Kidney Disease in the Cancer Patient

2014 ◽  
Author(s):  
Colm Magee ◽  
Lynn Redahan

The spectrum of kidney disease in the cancer patient is wide. Kidney dysfunction can result from the cancer itself or its treatment. The presentation in this population is varied and may manifest as acute kidney injury (AKI) or chronic kidney disease. In addition, other manifestations of kidney disease can include proteinuria, hypertension, and electrolyte disturbances. As new cancer treatments emerge, the range of therapy-associated renal syndromes increases. This chapter deals predominantly with causes and management of renal dysfunction that are specific to the cancer patient, including those caused by hypercalcemia; hepatorenal syndrome; the use of interleukin-2 (IL-2) and bisphosphonate; glomerular, tubular, interstitial, and vascular diseases; multiple myeloma (MM); and tumor infiltration. The chapter also examines postrenal causes of AKI, electrolyte disorders, and hematopoietic stem cell transplantation (HSCT). Tables provide the features of kidney disease in the cancer patient, the pathogenesis of hypercalcemia, strategies for preventing and managing AKI with IL-2 therapy, laboratory findings with hemolytic-uremic syndrome/thrombocytopenic purpura, the causes of acute tubular necrosis in MM, a summary of electrolyte disturbances in the cancer patient, indications for HSCT, and a summary of the management of patients with post-HSCT AKI. The chapter is also enhanced by ultrasound and computed tomographic scans, histology images, and an illustration of tumor lysis syndrome. This chapter contains 105 references, 8 tables, 4 highly rendered figures, and 5 MCQs.

2014 ◽  
Author(s):  
Colm Magee ◽  
Lynn Redahan

The spectrum of kidney disease in the cancer patient is wide. Kidney dysfunction can result from the cancer itself or its treatment. The presentation in this population is varied and may manifest as acute kidney injury (AKI) or chronic kidney disease. In addition, other manifestations of kidney disease can include proteinuria, hypertension, and electrolyte disturbances. As new cancer treatments emerge, the range of therapy-associated renal syndromes increases. This chapter deals predominantly with causes and management of renal dysfunction that are specific to the cancer patient, including those caused by hypercalcemia; hepatorenal syndrome; the use of interleukin-2 (IL-2) and bisphosphonate; glomerular, tubular, interstitial, and vascular diseases; multiple myeloma (MM); and tumor infiltration. The chapter also examines postrenal causes of AKI, electrolyte disorders, and hematopoietic stem cell transplantation (HSCT). Tables provide the features of kidney disease in the cancer patient, the pathogenesis of hypercalcemia, strategies for preventing and managing AKI with IL-2 therapy, laboratory findings with hemolytic-uremic syndrome/thrombocytopenic purpura, the causes of acute tubular necrosis in MM, a summary of electrolyte disturbances in the cancer patient, indications for HSCT, and a summary of the management of patients with post-HSCT AKI. The chapter is also enhanced by ultrasound and computed tomographic scans, histology images, and an illustration of tumor lysis syndrome. This chapter contains 105 references, 8 tables, 4 highly rendered figures, and 5 MCQs.


Author(s):  
Kianoush B. Kashani ◽  
Amy W. Williams

Renal failure is caused by acute kidney injury or chronic kidney disease. Acute kidney injury (AKI) is a common, devastating complication that increases mortality and morbidity among patients with various medical and surgical illnesses. Also known as acute renal failure, AKI is a rapid deterioration of kidney function that results in the accumulation of nitrogenous metabolites and medications and in electrolyte and acid-base imbalances. This chapter discusses the definition, epidemiology, pathophysiology, and etiology of AKI; the clinical approach to patients with AKI; and the management of AKI. Chronic kidney disease (CKD) has been categorized into 5 stages. When renal function decreases to stage 3, the complications of CKD become evident. These complications include hypertension, cardiovascular disease, lipid abnormalities, anemia, metabolic bone disease, and electrolyte disturbances. To prevent the progression of CKD, therapy must be directed toward preventing these complications and achieving adequate glucose control in diabetic patients with CKD.


Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 3463-3463
Author(s):  
Tatsunori Shimoi ◽  
Minoru Ando ◽  
Takeshi Kobayashi ◽  
Kazuhiko Kakihana ◽  
Takuya Yamashita ◽  
...  

Abstract Abstract 3463 Introduction: Chronic kidney disease (CKD) is common in survivors of hematopoietic stem cell transplantation (SCT). However, evolution over time of kidney dysfunction and its association with post-SCT acute kidney injury (AKI) are unclear. Methods: A retrospective cohort study was performed in 86 myeloablative allogenic SCT patients who received SCT between 1990 and 1999 and lived without relapse for 10 years or more. CKD was defined as a sustained decrease in estimated GFR less than 60 ml/min/1.73 m2 at least for a period more than 3 months. Post-SCT AKI was classified into three stages according to the acute kidney injury network (AKIN) criteria within 100 days after SCT. Incidence of new-onset CKD was studied by 1-year interval along the course of follow-up. Cumulative CKD incidence was evaluated by the Kaplan-Meier analysis. The factors associated with CKD at the time of 10 years after SCT were examined using Cox regression analysis. Results: The incident of new CKD was the highest (10.5%) at the first year after SCT and then remained almost constant (2.3 to 3.5%) (Figure 1). The prevalence of CKD increased along the follow-up time (Table 1). The cumulative incidence of CKD increased according to increasing AKI stages with significant difference between stages ≥1 and no AKI (Figure 2). Cox regression showed that each AKIN stage was a significant predictor of CKD: stage 3: hazard ratio (HR) 12.7, 95% confidence interval (CI) 2.42–97.6; stage 2: HR 7.75, 95% CI 1.83–53.6; and stage 1: HR 4.36, 95% CI 1.06–29.5. Other predictors included total body irradiation (TBI) (HR, 4.00; 95% CI, 1.63–10.5) and age on SCT (HR, 1.08; 95% CI, 1.03–1.13). Conclusions: CKD accumulated among long-term survivors receiving myeloablative allogenic SCT. Post-SCT AKI, regardless of the AKIN stages, is the most significant risk of CKD in such SCT population. Disclosures: No relevant conflicts of interest to declare.


2017 ◽  
Author(s):  
Shveta Motwani ◽  
Albert Q. Lam

Acute kidney injury (AKI) is a problem frequently encountered in patients with cancer that significantly impacts their well-being and outcomes. In addition to the usual prerenal, intrarenal, and postrenal etiologies of AKI, patients with cancer experience unique causes of AKI. Nephrologists caring for this population must be able to identify and manage these conditions, which often require distinguishing between causes resulting from the cancer itself and those related to chemotherapeutic or other concurrent treatment, to institute appropriate preventive or therapeutic strategies. In this review, we present a suggested systematic approach to the diagnosis of AKI in patients with cancer and discuss common clinical scenarios specific to this patient population, with a special emphasis on tumor infiltration of the kidney parenchyma, myeloma-related AKI, tumor lysis syndrome, thrombotic microangiopathy, AKI in the patient with hematopoietic stem cell transplantation, and renal disease in patients with renal cell carcinoma. We cover the latest evidence-based strategies for management of these disorders in this evolving field. In addition, we provide an updated table of potentially nephrotoxic chemotherapeutic agents with their associated mechanisms of kidney injury as a reference for clinicians to build on as they encounter the ever-expanding list of oncologic agents in practice. As the subspecialty of onconephrology continues to evolve, it will be increasingly important for clinicians to have the skills to effectively diagnose and treat AKI in cancer patients to minimize morbidity and mortality, decrease the incidence of subsequent chronic kidney disease, and maintain chemotherapeutic options for these patients. This review contains 5 figures, 5 tables, and 61 references. Key words: acute kidney injury, cancer, chemotherapy, onconephrology, renal failure


2017 ◽  
Author(s):  
Shveta Motwani ◽  
Albert Q. Lam

Acute kidney injury (AKI) is a problem frequently encountered in patients with cancer that significantly impacts their well-being and outcomes. In addition to the usual prerenal, intrarenal, and postrenal etiologies of AKI, patients with cancer experience unique causes of AKI. Nephrologists caring for this population must be able to identify and manage these conditions, which often require distinguishing between causes resulting from the cancer itself and those related to chemotherapeutic or other concurrent treatment, to institute appropriate preventive or therapeutic strategies. In this review, we present a suggested systematic approach to the diagnosis of AKI in patients with cancer and discuss common clinical scenarios specific to this patient population, with a special emphasis on tumor infiltration of the kidney parenchyma, myeloma-related AKI, tumor lysis syndrome, thrombotic microangiopathy, AKI in the patient with hematopoietic stem cell transplantation, and renal disease in patients with renal cell carcinoma. We cover the latest evidence-based strategies for management of these disorders in this evolving field. In addition, we provide an updated table of potentially nephrotoxic chemotherapeutic agents with their associated mechanisms of kidney injury as a reference for clinicians to build on as they encounter the ever-expanding list of oncologic agents in practice. As the subspecialty of onconephrology continues to evolve, it will be increasingly important for clinicians to have the skills to effectively diagnose and treat AKI in cancer patients to minimize morbidity and mortality, decrease the incidence of subsequent chronic kidney disease, and maintain chemotherapeutic options for these patients. This review contains 5 figures, 5 tables, and 61 references. Key words: acute kidney injury, cancer, chemotherapy, onconephrology, renal failure


2021 ◽  
pp. 1141-1146
Author(s):  
Sara E. Hocker ◽  
Ali Daneshmand

Electrolyte disorders are among the most common clinical problems encountered in critically ill patients. Disorders such as severe burns, trauma, sepsis, acute brain injury, and heart failure lead to disturbances in fluid and electrolyte homeostasis through complex mechanisms involving deregulation or activation of hormonal systems and ischemic or nephrotoxic kidney injury. Inappropriate fluid management should also be considered in the differential diagnosis of electrolyte disturbances in patients in intensive care units. Electrolyte imbalances produce both central and peripheral neurologic dysfunction because electrochemical membrane potentials in brain, nerve, and muscle tissues are particularly sensitive to chemical, ionic, and osmolar shifts.


2017 ◽  
Vol 1 (1) ◽  
pp. 24-29
Author(s):  
Deirdre Sawinski

Hematopoietic stem cell transplantation in the USA is growing, and stem cell transplant recipients are at risk for both acute and chronic renal injury. Some etiologies of acute kidney injury are shared with the general population, such as prerenal azotemia and acute tubular necrosis, while others are unique to aspects of the stem cell procedure and include hepatic veno-occlusive disease and BK cystitis. Long-term hematopoietic stem cell transplant survivors are also at increased risk for chronic kidney disease, and important etiologies include calcineurin inhibitor toxicity, nephrotic syndrome, and thrombotic microangiopathy. Stem cell transplant patient survival on chronic dialysis is poor, but well-selected patients can have excellent outcomes with renal transplantation.


2019 ◽  
Vol 143 (5) ◽  
pp. 452-464 ◽  
Author(s):  
Masahiro Sakaguchi ◽  
Kazutaka Nakayama ◽  
Hiroki Yamaguchi ◽  
Akiko Mii ◽  
Akira Shimizu ◽  
...  

Background: Acute kidney injury (AKI) and chronic kidney disease (CKD) are considered common complications after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Objectives and Method: In this study, 114 patients who had undergone allo-HSCT were retrospectively analyzed to investigate the risk factors for onset of posttransplant AKI and CKD as defined by the new Kidney Disease Improving Global Outcomes criteria. Results: Seventy-four patients (64.9%) developed AKI and 25 (21.9%) developed CKD. The multivariate analysis showed that the risk factors for developing stage 1 or higher AKI were age ≥46 years at the time of transplant (p = 0.001) and use of ≥3 nephrotoxic drugs (p = 0.036). For CKD, the associated risk factors were disease status other than complete remission at the time of transplantation (p = 0.018) and onset of AKI after transplant (p = 0.035). The 5-year overall survival (OS) was significantly reduced by development of AKI (p < 0.001), but not CKD. Posttransplant AKI significantly increased the 5-year nonrelapse mortality (p < 0.001), whereas posttransplant CKD showed an increasing tendency, but the difference was not significant. Conclusions: Posttransplant AKI impacts OS, significantly increases the risk of CKD, and is significantly associated with disseminated intravascular coagulation and use of ˃3 nephrotoxic drugs.


2016 ◽  
Vol 2016 ◽  
pp. 1-13 ◽  
Author(s):  
Vinod Krishnappa ◽  
Mohit Gupta ◽  
Gurusidda Manu ◽  
Shivani Kwatra ◽  
Osei-Tutu Owusu ◽  
...  

Hematopoietic stem cell transplantation (HSCT) is a highly effective treatment strategy for lymphoproliferative disorders and bone marrow failure states including aplastic anemia and thalassemia. However, its use has been limited by the increased treatment related complications, including acute kidney injury (AKI) with an incidence ranging from 20% to 73%. AKI after HSCT has been associated with an increased risk of mortality. The incidence of AKI reported in recipients of myeloablative allogeneic transplant is considerably higher in comparison to other subclasses mainly due to use of cyclosporine and development of graft-versus-host disease (GVHD) in allogeneic groups. Acute GVHD is by itself a major independent risk factor for the development of AKI in HSCT recipients. The other major risk factors are sepsis, nephrotoxic medications (amphotericin B, acyclovir, aminoglycosides, and cyclosporine), hepatic sinusoidal obstruction syndrome (SOS), thrombotic microangiopathy (TMA), marrow infusion toxicity, and tumor lysis syndrome. The mainstay of management of AKI in these patients is avoidance of risk factors contributing to AKI, including use of reduced intensity-conditioning regimen, close monitoring of nephrotoxic medications, and use of alternative antifungals for prophylaxis against infection. Also, early identification and effective management of sepsis, tumor lysis syndrome, marrow infusion toxicity, and hepatic SOS help in reducing the incidence of AKI in HSCT recipients.


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