Onco-Nephrology

Perazella, Mark A.

doi:10.2215/cjn.02780312

Cited by 276 publications

(213 citation statements)

References 43 publications

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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%

Predictors of Recurrent AKI

Siew

Parr

Abdel-Kader

et al. 2016

Journal of the American Society of Nephrology

133

114

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Recurrent AKI is common among patients after hospitalized AKI and is associated with progressive CKD. In this study, we identified clinical risk factors for recurrent AKI present during index AKI hospitalizations that occurred between 2003 and 2010 using a regional Veterans Administration database in the United States. AKI was defined as a 0.3 mg/dl or 50% increase from a baseline creatinine measure. The primary outcome was hospitalization with recurrent AKI within 12 months of discharge from the index hospitalization. Time to recurrent AKI was examined using Cox regression analysis, and sensitivity analyses were performed using a competing risk approach. Among 11,683 qualifying AKI hospitalizations, 2954 patients (25%) were hospitalized with recurrent AKI within 12 months of discharge. Median time to recurrent AKI within 12 months was 64 (interquartile range 19-167) days. In addition to known demographic and comorbid risk factors for AKI, patients with longer AKI duration and those whose discharge diagnosis at index AKI hospitalization included congestive heart failure (primary diagnosis), decompensated advanced liver disease, cancer with or without chemotherapy, acute coronary syndrome, or volume depletion, were at highest risk for being hospitalized with recurrent AKI. Risk factors identified were similar when a competing risk model for death was applied. In conclusion, several inpatient conditions associated with AKI may increase the risk for recurrent AKI. These findings should facilitate risk stratification, guide appropriate patient referral after AKI, and help generate potential risk reduction strategies. Efforts to identify modifiable factors to prevent recurrent AKI in these patients are warranted.

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Section: Discussionmentioning

confidence: 99%

Predictors of Recurrent AKI

Siew

Parr

Abdel-Kader

et al. 2016

Journal of the American Society of Nephrology

133

114

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“…Below, we review AKI specific to cancer patients. Chemotherapy-induced AKI will not be reviewed here, because it is the subject of the work by Perazella et al (19).…”

Section: Causes Of Aki In the Cancer Patientmentioning

confidence: 99%

“…In addition, hyperuricemia can cause AKI through crystal-independent mechanisms, such as renal vasoconstriction, reduced renal blood flow, reactive oxygen species, and inflammation (43). The management of TLS is reviewed elsewhere (19).…”

Section: Intrinsic Causesmentioning

confidence: 99%

Onco-Nephrology

Lam

Humphreys

2012

Clinical Journal of the American Society of Nephrology

115

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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.

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“…19 Previous interventions failed, because the renoprotective strategy either interfered with the chemotherapeutic efficacy of cisplatin or invoked a separate set of prohibitive side effects, such as immunosuppression in the case of global TNF blockade. Immunosuppression is particularly problematic given the immunocompromised state of many patients with malignancy receiving chemotherapy.…”

mentioning

confidence: 99%

Competing Actions of Type 1 Angiotensin II Receptors Expressed on T Lymphocytes and Kidney Epithelium during Cisplatin-Induced AKI

Zhang¹,

Rudemiller²,

Patel³

et al. 2016

JASN

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Inappropriate activation of the renin-angiotensin system (RAS) contributes to many CKDs. However, the role of the RAS in modulating AKI requires elucidation, particularly because stimulating type 1 angiotensin II (AT 1 ) receptors in the kidney or circulating inflammatory cells can have opposing effects on the generation of inflammatory mediators that underpin the pathogenesis of AKI. For example, TNF-a is a fundamental driver of cisplatin nephrotoxicity, and generation of TNF-a is suppressed or enhanced by AT 1 receptor signaling in T lymphocytes or the distal nephron, respectively. In this study, cell tracking experiments with CD4-Cre mT/mG reporter mice revealed robust infiltration of T lymphocytes into the kidney after cisplatin injection. Notably, knockout of AT 1 receptors on T lymphocytes exacerbated the severity of cisplatin-induced AKI and enhanced the cisplatin-induced increase in TNF-a levels locally within the kidney and in the systemic circulation. In contrast, knockout of AT 1 receptors on kidney epithelial cells ameliorated the severity of AKI and suppressed local and systemic TNF-a production induced by cisplatin. Finally, disrupting TNF-a production specifically within the renal tubular epithelium attenuated the AKI and the increase in circulating TNF-a levels induced by cisplatin. These results illustrate discrepant tissue-specific effects of RAS stimulation on cisplatin nephrotoxicity and raise the concern that inflammatory mediators produced by renal parenchymal cells may influence the function of remote organs by altering systemic cytokine levels. Our findings suggest selective inhibition of AT 1 receptors within the nephron as a promising intervention for protecting patients from cisplatin-induced nephrotoxicity.

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Onco-Nephrology

Cited by 276 publications

References 43 publications

Predictors of Recurrent AKI

Predictors of Recurrent AKI

Onco-Nephrology

Competing Actions of Type 1 Angiotensin II Receptors Expressed on T Lymphocytes and Kidney Epithelium during Cisplatin-Induced AKI

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