2012
DOI: 10.2215/cjn.03140312
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Onco-Nephrology

Abstract: SummaryAKI is common in patients with cancer, and it causes interruptions in therapy and increased hospital length of stay, cost, and mortality. Although cancer patients are susceptible to all of the usual causes of AKI in patients without cancer, there are a number of AKI syndromes that occur more frequently or are unique to this patient population. AKI also confers substantially increased risk of short-term death, and the ability to reverse AKI portends a better outcome in some cancers, such as multiple myel… Show more

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Cited by 115 publications
(97 citation statements)
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“…27 The improved survival along with advances in available, but potentially nephrotoxic therapies, has resulted in cancer becoming an increasingly important contributor to the changing AKI case mix. [28][29][30][31] Not surprisingly, the need to enhance our hospitalization with recurrent AKI (solid line) or death/hospice referral (dash-dotted line) as the first event experienced. The corresponding numbers and proportions of patients experiencing each event are shown in Table 2.…”
Section: Discussionmentioning
confidence: 99%
“…27 The improved survival along with advances in available, but potentially nephrotoxic therapies, has resulted in cancer becoming an increasingly important contributor to the changing AKI case mix. [28][29][30][31] Not surprisingly, the need to enhance our hospitalization with recurrent AKI (solid line) or death/hospice referral (dash-dotted line) as the first event experienced. The corresponding numbers and proportions of patients experiencing each event are shown in Table 2.…”
Section: Discussionmentioning
confidence: 99%
“…The incidence of hepatic SOS varies greatly among single-center case reports with a range of 5-60%; 50 the mean incidence reported in a recent meta-analysis was 13.7%. 51 Hepatic SOS is an early cause of AKI in HCT patients, usually encountered within the first month after HCT.…”
Section: Pathogenesismentioning
confidence: 99%
“…This injury causes obliteration of small intrahepatic venules and sinusoidal thrombosis, ultimately resulting in sinusoidal congestion, fibrosis and necrosis. 50,51 Patients clinically develop a syndrome constituted of hyperbilirubinemia, painful hepatomegaly, ascites, volume overload and AKI mirroring hepatorenal syndrome. AKI can occur in up to 80% of patients with SOS, but characteristically emerges only after the onset of the hepatic disease (as demonstrated by progressive hyperbilirubinemia).…”
Section: Pathogenesismentioning
confidence: 99%
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