en-usOver the past several decades, the acuity of hospitalized patients has increased, as has the percentage of time that nephrologists spend caring for patients in intensive care units (ICUs). This includes the care of patients with chronic kidney disease or dialysis-dependent kidney failure who are predisposed to the development of critical illness, as well as the management of patients with acute kidney injury (AKI). <p></p><p> The <i> Critical Care Nephrology and Acute Kidney Injury </i> series provides updates on broad aspects of critical care nephrology that are clinically relevant to seasoned clinicians as well as serving as a primer on topics that are important to trainees. The series begins with six articles that form a primer of critical care medicine for nephrologists, followed by topics on fluid and electrolyte issues, a primer on the management of kidney replacement therapy in the ICU, and, finally, several miscellaneous topics including medication management in the critically ill patient with AKI and the management of poisonings and intoxications.</p>Fri, 19 Apr 2024 10:30:03 GMThttp://cct.highwire.org/feeds/asn/critical-care-nephrology-and-acute-kidney-injury.rssThe medical management of the critically ill patient focuses predominantly on treatment of the underlying condition (e.g., sepsis or respiratory failure). However, in the past decade, the importance of initiating early prophylactic treatment for complications arising from care in the intensive care unit setting has become increasingly apparent. As survival from critical illness has improved, there is an increased prevalence of postintensive care syndrome—defined as a decline in physical, cognitive, or psychologic function among survivors of critical illness. The Intensive Care Unit Liberation Bundle, a major initiative of the Society of Critical Care Medicine, is centered on facilitating the return to normal function as early as possible, with the intent of minimizing iatrogenic harm during necessary critical care. These concepts are universally applicable to patients seen by nephrologists in the intensive care unit and may have particular relevance for patients with kidney failure either on dialysis or after kidney transplant. In this article, we will briefly summarize some known organ-based consequences associated with critical illness, review the components of the ABCDEF bundle (the conceptual framework for Intensive Care Unit Liberation), highlight the role nephrologists can play in implementing and complying with the ABCDEF bundle, and briefly discuss areas for additional research.10.2215/CJN.07130622Fri, 18 Nov 2022 05:09:20 GMT-08:00Overview of the Medical Management of the Critically Ill PatientThe medical management of the critically ill patient focuses predominantly on treatment of the underlying condition (e.g., sepsis or respiratory failure). However, in the past decade, the importance of initiating early prophylactic treatment for complications arising from care in the intensive care unit setting has become increasingly apparent. As survival from critical illness has improved, there is an increased prevalence of postintensive care syndrome—defined as a decline in physical, cognitive, or psychologic function among survivors of critical illness. The Intensive Care Unit Liberation Bundle, a major initiative of the Society of Critical Care Medicine, is centered on facilitating the return to normal function as early as possible, with the intent of minimizing iatrogenic harm during necessary critical care. These concepts are universally applicable to patients seen by nephrologists in the intensive care unit and may have particular relevance for patients with kidney failure either on dialysis or after kidney transplant. In this article, we will briefly summarize some known organ-based consequences associated with critical illness, review the components of the ABCDEF bundle (the conceptual framework for Intensive Care Unit Liberation), highlight the role nephrologists can play in implementing and complying with the ABCDEF bundle, and briefly discuss areas for additional research.Martinez, Rebecca H.Liu, Kathleen D.Aldrich, J. Matthew2022-11-18T05:09:20-08:00doi:10.2215/CJN.07130622hwp:resource-id:clinjasn;17/12/1805American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologyacute renal failure, renal injury, clinical epidemiologyCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-12-01December 202210.2215/CJN.071306221555-90411555-905X2022-11-18T05:09:20-08:002022-12Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury171218051813AKI is commonly encountered in patients with decompensated cirrhosis, and it is associated with unfavorable outcomes. Among factors specific to cirrhosis, hepatorenal syndrome type 1, also referred to as hepatorenal syndrome-AKI, is the most salient and unique etiology. Patients with cirrhosis are vulnerable to traditional causes of AKI, such as prerenal azotemia, acute tubular injury, and acute interstitial nephritis. In addition, other less common etiologies of AKI specifically related to chronic liver disease should be considered, including abdominal compartment syndrome, cardiorenal processes linked to cirrhotic cardiomyopathy and portopulmonary hypertension, and cholemic nephropathy. Furthermore, certain types of GN can cause AKI in cirrhosis, such as IgA nephropathy or viral hepatitis related. Therefore, a comprehensive diagnostic approach is needed to evaluate patients with cirrhosis presenting with AKI. Management should be tailored to the specific underlying etiology. Albumin-based volume resuscitation is recommended in prerenal AKI. Acute tubular injury and acute interstitial nephritis are managed with supportive care, withdrawal of the offending agent, and, potentially, corticosteroids in acute interstitial nephritis. Short of liver transplantation, vasoconstrictor therapy is the primary treatment for hepatorenal syndrome type 1. Timing of initiation of vasoconstrictors, the rise in mean arterial pressure, and the degree of cholestasis are among the factors that determine vasoconstrictor responsiveness. Large-volume paracentesis and diuretics are indicated to relieve intra-abdominal hypertension and renal vein congestion. Direct-acting antivirals with or without immunosuppression are used to treat hepatitis B/C–associated GN. In summary, AKI in cirrhosis requires careful consideration of multiple potentially pathogenic factors and the implementation of targeted therapeutic interventions.10.2215/CJN.03040322Thu, 28 Jul 2022 06:55:06 GMT-07:00Acute Kidney Injury in Patients with Liver DiseaseAKI is commonly encountered in patients with decompensated cirrhosis, and it is associated with unfavorable outcomes. Among factors specific to cirrhosis, hepatorenal syndrome type 1, also referred to as hepatorenal syndrome-AKI, is the most salient and unique etiology. Patients with cirrhosis are vulnerable to traditional causes of AKI, such as prerenal azotemia, acute tubular injury, and acute interstitial nephritis. In addition, other less common etiologies of AKI specifically related to chronic liver disease should be considered, including abdominal compartment syndrome, cardiorenal processes linked to cirrhotic cardiomyopathy and portopulmonary hypertension, and cholemic nephropathy. Furthermore, certain types of GN can cause AKI in cirrhosis, such as IgA nephropathy or viral hepatitis related. Therefore, a comprehensive diagnostic approach is needed to evaluate patients with cirrhosis presenting with AKI. Management should be tailored to the specific underlying etiology. Albumin-based volume resuscitation is recommended in prerenal AKI. Acute tubular injury and acute interstitial nephritis are managed with supportive care, withdrawal of the offending agent, and, potentially, corticosteroids in acute interstitial nephritis. Short of liver transplantation, vasoconstrictor therapy is the primary treatment for hepatorenal syndrome type 1. Timing of initiation of vasoconstrictors, the rise in mean arterial pressure, and the degree of cholestasis are among the factors that determine vasoconstrictor responsiveness. Large-volume paracentesis and diuretics are indicated to relieve intra-abdominal hypertension and renal vein congestion. Direct-acting antivirals with or without immunosuppression are used to treat hepatitis B/C–associated GN. In summary, AKI in cirrhosis requires careful consideration of multiple potentially pathogenic factors and the implementation of targeted therapeutic interventions.Cullaro, GiuseppeKanduri, Swetha RaniVelez, Juan Carlos Q.2022-07-28T06:55:06-07:00doi:10.2215/CJN.03040322hwp:resource-id:clinjasn;17/11/1674American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologyacute kidney injury, cirrhosis, liver failure, hepatorenal syndrome, Critical Care Nephrology and Acute Kidney Injury SeriesCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-11-01November 202210.2215/CJN.030403221555-90411555-905X2022-07-28T06:55:06-07:002022-11Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury171116741684Postoperative AKI is a common complication of major surgery and is associated with significant morbidity and mortality. The Kidney Disease Improving Global Outcomes AKI definition allows consensus classification and identification of postoperative AKI through changes in serum creatinine and/or urine output. However, such conventional diagnostic criteria may be inaccurate in the postoperative period, suggesting a potential to refine diagnosis by application of novel diagnostic biomarkers. Risk factors for the development of postoperative AKI can be thought of in terms of preoperative, intraoperative, and postoperative factors and, as such, represent areas that may be targeted perioperatively to minimize the risk of AKI. The treatment of postoperative AKI remains predominantly supportive, although application of management bundles may translate into improved outcomes.10.2215/CJN.16541221Thu, 16 Jun 2022 09:33:17 GMT-07:00Postoperative Acute Kidney InjuryPostoperative AKI is a common complication of major surgery and is associated with significant morbidity and mortality. The Kidney Disease Improving Global Outcomes AKI definition allows consensus classification and identification of postoperative AKI through changes in serum creatinine and/or urine output. However, such conventional diagnostic criteria may be inaccurate in the postoperative period, suggesting a potential to refine diagnosis by application of novel diagnostic biomarkers. Risk factors for the development of postoperative AKI can be thought of in terms of preoperative, intraoperative, and postoperative factors and, as such, represent areas that may be targeted perioperatively to minimize the risk of AKI. The treatment of postoperative AKI remains predominantly supportive, although application of management bundles may translate into improved outcomes.Boyer, NaomiEldridge, JackProwle, John R.Forni, Lui G.2022-06-16T09:33:17-07:00doi:10.2215/CJN.16541221hwp:resource-id:clinjasn;17/10/1535American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, acute kidney injury, perioperative, postoperative, surgery, biomarkers, kidney replacement therapyCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-10-01October 202210.2215/CJN.165412211555-90411555-905X2022-06-16T09:33:17-07:002022-10Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury171015351545Acid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non–gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non–gap acidoses result from disorders of renal tubular H+ transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO2 can be considered.10.2215/CJN.04500422Tue, 23 Aug 2022 07:06:40 GMT-07:00Acid-Base Disorders in the Critically Ill PatientAcid-base disorders are common in the intensive care unit. By utilizing a systematic approach to their diagnosis, it is easy to identify both simple and mixed disturbances. These disorders are divided into four major categories: metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis. Metabolic acidosis is subdivided into anion gap and non–gap acidosis. Distinguishing between these is helpful in establishing the cause of the acidosis. Anion gap acidosis, caused by the accumulation of organic anions from sepsis, diabetes, alcohol use, and numerous drugs and toxins, is usually present on admission to the intensive care unit. Lactic acidosis from decreased delivery or utilization of oxygen is associated with increased mortality. This is likely secondary to the disease process, as opposed to the degree of acidemia. Treatment of an anion gap acidosis is aimed at the underlying disease or removal of the toxin. The use of therapy to normalize the pH is controversial. Non–gap acidoses result from disorders of renal tubular H+ transport, decreased renal ammonia secretion, gastrointestinal and kidney losses of bicarbonate, dilution of serum bicarbonate from excessive intravenous fluid administration, or addition of hydrochloric acid. Metabolic alkalosis is the most common acid-base disorder found in patients who are critically ill, and most often occurs after admission to the intensive care unit. Its etiology is most often secondary to the aggressive therapeutic interventions used to treat shock, acidemia, volume overload, severe coagulopathy, respiratory failure, and AKI. Treatment consists of volume resuscitation and repletion of potassium deficits. Aggressive lowering of the pH is usually not necessary. Respiratory disorders are caused by either decreased or increased minute ventilation. The use of permissive hypercapnia to prevent barotrauma has become the standard of care. The use of bicarbonate to correct the acidemia is not recommended. In patients at the extreme, the use of extracorporeal therapies to remove CO2 can be considered.Achanti, AnandSzerlip, Harold M.2022-08-23T07:06:40-07:00doi:10.2215/CJN.04500422hwp:resource-id:clinjasn;CJN.04500422v3American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologyacid-base, critical illness, metabolic acidosis, metabolic alkalosis, anion gap, lactic acidosis, ketoacidosisCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article202210.2215/CJN.045004221555-90411555-905X2022-08-23T07:06:40-07:00Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney InjuryCJN.04500422KRT is considered for patients with severe AKI and associated complications. The exact indications for initiating KRT have been debated for decades. There is a general consensus that KRT should be considered in patients with AKI and medically refractory complications (“urgent indications”). “Relative indications” are more common but defined with less precision. In this review, we summarize the latest evidence from recent landmark clinical trials, discuss strategies to anticipate the need for KRT in individual patients, and propose an algorithm for decision making. We emphasize that the decision to consider KRT should be made in conjunction with other forms of organ support therapies and important nonkidney factors, including the patient’s preferences and overall goals of care. We also suggest future research to differentiate patients who benefit from timely initiation of KRT from those with imminent recovery of kidney function. Until then, efforts are needed to optimize the initiation and delivery of KRT in routine clinical practice, to minimize nonessential variation, and to ensure that patients with persistent AKI or progressive organ failure affected by AKI receive KRT in a timely manner.10.2215/CJN.05450522Tue, 13 Sep 2022 05:36:59 GMT-07:00Indications for and Timing of Initiation of KRTKRT is considered for patients with severe AKI and associated complications. The exact indications for initiating KRT have been debated for decades. There is a general consensus that KRT should be considered in patients with AKI and medically refractory complications (“urgent indications”). “Relative indications” are more common but defined with less precision. In this review, we summarize the latest evidence from recent landmark clinical trials, discuss strategies to anticipate the need for KRT in individual patients, and propose an algorithm for decision making. We emphasize that the decision to consider KRT should be made in conjunction with other forms of organ support therapies and important nonkidney factors, including the patient’s preferences and overall goals of care. We also suggest future research to differentiate patients who benefit from timely initiation of KRT from those with imminent recovery of kidney function. Until then, efforts are needed to optimize the initiation and delivery of KRT in routine clinical practice, to minimize nonessential variation, and to ensure that patients with persistent AKI or progressive organ failure affected by AKI receive KRT in a timely manner.Ostermann, MarliesBagshaw, Sean M.Lumlertgul, NutthaWald, Ron2022-09-13T05:36:59-07:00doi:10.2215/CJN.05450522hwp:resource-id:clinjasn;CJN.05450522v1American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, acute kidney injury, renal replacement therapy, critical care nephrology, CRRT, CKRTCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article202210.2215/CJN.054505221555-90411555-905X2022-09-13T05:36:59-07:00Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney InjuryCJN.05450522Advances in cancer therapy have significantly improved overall patient survival; however, AKI remains a common complication in patients with cancer, occurring in anywhere from 11% to 22% of patients, depending on patient-related or cancer-specific factors. Critically ill patients with cancer as well as patients with certain malignancies (e.g., leukemias, lymphomas, multiple myeloma, and renal cell carcinoma) are at highest risk of developing AKI. AKI may be a consequence of the underlying malignancy itself or from the wide array of therapies used to treat it. Cancer-associated AKI can affect virtually every compartment of the nephron and can present as subclinical AKI or as overt acute tubular injury, tubulointerstitial nephritis, or thrombotic microangiopathy, among others. AKI can have major repercussions for patients with cancer, potentially jeopardizing further eligibility for therapy and leading to greater morbidity and mortality. This review highlights the epidemiology of AKI in critically ill patients with cancer, risk factors for AKI, and common pathologies associated with certain cancer therapies, as well as the management of AKI in different clinical scenarios. It highlights gaps in our knowledge of AKI in patients with cancer, including the lack of validated biomarkers, as well as evidence-based therapies to prevent AKI and its deleterious consequences.10.2215/CJN.15681221Fri, 25 Mar 2022 07:54:20 GMT-07:00Acute Kidney Injury in Critically Ill Patients with CancerAdvances in cancer therapy have significantly improved overall patient survival; however, AKI remains a common complication in patients with cancer, occurring in anywhere from 11% to 22% of patients, depending on patient-related or cancer-specific factors. Critically ill patients with cancer as well as patients with certain malignancies (e.g., leukemias, lymphomas, multiple myeloma, and renal cell carcinoma) are at highest risk of developing AKI. AKI may be a consequence of the underlying malignancy itself or from the wide array of therapies used to treat it. Cancer-associated AKI can affect virtually every compartment of the nephron and can present as subclinical AKI or as overt acute tubular injury, tubulointerstitial nephritis, or thrombotic microangiopathy, among others. AKI can have major repercussions for patients with cancer, potentially jeopardizing further eligibility for therapy and leading to greater morbidity and mortality. This review highlights the epidemiology of AKI in critically ill patients with cancer, risk factors for AKI, and common pathologies associated with certain cancer therapies, as well as the management of AKI in different clinical scenarios. It highlights gaps in our knowledge of AKI in patients with cancer, including the lack of validated biomarkers, as well as evidence-based therapies to prevent AKI and its deleterious consequences.Gupta, ShrutiGudsoorkar, PrakashJhaveri, Kenar D.2022-03-25T07:54:20-07:00doi:10.2215/CJN.15681221hwp:resource-id:clinjasn;17/9/1385American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, onconephrology, cancer, AKI, drug nephrotoxicity, acute kidney injuryCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-09-01September 202210.2215/CJN.156812211555-90411555-905X2022-03-25T07:54:20-07:002022-09Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17913851398Kidney replacement therapy (KRT) is a vital, supportive treatment for patients with critical illness and severe AKI. The optimal timing, dose, and modality of KRT have been studied extensively, but gaps in knowledge remain. With respect to modalities, continuous KRT and intermittent hemodialysis are well-established options, but prolonged intermittent KRT is becoming more prevalent worldwide, particularly in emerging countries. Compared with continuous KRT, prolonged intermittent KRT offers similar hemodynamic stability and overall cost savings, and its intermittent nature allows patients time off therapy for mobilization and procedures. When compared with intermittent hemodialysis, prolonged intermittent KRT offers more hemodynamic stability, particularly in patients who remain highly vulnerable to hypotension from aggressive ultrafiltration over a shorter duration of treatment. The prescription of prolonged intermittent KRT can be tailored to patients’ progression in their recovery from critical illness, and the frequency, flow rates, and duration of treatment can be modified to avert hemodynamic instability during de-escalation of care. Dosing of prolonged intermittent KRT can be extrapolated from urea kinetics used to calculate clearance for continuous KRT and intermittent hemodialysis. Practice variations across institutions with respect to terminology, prescription, and dosing of prolonged intermittent KRT create significant challenges, especially in creating specific drug dosing recommendations during prolonged intermittent KRT. During the coronavirus disease 2019 pandemic, prolonged intermittent KRT was rapidly implemented to meet the KRT demands during patient surges in some of the medical centers overwhelmed by sheer volume of patients with AKI. Ideally, implementation of prolonged intermittent KRT at any institution should be conducted in a timely manner, with judicious planning and collaboration among nephrology, critical care, dialysis and intensive care nursing, and pharmacy leadership. Future analyses and clinical trials with respect to prescription and delivery of prolonged intermittent KRT and clinical outcomes will help to guide standardization of practice.10.2215/CJN.04310422Mon, 29 Aug 2022 06:04:11 GMT-07:00Prolonged Intermittent Kidney Replacement TherapyKidney replacement therapy (KRT) is a vital, supportive treatment for patients with critical illness and severe AKI. The optimal timing, dose, and modality of KRT have been studied extensively, but gaps in knowledge remain. With respect to modalities, continuous KRT and intermittent hemodialysis are well-established options, but prolonged intermittent KRT is becoming more prevalent worldwide, particularly in emerging countries. Compared with continuous KRT, prolonged intermittent KRT offers similar hemodynamic stability and overall cost savings, and its intermittent nature allows patients time off therapy for mobilization and procedures. When compared with intermittent hemodialysis, prolonged intermittent KRT offers more hemodynamic stability, particularly in patients who remain highly vulnerable to hypotension from aggressive ultrafiltration over a shorter duration of treatment. The prescription of prolonged intermittent KRT can be tailored to patients’ progression in their recovery from critical illness, and the frequency, flow rates, and duration of treatment can be modified to avert hemodynamic instability during de-escalation of care. Dosing of prolonged intermittent KRT can be extrapolated from urea kinetics used to calculate clearance for continuous KRT and intermittent hemodialysis. Practice variations across institutions with respect to terminology, prescription, and dosing of prolonged intermittent KRT create significant challenges, especially in creating specific drug dosing recommendations during prolonged intermittent KRT. During the coronavirus disease 2019 pandemic, prolonged intermittent KRT was rapidly implemented to meet the KRT demands during patient surges in some of the medical centers overwhelmed by sheer volume of patients with AKI. Ideally, implementation of prolonged intermittent KRT at any institution should be conducted in a timely manner, with judicious planning and collaboration among nephrology, critical care, dialysis and intensive care nursing, and pharmacy leadership. Future analyses and clinical trials with respect to prescription and delivery of prolonged intermittent KRT and clinical outcomes will help to guide standardization of practice.Levine, ZoeyVijayan, Anitha2022-08-29T06:04:11-07:00doi:10.2215/CJN.04310422hwp:resource-id:clinjasn;CJN.04310422v1American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and AKI series, intermittent RRT, PIRRTCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article202210.2215/CJN.043104221555-90411555-905X2022-08-29T06:04:11-07:00Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney InjuryCJN.04310422AKI is a common complication of critical illness and is associated with substantial morbidity and risk of death. Continuous KRT comprises a spectrum of dialysis modalities preferably used to provide kidney support to patients with AKI who are hemodynamically unstable and critically ill. The various continuous KRT modalities are distinguished by different mechanisms of solute transport and use of dialysate and/or replacement solutions. Considerable variation exists in the application of continuous KRT due to a lack of standardization in how the treatments are prescribed, delivered, and optimized to improve patient outcomes. In this manuscript, we present an overview of the therapy, recent clinical trials, and outcome studies. We review the indications for continuous KRT and the technical aspects of the treatment, including continuous KRT modality, vascular access, dosing of continuous KRT, anticoagulation, volume management, nutrition, and continuous KRT complications. Finally, we highlight the need for close collaboration of a multidisciplinary team and development of quality assurance programs for the provision of high-quality and effective continuous KRT.10.2215/CJN.04350422Thu, 18 Aug 2022 10:25:48 GMT-07:00Continuous KRTAKI is a common complication of critical illness and is associated with substantial morbidity and risk of death. Continuous KRT comprises a spectrum of dialysis modalities preferably used to provide kidney support to patients with AKI who are hemodynamically unstable and critically ill. The various continuous KRT modalities are distinguished by different mechanisms of solute transport and use of dialysate and/or replacement solutions. Considerable variation exists in the application of continuous KRT due to a lack of standardization in how the treatments are prescribed, delivered, and optimized to improve patient outcomes. In this manuscript, we present an overview of the therapy, recent clinical trials, and outcome studies. We review the indications for continuous KRT and the technical aspects of the treatment, including continuous KRT modality, vascular access, dosing of continuous KRT, anticoagulation, volume management, nutrition, and continuous KRT complications. Finally, we highlight the need for close collaboration of a multidisciplinary team and development of quality assurance programs for the provision of high-quality and effective continuous KRT.Teixeira, J. PedroNeyra, Javier A.Tolwani, Ashita2022-08-18T10:25:48-07:00doi:10.2215/CJN.04350422hwp:resource-id:clinjasn;CJN.04350422v1American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, CRRT, AKI, ICU, renal replacement therapy, continuous KRT, acute kidney injuryInvited FeaturesCritical Care Nephrology and Acute Kidney InjuryInvited FeaturesCritical Care Nephrology and Acute Kidney Injuryresearch-article202210.2215/CJN.043504221555-90411555-905X2022-08-18T10:25:48-07:00Clinical Journal of the American Society of NephrologyInvited FeaturesCJN.04350422Medications are a common cause of AKI, especially for patients admitted to hospital wards and the intensive care unit. Although drug-related kidney injury occurs through different mechanisms, this review will focus on three specific types of tubulointerstitial injury. Direct acute tubular injury develops from several medications, which are toxic to various cellular functions. Their excretory pathways through the proximal tubules contribute further to AKI. Drug-induced AKI may also develop through induction of inflammation within the tubulointerstitium. Medications can elicit a T cell–mediated immune response that promotes the development of acute interstitial nephritis leading to AKI. Although less common, a third pathway to kidney injury results from the insolubility of drugs in the urine leading to their precipitation as crystals within distal tubular lumens, causing a crystalline-related AKI. Intratubular obstruction, direct tubular injury, and localized inflammation lead to AKI. Clinicians should be familiar with the pathogenesis and clinical-pathologic manifestations of these forms of kidney injury. Prevention and treatment of AKI relies on understanding the pathogenesis and judiciously using these agents in settings where AKI risk is high.10.2215/CJN.11290821Thu, 10 Mar 2022 07:00:02 GMT-08:00Drug-Induced Acute Kidney InjuryMedications are a common cause of AKI, especially for patients admitted to hospital wards and the intensive care unit. Although drug-related kidney injury occurs through different mechanisms, this review will focus on three specific types of tubulointerstitial injury. Direct acute tubular injury develops from several medications, which are toxic to various cellular functions. Their excretory pathways through the proximal tubules contribute further to AKI. Drug-induced AKI may also develop through induction of inflammation within the tubulointerstitium. Medications can elicit a T cell–mediated immune response that promotes the development of acute interstitial nephritis leading to AKI. Although less common, a third pathway to kidney injury results from the insolubility of drugs in the urine leading to their precipitation as crystals within distal tubular lumens, causing a crystalline-related AKI. Intratubular obstruction, direct tubular injury, and localized inflammation lead to AKI. Clinicians should be familiar with the pathogenesis and clinical-pathologic manifestations of these forms of kidney injury. Prevention and treatment of AKI relies on understanding the pathogenesis and judiciously using these agents in settings where AKI risk is high.Perazella, Mark A.Rosner, Mitchell H.2022-03-10T07:00:02-08:00doi:10.2215/CJN.11290821hwp:resource-id:clinjasn;17/8/1220American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, acute kidney injury, drugs, nephrotoxins, acute tubular injury, acute interstitial nephritis, crystalline nephropathy, chronic kidney disease, inflammation, apoptosisCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-08-01August 202210.2215/CJN.112908211555-90411555-905X2022-03-10T07:00:02-08:002022-08Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17812201233AKI is a potential complication of intravascular iodinated contrast exposure. Contrast-associated AKI, which typically manifests as small and transient decrements in kidney function that develop within several days of contrast administration, is associated with serious adverse outcomes, including progressive kidney dysfunction and death. However, a causal link between the small increases in serum creatinine that characteristically occur with contrast-associated AKI and serious adverse outcomes remains unproven. This is important given mounting evidence that clinically indicated, potentially lifesaving radiographic procedures are underutilized in patients with CKD. This has been hypothesized to be related to provider concern about precipitating contrast-associated AKI. Intravascular gadolinium-based contrast, an alternative to iodinated contrast that is administered with magnetic resonance imaging, has also been linked with potential serious adverse events, notably the development of nephrogenic systemic fibrosis in patients with severe impairment in kidney function. Patients hospitalized in the intensive care unit frequently have clinical indications for diagnostic and therapeutic procedures that involve the intravascular administration of contrast media. Accordingly, critical care providers and others treating critically ill patients should possess a sound understanding of the risk factors for and incidence of such outcomes, the ability to perform evidence-based risk-benefit assessments regarding intravascular contrast administration, and knowledge of empirical data on the prevention of these iatrogenic complications.10.2215/CJN.16311221Fri, 01 Jul 2022 06:35:28 GMT-07:00Radiographic Contrast Media and the KidneyAKI is a potential complication of intravascular iodinated contrast exposure. Contrast-associated AKI, which typically manifests as small and transient decrements in kidney function that develop within several days of contrast administration, is associated with serious adverse outcomes, including progressive kidney dysfunction and death. However, a causal link between the small increases in serum creatinine that characteristically occur with contrast-associated AKI and serious adverse outcomes remains unproven. This is important given mounting evidence that clinically indicated, potentially lifesaving radiographic procedures are underutilized in patients with CKD. This has been hypothesized to be related to provider concern about precipitating contrast-associated AKI. Intravascular gadolinium-based contrast, an alternative to iodinated contrast that is administered with magnetic resonance imaging, has also been linked with potential serious adverse events, notably the development of nephrogenic systemic fibrosis in patients with severe impairment in kidney function. Patients hospitalized in the intensive care unit frequently have clinical indications for diagnostic and therapeutic procedures that involve the intravascular administration of contrast media. Accordingly, critical care providers and others treating critically ill patients should possess a sound understanding of the risk factors for and incidence of such outcomes, the ability to perform evidence-based risk-benefit assessments regarding intravascular contrast administration, and knowledge of empirical data on the prevention of these iatrogenic complications.Cashion, WinnWeisbord, Steven D.2022-07-01T06:35:28-07:00doi:10.2215/CJN.16311221hwp:resource-id:clinjasn;17/8/1234American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, contrast mediaCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-08-01August 202210.2215/CJN.163112211555-90411555-905X2022-07-01T06:35:28-07:002022-08Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17812341242Intermittent hemodialysis remains a cornerstone of extracorporeal KRT in the intensive care unit, either as a first-line therapy for AKI or a second-line therapy when patients transition from a continuous or prolonged intermittent therapy. Intermittent hemodialysis is usually provided 3 days per week in this setting on the basis that no clinical benefits have been demonstrated with more frequent hemodialysis. This should not detract from the importance of continually assessing and refining the hemodialysis prescription (including the need for extra treatments) according to dynamic changes in extracellular volume and other parameters, and ensuring that an adequate dose of hemodialysis is being delivered to the patient. Compared with other KRT modalities, the cardinal challenge encountered during intermittent hemodialysis is hemodynamic instability. This phenomenon occurs when reductions in intravascular volume, as a consequence of ultrafiltration and/or osmotic shifts, outpace compensatory plasma refilling from the extravascular space. Myocardial stunning, triggered by intermittent hemodialysis, and independent of ultrafiltration, may also contribute. The hemodynamic effect of intermittent hemodialysis is likely magnified in patients who are critically ill due to an inability to mount sufficient compensatory physiologic responses in the context of multiorgan dysfunction. Of the many interventions that have undergone testing to mitigate hemodynamic instability related to KRT, the best evidence exists for cooling the dialysate and raising the dialysate sodium concentration. Unfortunately, the evidence supporting routine use of these and other interventions is weak owing to poor study quality and limited sample sizes. Intermittent hemodialysis will continue to be an important and commonly used KRT modality for AKI in patients with critical illness, especially in jurisdictions where resources are limited. There is an urgent need to harmonize the definition of hemodynamic instability related to KRT in clinical trials and robustly test strategies to combat it in this vulnerable patient population.10.2215/CJN.04000422Fri, 15 Jul 2022 10:44:05 GMT-07:00Management of Intermittent Hemodialysis in the Critically Ill PatientIntermittent hemodialysis remains a cornerstone of extracorporeal KRT in the intensive care unit, either as a first-line therapy for AKI or a second-line therapy when patients transition from a continuous or prolonged intermittent therapy. Intermittent hemodialysis is usually provided 3 days per week in this setting on the basis that no clinical benefits have been demonstrated with more frequent hemodialysis. This should not detract from the importance of continually assessing and refining the hemodialysis prescription (including the need for extra treatments) according to dynamic changes in extracellular volume and other parameters, and ensuring that an adequate dose of hemodialysis is being delivered to the patient. Compared with other KRT modalities, the cardinal challenge encountered during intermittent hemodialysis is hemodynamic instability. This phenomenon occurs when reductions in intravascular volume, as a consequence of ultrafiltration and/or osmotic shifts, outpace compensatory plasma refilling from the extravascular space. Myocardial stunning, triggered by intermittent hemodialysis, and independent of ultrafiltration, may also contribute. The hemodynamic effect of intermittent hemodialysis is likely magnified in patients who are critically ill due to an inability to mount sufficient compensatory physiologic responses in the context of multiorgan dysfunction. Of the many interventions that have undergone testing to mitigate hemodynamic instability related to KRT, the best evidence exists for cooling the dialysate and raising the dialysate sodium concentration. Unfortunately, the evidence supporting routine use of these and other interventions is weak owing to poor study quality and limited sample sizes. Intermittent hemodialysis will continue to be an important and commonly used KRT modality for AKI in patients with critical illness, especially in jurisdictions where resources are limited. There is an urgent need to harmonize the definition of hemodynamic instability related to KRT in clinical trials and robustly test strategies to combat it in this vulnerable patient population.Chan, Ryan J.Helmeczi, WryanCanney, MarkClark, Edward G.2022-07-15T10:44:05-07:00doi:10.2215/CJN.04000422hwp:resource-id:clinjasn;CJN.04000422v1American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologyacute kidney injury, hemodialysis, hypotensionInvited FeaturesCritical Care Nephrology and Acute Kidney InjuryInvited FeaturesCritical Care Nephrology and Acute Kidney Injuryresearch-article202210.2215/CJN.040004221555-90411555-905X2022-07-15T10:44:05-07:00Clinical Journal of the American Society of NephrologyInvited FeaturesCJN.04000422AKI is a syndrome, not a disease. It results from many different primary and/or secondary etiologies and is often multifactorial, especially in the hospitalized patient. This review discusses the pathophysiology of three etiologies that cause AKI, those being kidney hypoperfusion, abdominal compartment syndrome, and urinary tract obstruction. The pathophysiology of these three causes of AKI differs but is overlapping. They all lead to a low urine flow rate and low urine sodium initially. In all three cases, with early recognition and correction of the underlying process, the resulting functional AKI can be rapidly reversed. However, with continued duration and/or increased severity, cell injury occurs within the kidney, resulting in structural AKI and a longer and more severe disease state with increased morbidity and mortality. This is why early recognition and reversal are critical.10.2215/CJN.15341121Wed, 18 May 2022 10:59:11 GMT-07:00Low-Flow Acute Kidney InjuryAKI is a syndrome, not a disease. It results from many different primary and/or secondary etiologies and is often multifactorial, especially in the hospitalized patient. This review discusses the pathophysiology of three etiologies that cause AKI, those being kidney hypoperfusion, abdominal compartment syndrome, and urinary tract obstruction. The pathophysiology of these three causes of AKI differs but is overlapping. They all lead to a low urine flow rate and low urine sodium initially. In all three cases, with early recognition and correction of the underlying process, the resulting functional AKI can be rapidly reversed. However, with continued duration and/or increased severity, cell injury occurs within the kidney, resulting in structural AKI and a longer and more severe disease state with increased morbidity and mortality. This is why early recognition and reversal are critical.Molitoris, Bruce A.2022-05-18T10:59:11-07:00doi:10.2215/CJN.15341121hwp:resource-id:clinjasn;17/7/1039American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, renal hypoperfusion, intraabdominal hypertension, glomerulus, proximal tubule, renal hemodynamics, acute kidney injuryCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-07-01July 202210.2215/CJN.153411211555-90411555-905X2022-05-18T10:59:11-07:002022-07Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17710391049Sepsis-associated AKI is a life-threatening complication that is associated with high morbidity and mortality in patients who are critically ill. Although it is clear early supportive interventions in sepsis reduce mortality, it is less clear that they prevent or ameliorate sepsis-associated AKI. This is likely because specific mechanisms underlying AKI attributable to sepsis are not fully understood. Understanding these mechanisms will form the foundation for the development of strategies for early diagnosis and treatment of sepsis-associated AKI. Here, we summarize recent laboratory and clinical studies, focusing on critical factors in the pathophysiology of sepsis-associated AKI: microcirculatory dysfunction, inflammation, NOD-like receptor protein 3 inflammasome, microRNAs, extracellular vesicles, autophagy and efferocytosis, inflammatory reflex pathway, vitamin D, and metabolic reprogramming. Lastly, identifying these molecular targets and defining clinical subphenotypes will permit precision approaches in the prevention and treatment of sepsis-associated AKI.10.2215/CJN.00850122Tue, 28 Jun 2022 11:05:04 GMT-07:00The Pathophysiology of Sepsis-Associated AKISepsis-associated AKI is a life-threatening complication that is associated with high morbidity and mortality in patients who are critically ill. Although it is clear early supportive interventions in sepsis reduce mortality, it is less clear that they prevent or ameliorate sepsis-associated AKI. This is likely because specific mechanisms underlying AKI attributable to sepsis are not fully understood. Understanding these mechanisms will form the foundation for the development of strategies for early diagnosis and treatment of sepsis-associated AKI. Here, we summarize recent laboratory and clinical studies, focusing on critical factors in the pathophysiology of sepsis-associated AKI: microcirculatory dysfunction, inflammation, NOD-like receptor protein 3 inflammasome, microRNAs, extracellular vesicles, autophagy and efferocytosis, inflammatory reflex pathway, vitamin D, and metabolic reprogramming. Lastly, identifying these molecular targets and defining clinical subphenotypes will permit precision approaches in the prevention and treatment of sepsis-associated AKI.Kuwabara, ShuheiGoggins, EibhlinOkusa, Mark D.2022-06-28T11:05:04-07:00doi:10.2215/CJN.00850122hwp:resource-id:clinjasn;17/7/1050American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, sepsis, AKI, inflammation, microcirculatory dysfunction, metabolic reprogrammingCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-07-01July 202210.2215/CJN.008501221555-90411555-905X2022-06-28T11:05:04-07:002022-07Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17710501069Mechanical life support therapies exist in many forms to temporarily replace the function of vital organs. Generally speaking, these tools are supportive therapy to allow for organ recovery but, at times, require transition to long-term mechanical support. This review will examine nonrenal extracorporeal life support for cardiac and pulmonary support as well as other mechanical circulatory support options. This is intended as a general primer and overview to assist nephrologist consultants participating in the care of these critically ill patients who often experience acute renal injury as a result of cardiopulmonary shock and from their exposure to mechanical circulatory support.10.2215/CJN.13341021Fri, 20 May 2022 09:56:38 GMT-07:00Mechanical Circulatory SupportMechanical life support therapies exist in many forms to temporarily replace the function of vital organs. Generally speaking, these tools are supportive therapy to allow for organ recovery but, at times, require transition to long-term mechanical support. This review will examine nonrenal extracorporeal life support for cardiac and pulmonary support as well as other mechanical circulatory support options. This is intended as a general primer and overview to assist nephrologist consultants participating in the care of these critically ill patients who often experience acute renal injury as a result of cardiopulmonary shock and from their exposure to mechanical circulatory support.Tam, Christopher W.Shen, LiangZeidman, Amanda DijanicSrivastava, AnkurIvascu, Natalia S.2022-05-20T09:56:38-07:00doi:10.2215/CJN.13341021hwp:resource-id:clinjasn;17/6/890American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, cardiovascular, cardiovascular disease, heart failureCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-06-01June 202210.2215/CJN.133410211555-90411555-905X2022-05-20T09:56:38-07:002022-06Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury176890901The definition of sepsis has evolved significantly over the past three decades. Today, sepsis is defined as a dysregulated host immune response to microbial invasion leading to end organ dysfunction. Septic shock is characterized by hypotension requiring vasopressors after adequate fluid resuscitation with elevated lactate. Early recognition and intervention remain hallmarks for sepsis management. We addressed the current literature and assimilated thought regarding optimum initial resuscitation of the patient with sepsis. A nuanced understanding of the physiology of lactate is provided in our review. Physiologic and practical knowledge of steroid and vasopressor therapy for sepsis is crucial and addressed. As blood purification may interest the nephrologist treating sepsis, we have also added a brief discussion of its status.10.2215/CJN.14381121Thu, 12 May 2022 08:19:26 GMT-07:00Sepsis Management for the NephrologistThe definition of sepsis has evolved significantly over the past three decades. Today, sepsis is defined as a dysregulated host immune response to microbial invasion leading to end organ dysfunction. Septic shock is characterized by hypotension requiring vasopressors after adequate fluid resuscitation with elevated lactate. Early recognition and intervention remain hallmarks for sepsis management. We addressed the current literature and assimilated thought regarding optimum initial resuscitation of the patient with sepsis. A nuanced understanding of the physiology of lactate is provided in our review. Physiologic and practical knowledge of steroid and vasopressor therapy for sepsis is crucial and addressed. As blood purification may interest the nephrologist treating sepsis, we have also added a brief discussion of its status.Patel, SharadPuri, NitinDellinger, R. Phillip2022-05-12T08:19:26-07:00doi:10.2215/CJN.14381121hwp:resource-id:clinjasn;17/6/880American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, sepsis, acute kidney injury, septic shockCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-06-01June 202210.2215/CJN.143811211555-90411555-905X2022-05-12T08:19:26-07:002022-06Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury176880889Since the description ischuria renalis by William Heberden (1), AKI has remained a prominent complication of critical illness. Beyond KRT, treatment has been limited by the capacity to phenotype this condition. Here, we chronicle the evolution of attempts to classify AKI, including the adoption of consensus definitions, the expansion of diagnosis and prognosis with novel biomarkers, and emerging tools such as artificial intelligence (AI).10.2215/CJN.14181021Tue, 15 Mar 2022 08:22:04 GMT-07:00Overview of Diagnostic Criteria and Epidemiology of Acute Kidney Injury and Acute Kidney Disease in the Critically Ill PatientSince the description ischuria renalis by William Heberden (1), AKI has remained a prominent complication of critical illness. Beyond KRT, treatment has been limited by the capacity to phenotype this condition. Here, we chronicle the evolution of attempts to classify AKI, including the adoption of consensus definitions, the expansion of diagnosis and prognosis with novel biomarkers, and emerging tools such as artificial intelligence (AI).Birkelo, Bethany C.Pannu, NeeshSiew, Edward D.2022-03-15T08:22:04-07:00doi:10.2215/CJN.14181021hwp:resource-id:clinjasn;17/5/717American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury Series, acute kidney injury, epidemiologyCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-05-01May 202210.2215/CJN.141810211555-90411555-905X2022-03-15T08:22:04-07:002022-05Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury175717735One of the primary reasons for intensive care admission is shock. Identifying the underlying cause of shock (hypovolemic, distributive, cardiogenic, and obstructive) may lead to entirely different clinical pathways for management. Among patients with hypovolemic and distributive shock, fluid therapy is one of the leading management strategies. Although an appropriate amount of fluid administration might save a patient's life, inadequate (or excessive) fluid use could lead to more complications, including organ failure and mortality due to either hypovolemia or volume overload. Currently, intensivists have access to a wide variety of information sources and tools to monitor the underlying hemodynamic status, including medical history, physical examination, and specific hemodynamic monitoring devices. Although appropriate and timely assessment and interpretation of this information can promote adequate fluid resuscitation, misinterpretation of these data can also lead to additional mortality and morbidity. This article provides a narrative review of the most commonly used hemodynamic monitoring approaches to assessing fluid responsiveness and fluid tolerance. In addition, we describe the benefits and disadvantages of these tools.10.2215/CJN.14191021Mon, 04 Apr 2022 07:46:06 GMT-07:00The Intensivist's Perspective of Shock, Volume Management, and Hemodynamic MonitoringOne of the primary reasons for intensive care admission is shock. Identifying the underlying cause of shock (hypovolemic, distributive, cardiogenic, and obstructive) may lead to entirely different clinical pathways for management. Among patients with hypovolemic and distributive shock, fluid therapy is one of the leading management strategies. Although an appropriate amount of fluid administration might save a patient's life, inadequate (or excessive) fluid use could lead to more complications, including organ failure and mortality due to either hypovolemia or volume overload. Currently, intensivists have access to a wide variety of information sources and tools to monitor the underlying hemodynamic status, including medical history, physical examination, and specific hemodynamic monitoring devices. Although appropriate and timely assessment and interpretation of this information can promote adequate fluid resuscitation, misinterpretation of these data can also lead to additional mortality and morbidity. This article provides a narrative review of the most commonly used hemodynamic monitoring approaches to assessing fluid responsiveness and fluid tolerance. In addition, we describe the benefits and disadvantages of these tools.Kashani, KianoushOmer, TarigShaw, Andrew D.2022-04-04T07:46:06-07:00doi:10.2215/CJN.14191021hwp:resource-id:clinjasn;17/5/706American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, hemodynamic monitoring, shock, fluid therapy, fluid responsiveness, POCUSCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-05-01May 202210.2215/CJN.141910211555-90411555-905X2022-04-04T07:46:06-07:002022-05Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury17570671610.2215/CJN.01400222Thu, 10 Mar 2022 07:00:01 GMT-08:00Introduction to Critical Care Nephrology and Acute Kidney InjuryLiu, Kathleen D.Palevsky, Paul M.2022-03-10T07:00:01-08:00doi:10.2215/CJN.01400222hwp:resource-id:clinjasn;17/4/570American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury SeriesCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-04-01April 202210.2215/CJN.014002221555-90411555-905X2022-03-10T07:00:01-08:002022-04Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury174570571Mechanical ventilation is a lifesaving therapy for critically ill patients with respiratory failure, but like all treatments, it has the potential to cause harm if not administered appropriately. This review aims to give an overview of the basic principles of invasive and noninvasive mechanical ventilation. Topics covered include modes of mechanical ventilation, respiratory mechanics and ventilator waveform interpretation, strategies for initial ventilator settings, indications and contraindications for noninvasive ventilation, and the effect of the ventilator on kidney function.10.2215/CJN.13091021Thu, 10 Mar 2022 07:00:01 GMT-08:00Management of Respiratory FailureMechanical ventilation is a lifesaving therapy for critically ill patients with respiratory failure, but like all treatments, it has the potential to cause harm if not administered appropriately. This review aims to give an overview of the basic principles of invasive and noninvasive mechanical ventilation. Topics covered include modes of mechanical ventilation, respiratory mechanics and ventilator waveform interpretation, strategies for initial ventilator settings, indications and contraindications for noninvasive ventilation, and the effect of the ventilator on kidney function.Pearson, Steven D.Koyner, Jay L.Patel, Bhakti K.2022-03-10T07:00:01-08:00doi:10.2215/CJN.13091021hwp:resource-id:clinjasn;17/4/572American Society of NephrologyCopyright © 2022 by the American Society of NephrologyClinical Journal of the American Society of Nephrologycritical care nephrology and acute kidney injury series, respiratory failure, mechanical ventilationCritical Care Nephrology and Acute Kidney InjuryCritical Care Nephrology and Acute Kidney Injuryresearch-article20222022-04-01April 202210.2215/CJN.130910211555-90411555-905X2022-03-10T07:00:01-08:002022-04Clinical Journal of the American Society of NephrologyCritical Care Nephrology and Acute Kidney Injury174572580