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      Kidney diseases associated with haematological cancers

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          Abstract

          Advances in chemotherapy for haematological malignancies, resulting from a greater understanding of the complex pathophysiology of these diseases, have improved the survival of patients with these disorders. Clinicians must now, therefore, be more aware of the issues related to fluid, electrolyte, and acid-base disorders, as well as acute and chronic kidney injuries that can develop in such patients as a result of the underlying malignancy and its treatment. Patients with acute kidney injury associated with haematological malignancy have a worse prognosis than do other patients with acute kidney injury. Glomerular diseases associated with haematological malignancies are thought to be paraneoplastic syndromes with variable histological presentations. Some of the newest therapeutic agents used to treat haematological malignancies have adverse renal effects that can preclude continuation of treatment, often leading to difficult clinical decisions when patients have advanced disease and alternative treatment options are limited. Haematopoietic stem cell transplantation has an expanding role as a therapy for haematological malignancies but is also associated with important renal complications. Here, we review the literature that examines the incidences, aetiologies, mechanisms and treatment options for renal disorders associated with haematological malignancies.

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          Most cited references92

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          Acute renal failure in the ICU: risk factors and outcome evaluated by the SOFA score.

          To describe risk factors for the development of acute renal failure (ARF) in a population of intensive care unit (ICU) patients, and the association of ARF with multiple organ failure (MOF) and outcome using the sequential organ failure assessment (SOFA) score. Prospective, multicenter, observational cohort analysis. Forty ICUs in 16 countries. All patients admitted to one of the participating ICUs in May 1995, except those who stayed in the ICU for less than 48 h after uncomplicated surgery, were included. After the exclusion of 38 patients with a history of chronic renal failure requiring renal replacement therapy, a total of 1411 patients were studied. Of the patients, 348 (24.7%) developed ARF, as diagnosed by a serum creatinine of 300 micromol/l (3.5 mg/dl) or more and/or a urine output of less than 500 ml/day. The most important risk factors for the development of ARF present on admission were acute circulatory or respiratory failure; age more than 65 years, presence of infection, past history of chronic heart failure (CHF), lymphoma or leukemia, or cirrhosis. ARF patients developed MOF earlier than non-ARF patients (median 24 vs 48 h after ICU admission, p < 0.05). ARF patients older than 65 years with a past history of CHF or with any organ failure on admission were most likely to develop MOF. ICU mortality was 3 times higher in ARF than in other patients (42.8% vs 14.0%, p < 0.01). Oliguric ARF was an independent risk factor for overall mortality as determined by a multivariate regression analysis (OR = 1.59 [CI 95%: 1.23-2.06], p < 0.01). Infection increased the risk of death associated with all factors. Factors that increased the ICU mortality of ARF patients were a past history of hematologic malignancy, age more than 65 years, the number of failing organs on admission and the presence of acute cardiovascular failure. In ICU patients, the most important risk factors for ARF or mortality from ARF are often present on admission. During the ICU stay, other organ failures (especially cardiovascular) are important risk factors. Oliguric ARF was an independent risk factor for ICU mortality, and infection increased the contribution to mortality by other factors. The severity of circulatory shock was the most important factor influencing outcome in ARF patients.
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            Incidence of acute kidney injury in cancer patients: a Danish population-based cohort study.

            Cancer patients may be at increased risk of acute kidney injury, but evidence is limited. We assembled a cohort of incident cancer patients diagnosed within a population-based hospital setting in Northern Denmark (population:~1.2 million) between 1999 and 2006. Patients were followed up to five years for acute kidney injury, identified using creatinine measurements recorded in a laboratory database covering the study area. Acute kidney injury was defined according to recent consensus criteria as a 50% increase in creatinine level. We computed incidence rate, 1-year, and 5-year risks of acute kidney injury, accounting for competing risk from death. Acute kidney injury incidence was compared between cancers using a Cox regression model adjusted for important confounders. Among 37,267 incident cancer patients with a creatinine measurement, 9613 (25.8%) developed acute kidney injury during 77,376 person-years. The incidence was 258 (95%CI: 252-264) per 1000 person-years the first year after cancer diagnosis decreasing to 43 (95%CI: 41-44) thereafter. The 1-year risk was 17.5% (95%CI: 17.1-17.9%), and the 5-year risk was 27.0% (95%CI: 26.5-27.5%). We observed the highest 1-year risk in patients with kidney cancer [44.0% (95%CI: 40.5-47.5)], liver cancer [33.0% (95%CI: 28.2-37.8%)], or multiple myeloma [31.8% (95%CI: 27.3-36.3%)]. Similar results were observed after adjustment for confounders. Both overall and for most specific cancer sites, risks were higher among patients with distant metastases at cancer diagnosis. Acute kidney injury is a common complication in cancer patients, particularly in patients with kidney cancer, liver cancer, or multiple myeloma. Copyright © 2011 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
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              Small vessels, big trouble in the kidneys and beyond: hematopoietic stem cell transplantation-associated thrombotic microangiopathy.

              Transplantation-associated thrombotic microangiopathy (TA-TMA) is a challenging diagnosis after hematopoietic stem cell transplantation. Although endothelial injury represents the final common pathway of disease, the exact pathophysiology of TA-TMA remains unclear. Potential causes include infections, chemotherapy, radiation, and calcineurin inhibitors. Recent literature addresses the roles of cytokines, graft-versus-host disease, the coagulation cascade, and complement in the pathogenesis of TA-TMA. Current diagnostic criteria are unsatisfactory, because patients who have received a transplant can have multiple other reasons for the laboratory abnormalities currently used to diagnose TA-TMA. Moreover, our lack of understanding of the exact mechanism of disease limits the development and evaluation of potential treatments. Short- and long-term renal complications contribute to TA-TMA's overall poor prognosis. In light of these challenges, future research must validate novel markers of disease to aid in early diagnosis, guide current and future treatments, prevent long-term morbidity, and improve outcomes. We focus on TA-TMA as a distinct complication of hematopoietic stem cell transplantation, emphasizing the central role of the kidney in this disease.
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                Author and article information

                Journal
                Nature Reviews Nephrology
                Nat Rev Nephrol
                Springer Science and Business Media LLC
                1759-5061
                1759-507X
                August 2015
                June 2 2015
                August 2015
                : 11
                : 8
                : 478-490
                Article
                10.1038/nrneph.2015.81
                26035773
                7be58eef-cf82-4ded-8c95-c733f5561510
                © 2015

                http://www.springer.com/tdm

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