patients identified as white and 16.32% (4929) identified as black. The distribution of stages in blacks was the following: Stage 0: 10.49% (517), I: 25.10% (1237), II: 18.58% (916), III: 17.73% (874) and IV: 17.91% (883). By comparison, CC cases in whites presented as Stage 0: 8.92% (1781), I: 26.62% (5316), II: 22.29% (4450), III 18.75% (3744) and IV 13.71% (2738) (P value for X2 trend test = .021). Interestingly, in contrast to the results of the CONCORD study, the overall 5-year survival for all stages of CC in blacks and whites was similar [blacks: 2,854 (57.90%); whites 11,897 (59.58%); P = .2750]. The same holds true for the 5-year survival for Stage 0 [blacks: 423 (81.82%) whites: 1391 (78.10%); P = .5338], Stage I [blacks: 932 (75.34%) whites: 3973 (74.74%); P = .8667], Stage II [blacks: 605(66.05%) whites:2927 (65.78%); P = .9427], Stage III [blacks:509 (58.24%) whites:2138 (57.10%); P = .7513], Stage IV blacks:101 (11.44%) whites:364 (13.29%); P = .2058].

Conclusions: The racial disparity in survival highlighted in CONCORD-2 (9-10% lower 5-year survival for blacks) is not replicable in the VA system. This difference is likely due to the uniformity of the VA in providing screening and treatment services and in leveling the playing field in terms of access to care. We believe these results should be taken into consideration in the current discussion of the shape of the healthcare system the US should adopt.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.

Background: A 69-year-old male with history of stage IV left kidney clear cell carcinoma presented with 4-day history of gross hematuria, fever of 101.4 F and fatigue. He had been started on sunitinib, a VEGF Tyrosine Kinase Inhibitor (TKI) two weeks previously. Vitals were significant
for systolic BP of 160. Renal ultrasound showed perinephric hematoma. Labs were significant for platelets of 68,000, sodium of 120 and creatinine of 2.7 (baseline creatinine of 1.0). Urine sodium was less than 10 and 24 hours urine protein was 484 mg. Peripheral smear was negative for schistocytes. Renal biopsy performed after platelet infusion showed extensive interstitial inflammation with frequent eosinophils and interstitial edema, consistent with druginduced acute interstitial nephritis. He was started on oral steroids and required intermittent hemodialysis.

Discussion: This report describes the second known case of biopsy-proven sunitinib-induced acute interstitial nephritis (AIN). Similar case reports involving the VEGF-targeting drugs sorafenib (TKI), and bevacizumab (monoclonal antibody) imply a class effect. Previously reported renal adverse events of sunitinib include hypertension, proteinuria, renal insufficiency, and thrombotic microangiopathy; all present in this case except thrombotic microangiopathy. Thus, thrombocytopenia in this case may be secondary to bone marrow suppression.

Interestingly, while sunitinib is also used for the treatment of gastrointestinal stromal tumor (GIST) and pancreatic neuroendocrine tumors (PNET); thus far, cases of sunitinib-induced AIN have only been described in patients with metastatic renal cell carcinoma.

Given the risk of bleeding associated with a renal biopsy in the setting of thrombocytopenia on one hand; and the lethal complications that may ensue from delayed diagnosis and the possibility of permanent dialysis associated with AIN on the other, the decision to proceed with a renal biopsy is a controversial one and must be weighed carefully.

Conclusions: While sunitinib-induced AIN is exceedingly rare, it should be considered in patients with acute renal failure. Given the literature implicating VEGF-targeting drugs in cases of AIN, further study is required to elicit the link between the VEGF pathway and AIN.