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 myeloma. Several trends in oncology, including increased survival, better supportive care, older patients who have received multiple chemotherapy regimens, and new therapeutic options, are driving an increase in the numbers of cancer patients who develop AKI. As a result, nephrologists should be increasingly familiar with the diagnosis, management, and treatment of AKI in this setting. Here, we summarize recent data on epidemiology of AKI in cancer patients, describe the most common AKI syndromes in this population, and highlight emerging areas in the growing field of onconephrology.

Predictors of Recurrent AKI

“…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.…”

Acute kidney injury in HCT: an update

“…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.…”

“…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).…”

“…The appearance of AKI is frequently prompted by a superimposed incident, such as sepsis. 50,52,53 Hepatic SOS is an event almost exclusively recognized in the setting of HCT, and is more commonly associated with myeloablative allogeneic HCT than with myeloablative autologous HCT. Factors associated with increased risk of hepatic SOS development include allogeneic transplant, high-dose chemotherapy, pretransplant liver abnormalities, abdominal radiation and poor functional status.…”

“…52 As many patients will recover spontaneously, treatment of hepatic SOS is mostly supportive with diuretics, transfusions, analgesics, paracentesis and dialysis if needed. 50 There are case reports 57,58 describing the use of tissue plasminogen activator, heparin or defibrotide for treatment but there are no large, randomized controlled trials to support their use in hepatic SOS.…”