The Impact of July Admission on Outcome in Patients with Hematopoietic and Lymphoid Malignancy Admitted with Tumor Lysis Syndrome

Tumor lysis syndrome (TLS) defines a constellation of metabolic abnormalities resulting from tumor cell death leading to dreaded clinical complications, including acute kidney injury (AKI). The incidence of AKI in TLS varies from 14% to 76% and is associated with mortality in 36% cases, and up to 20% of patients require renal replacement therapy (RRT). This study was done to evaluate the therapeutic efficacy and safety of RRT in children with hematological malignancies who develop AKI with TLS. We retrospectively reviewed case records of patients, up to 5 years old,with AKI due to TLS who required RRT during November 2017–October 2019 admitted in the pediatric intensive care unit (PICU). The diagnosis of TLS was based on Bishop–Cairo criteria. The primary outcome was recorded as recovery of renal function. Out of total 400 patients with newly diagnosed hematological malignancy admitted in the PICU during the study period, 122 (30.5%) developed TLS with 32 (26.2%) having AKI, of which eight patients (2%) underwent dialysis. The mean estimated glomerular filtration rate on admission was 36.6 ± 9.8 mg/ml/1.73 m2 with a mean urine output being 0.32 ± 0.1 ml/kg/h. Seven of eight patients underwent hemodialysis. All cases had successful RRT with normalization of renal function and establishment of adequate urine output. RRT is safe and effective in children for AKI with TLS with the recovery of renal functions.

e19000 Background: Tumor lysis syndrome (TLS) is a known complication of hematologic malignancy treatments, often leading to fatal arrhythmias, acute kidney injury, and seizures. Chimeric Antigen Receptor T-cell (CAR-T) therapy, used for relapsed or refractory non-Hodgkin's lymphoma (NHL), B-cell acute lymphoblastic leukemia (ALL), and multiple myeloma (MM), has been increasingly associated with TLS. Single-center studies suggest that TLS in CAR-T patients correlates with lower overall survival, but its population-level impact remains underexplored. This study evaluates the effect of TLS on in-hospital outcomes in CAR-T patients using United States population data. Methods: We used the National Inpatient Sample to identify adult patients with ALL, NHL, and MM who underwent CAR-T between 2018 and 2021, based on ICD-10 codes. The cohort was stratified by TLS presence, with complex sampling weights used for national representation. We compared socio-demographic characteristics and comorbidities between groups. The primary outcome was all-cause mortality, with secondary outcomes assessed. Multivariate regression models evaluated outcome disparities, with significance set at p < 0.05. Results: We identified 4,120 adults who received CAR-T between 2018 and 2021 (82.5% NHL, 12.6% MM, 4.9% ALL), of whom 260 (6.3%) had concurrent TLS. A higher proportion of TLS patients had Medicare coverage (42.3% vs. 39.4%, p < 0.05), with no other significant demographic differences. The overall mortality rate was 3.0%, compared to 17.3% in the TLS group. TLS was associated with higher odds of all-cause mortality (adjusted odds ratio [aOR] 8.5, 95% CI 3.5–20.5), respiratory failure (aOR 3.9, 95% CI 1.9–8.1), acute kidney injury (aOR 3.8, 95% CI 2.0–7.3), shock (aOR 3.7, 95% CI 1.7–8.1), and gastrointestinal hemorrhage (aOR 6.8, 95% CI 1.6–28.5). TLS was also linked to higher odds of requiring mechanical ventilation (aOR 5.2, 95% CI 2.3–11.5), vasopressors (aOR 5.7, 95% CI 2.4–13.3), and renal replacement therapy (aOR 8.8, 95% CI 1.8–43.8). TLS patients had longer hospital stays (21.5 vs. 16.7 days, p < 0.05; adjusted incidence rate ratio [aIRR] 1.2, 95% CI 1.0–1.5). There were no significant differences in the risks of sudden cardiac death, new-onset seizures, acute venous thromboembolism, immune effector cell-associated neurotoxicity, intracerebral hemorrhage, or disseminated intravascular coagulation. Mean hospitalization charges for CAR-T patients were $1,196,413, with no significant difference between groups. Conclusions: Our study found that CAR-T patients with TLS had higher odds of all-cause mortality, adverse outcomes, longer hospital stays, and increased need for intensive care. These findings highlight the importance of early TLS detection and management to reduce complications and optimize healthcare resource use.

The term acute kidney injury has replaced acute renal failure and represents a spectrum of clinically meaningful kidney damage.After completing this article, readers should be able to:Acute kidney injury (AKI), formerly called acute renal failure, is characterized by multiple abnormalities, including increases in serum creatinine and blood urea nitrogen, electrolyte abnormalities, acidosis, and difficulties with fluid management. We have come to realize that what was previously thought to be relatively minor damage to the kidney can have significant short-term effects on morbidity and mortality and potential long-term implications for the development of chronic kidney disease. Thus, the term acute kidney injury has replaced acute renal failure, suggesting the spectrum of kidney damage that can occur.AKI is classically defined as an acute decrease in glomerular filtration rate, which results in an increase in serum creatinine. It is important to recognize the limitations of creatinine as a marker of AKI because an increase in creatinine can be delayed by as much as 48 hours after damage to the kidney has occurred. Despite this limitation, change in creatinine remains the gold standard for the diagnosis of AKI. An evolution in the definition of AKI to better understand, characterize, and study the disease spectrum, has occurred, which has sought to capture the clinical importance of even small variations in kidney function. In addition, previous definitions used in the literature were widely disparate; this lack of standardization made the understanding of AKI challenging. These circumstances have led to the development of 2 systems to define pediatric AKI that rely on changes in creatinine, estimated creatinine clearance, or urine output. The first of these definitions is the pediatric Risk, Injury, Failure, Loss, and End-stage (RIFLE) criteria, (1) which are modified from similar adult criteria. (2) The second is the Acute Kidney Injury Network (AKIN) definition, which relies on an increase in creatinine from a previous trough level. (3) The Kidney Disease: Improving Global Outcomes (KDIGO) consortium has put forth modifications to reconcile subtle differences in the adult AKIN and RIFLE criteria. (4) KDIGO is an international initiative composed of experts who, based on systematic review of evidence, develop and standardize clinical practice guidelines for children and adults with a variety of kidney diseases (including AKI). At this time, in practice and research, the pediatric RIFLE and modified AKIN criteria are most frequently used to define AKI in children (Table 1).A basic knowledge of renal development and normal renal physiology is necessary to better understand the pathophysiologic mechanisms of AKI. The kidney is immature at birth and continues to develop early in life. Term neonates are born with a full complement of nephrons but have only approximately 25% of their adult glomerular filtration rates. The renal function of a healthy child progressively increases, reaching a mature glomerular filtration rate by age 2 years. Neonates have immature compensatory mechanisms to handle changes in renal blood flow and are not able to fully concentrate their urine.Renal blood flow helps to drive a number of physiologic processes, including glomerular filtration, oxygen delivery to the kidneys, and solute or water reabsorption. Renal blood flow is under intricate control by a combination of hormones and reflex mechanisms. The afferent and efferent arterioles control renal blood flow to and from the glomerulus, respectively. The stretch of these arterioles (myogenic feedback) and delivery of sodium chloride sensed by the juxtaglomerular apparatus (tubuloglomerular feedback) drive a number of local and systemic hormone responses to low renal blood flow. In decreased renal perfusion, afferent arteriolar vasodilation occurs in response to prostaglandins (progtaglandins E and I), nitric oxide, and bradykinins to maintain glomerular filtration and renal blood flow. At the same time, the efferent arteriole is reflexively constricted by sympathetic nerve activation, endothelin, and activation of the renin-angiotensin system, leading to the production of angiotensin II. These mechanisms work in concert to maintain glomerular filtration and renal blood flow. Disease states and certain medical interventions may interfere with these mechanisms, leading to negative effects on glomerular filtration. Further, some of these compensatory mechanisms, when stressed beyond normal parameters, may themselves lead to diminished urinary output and clinical findings one would associate with AKI.With decreased renal perfusion, a number of these compensatory mechanisms also drive sodium and water reabsorption to increase extracellular volume. Increased activity of the renin-angiotensin system and production of angiotensin II (active in the proximal tubule) leads to increased secretion of aldosterone (active in the distal tubule), resulting in increased sodium reabsorption. Increased sympathetic nerve activity also drives sodium reabsorption. The reabsorption of urea and water is driven by antidiuretic hormone. The activity of these reflex mechanisms explains a number of the changes in urine electrolyte concentrations and clinical findings that help to differentiate the causes of AKI. The immaturity of these mechanisms in the neonate also explains why the diagnosis and evaluation of the cause of AKI in the neonate differs from that in older children.The epidemiology of AKI has evolved over the years and reflects the patient population under study. In developing countries the most common causes of AKI continue to be volume depletion, infection, and primary renal diseases (hemolytic uremic syndrome, glomerulonephritis). In developed countries, volume depletion and primary renal disease remain common causes of AKI in previously healthy children. In hospitalized children in developed countries, particularly in tertiary care centers, there has been a shift in the etiology of AKI from primary renal disease to secondary causes of AKI that are often multifactorial in nature and often complicate another diagnosis or its treatment (eg, heart disease, sepsis, and nephrotoxic drug exposure). (5) Despite this shift in epidemiology, an ordered approach to the diagnosis of AKI divides the potential origins into prerenal, intrinsic, and postrenal causes.Prerenal AKI results from a decrease in renal blood flow, leading to hypoperfusion (Table 2). The underlying pathophysiologic states may be due to a decrease in effective circulating volume, loss of vascular tone, or decreased cardiac output or blood delivery to the kidneys. Renal losses, gastrointestinal tract losses, or hemorrhage can lead to direct reduction in volume and decreased renal perfusion. Alternatively, a redistribution of fluid may occur from either reduced oncotic pressure within the blood (low albumin from liver disease, nephrotic syndrome, or protein losing enteropathy) or increased leak from vessels (systemic inflammatory response syndrome or sepsis), leading to suboptimal renal perfusion. Systemic vasodilation or poor vascular tone complicates a number of illnesses in critically ill children and may result in hypoperfusion of the kidneys. Finally, there may be a decrease in the delivery of blood to the kidneys because of an overall decrease in cardiac output (underlying heart disease or myocarditis) or increased resistance to flow (abdominal compartment syndrome or renal artery stenosis). In practice, previously healthy children frequently present with a decreased effective circulating volume from a single cause, whereas chronically ill or hospitalized children may have multifactorial processes.As noted above, low renal blood flow stimulates compensatory mechanisms, including increased sympathetic tone, activation of the renin-angiotensin system, release of antidiuretic hormone, and local paracrine activities (prostaglandin release). In the prerenal state, the afferent arterioles vasodilate in response to the local effects of prostaglandins in an effort to maintain renal blood flow and glomerular filtration. Consequently, nonsteroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, in volume-depleted children may worsen AKI by preventing this compensatory afferent arteriolar vasodilation. At the same time, angiotensin II causes efferent arteriolar constriction. Interruption of this compensatory mechanism by angiotensin-converting enzyme (ACE) inhibitors predisposes patients to prerenal AKI. The effects of renin-angiotensin system activation and antidiuretic hormone release result in increased sodium and urea reabsorption, respectively. The reabsorption of sodium, urea, and water leads to oliguria and the characteristic urine findings in prerenal AKI (Table 3).Neonates are a special group when considering prerenal AKI. Neonates have increased insensible losses because of a high body surface area to mass ratio, which can be exacerbated by the use of radiant warmers for critically ill newborns. Neonates are further at risk for prerenal AKI due to immature compensatory mechanisms, including poor urine concentrating abilities. This inability to concentrate urine explains why AKI in neonates is often nonoliguric, making its recognition more difficult.Patients with sickle cell disease are predisposed to prerenal AKI because of a number of pathophysiologic mechanisms inherent to the disease that may affect the kidney. The renal medulla represents an area of the kidney at risk in sickle cell disease because of a low oxygen concentration and high tonicity; this predisposes patients to sickling. Repeated episodes of sickling in the renal medulla result in vascular congestion and the loss of vasa recta of the juxtaglomerular nephrons, which can lead to chronic interstitial fibrosis and urine concentrating defects. In early childhood, the urinary concentrating defects frequently are reversible with treatment of the sickle cell disease but can progress to chronic concentrating defects over time.Intrinsic AKI refers to direct renal parenchymal damage or dysfunction. Categories include AKI associated with tubular, interstitial, glomerular, or vascular damage and nephrotoxin exposure (Table 4).The most common cause of intrinsic AKI in tertiary care centers is transformation of prerenal AKI to acute tubular necrosis (ATN) after prolonged hypoperfusion. The areas of the kidney that are most susceptible to damage with prolonged renal hypoperfusion include the third segment of the proximal tubule (high energy requirement) and the region of the thick ascending limb of the loop of Henle located within the medulla (low oxygen tension in the medulla). The damage seen from prolonged hypoperfusion can range from mild tubular injury to cell death. As cellular necrosis occurs, debris may build up in the tubules and further block tubular flow. Tubular dysfunction, a frequent hallmark of ATN, will not be evident during periods of oliguria but may become apparent during the recovery phase.In previously healthy children, glomerular and vascular causes of intrinsic AKI are more common. Where there is concern for glomerulonephritis, the clinical presentation and timing often suggest the origin, including isolated glomerulonephritides (eg, postinfectious glomerulonephritis) and multisystem immune complex–mediated processes that involve the kidney (eg, systemic lupus erythematosus). Vascular causes of intrinsic AKI include microangiopathic processes (hemolytic uremic syndrome and thrombotic thrombocytopenic purpura) and systemic vasculitides that involve larger vessels.Acute interstitial nephritis occurs after exposure to an offending agent, such as certain medications, including antibiotics, proton pump inhibitors, NSAIDs, and diuretics. Signs and symptoms may develop 3 to 5 days after a second exposure to as long as weeks to months after an initial exposure. Drugs can cause AKI in ways other than acute interstitial nephritis. Nephrotoxin exposure is an increasingly common cause of intrinsic AKI, particularly in hospitalized patients. As previously mentioned, drugs such as NSAIDs and ACE inhibitors can contribute to AKI by inhibiting renal vascular autoregulation. Other common drugs implicated in AKI include aminoglycosides, amphotericin, chemotherapeutic agents (cisplatin, ifosfamide, and methotrexate), and calcineurin inhibitors (cyclosporine and tacrolimus). Radiocontrast agents are a significant cause of nephrotoxin-related AKI; newer iso-osmolar agents are somewhat less nephrotoxic, but the risk remains. In instances of massive hemolysis or rhabdomyolysis, endogenous elements, such as myoglobin and hemoglobin, can obstruct tubules and/or cause direct toxic effects to the kidney.Postrenal AKI results from obstructive processes that block urine flow. Acquired causes of urinary tract obstruction include those that result from local mass effect (bilateral ureteral obstruction by a tumor), renal calculi, or clots within the bladder.An important developing paradigm in the study and treatment of AKI is the idea of renal angina, a term used to describe a high-risk state that occurs before AKI. (6) Earlier recognition of a prerenal state defines a period before significant parenchymal damage (eg, the development of ATN) where AKI can be reversed. Furthermore, patients who are identified as being at risk may have nephrotoxic medications held or dosages adjusted to potentially prevent the development of intrinsic AKI. Research using renal angina scoring systems is an active area that aims to identify patients at risk for AKI. Concurrently, investigation is under way to study novel biomarkers (urine neutrophil gelatinase–associated lipocalin and urine kidney injury molecule 1) that will allow for the earlier identification of kidney injury in critically ill children (often up to 48 hours before an increase in creatinine) to allow prevention and potentially earlier intervention.A detailed history and physical examination are invaluable for children who develop AKI. Quantifying the urine output during the previous several days may provide insight to the cause and severity of the episode of AKI and serves to categorize the event as oliguric (defined as urine output <1 mL/kg/h) or nonoliguric. Systematic evaluation of potential prerenal, intrinsic, and postrenal causes is key to diagnosing the origin of AKI. Frequently, the history will provide insight into causes or risk factors for prerenal AKI, including decreased circulatory volume (gastroenteritis and hemorrhage), redistribution of circulatory volume (edematous states, nephrotic syndrome, and sepsis), decreased cardiac output (heart disease), or increased resistance to blood flow (abdominal compartment syndrome and renal artery stenosis). In previously healthy children, the history and physical examination may offer clues (Table 4) to the underlying intrinsic renal origin, including volume depletion, recent viral illness or sore throat (possibly consistent with acute glomerulonephritis), rashes, swollen joints (suggesting systemic disorders such as lupus), hematuria, or medication exposures. In newborns with a suspected obstruction, a good prenatal history is important. For example, abnormalities on fetal ultrasonogram, including enlarged bladder, hydronephrosis, or decreased amniotic fluid, may suggest posterior urethral valves in a male infant. When evaluating AKI, it is important to remember that an increase in creatinine typically occurs up to 48 hours after renal injury and may reflect events that occurred 2 to 3 days earlier. Therefore, it is important to review episodes of hypotension, hypoxia, sepsis, surgery, contrast exposures, and drug exposures that occur 48 to 72 hours before the episode of AKI becomes apparent.As part of the initial evaluation for AKI, patients should have the following tests performed: basic electrolyte panel, serum creatinine measurement, urinalysis, urine sodium measurement, urine urea measurement, urine creatine measurement, urinalysis, and a renal ultrasound study. Frequently, urine studies will allow differentiation between prerenal AKI and intrinsic AKI (eg, ATN). Typical laboratory findings for prerenal AKI include a normal urinalysis result, concentrated urine (osmolality >500 mOsm/kg [>500 mmol/kg]), fractional excretion of sodium (FENa) less than 1% (<2% in neonates), fractional excretion of urea (FEurea) less than 35%, urine sodium less than 20 mEq/L (<20 mmol/L), and urea nitrogen to creatinine ratio greater than 20 (Table 3). A loss of urine concentrating ability is classically seen in ATN and results in the characteristic urine studies that differentiate it from prerenal AKI (Table 3). Urinalysis with accompanying urine microscopy can be illuminating and point toward particular diagnostic categories. Muddy granular casts on microscopy suggest ATN; red blood cell casts suggest glomerulonephritis. A urinalysis positive for blood on dipstick evaluation without evidence of red blood cells on microscopy should raise concerns for hemoglobinuria (hemolysis) or myoglobinuria (rhabdomyolysis).The presence of hematuria, proteinuria, and/or red blood cell casts in the right clinical scenario should raise concern for possible glomerulonephritis. In the context of a recent upper respiratory tract infection, one should consider the diagnosis of postinfectious glomerulonephritis (classically with pharyngitis 2-3 weeks earlier or skin infections 4-6 weeks earlier) and should evaluate serum complements (low C3 and normal C4). In patients with a more recent upper respiratory tract infection (2-3 days) with gross hematuria on urinalysis, one must consider IgA nephropathy (normal complement levels). A urinalysis consistent with glomerulonephritis in the context of the appropriate systemic symptoms (eg, rash and arthritis) may point toward systemic lupus erythematosus (low C3 and low C4) and may warrant further antibody testing (antinuclear and anti–double-stranded DNA antibodies). If there is involvement of the pulmonary system (cough, infiltrate on radiographs, and hemoptysis) and evidence of active glomerulonephritis, the pulmonary renal syndromes should be considered. These syndromes include granulomatosis with polyangiitis (formerly Wegener granulomatosis and cytoplasmic antineutrophil cytoplasmic antibody [ANCA]), microscopic polyangiitis (perinuclear ANCA), eosinophilic granulomatosis (formerly and ANCA), and syndrome A more detailed of glomerulonephritides is beyond the of this In the of a clinical and laboratory presentation of postinfectious glomerulonephritis, a renal is not but to the diagnosis and treatment of the a is of the glomerulonephritides is of glomerulonephritis, which is defined by blood urea nitrogen and creatine In this a renal and treatment are because renal injury may develop without for interstitial nephritis of and is not often seen in the and is in less than of patients. This is due to a change over in the most common offending In patients with suspected interstitial there is frequently urine that not have red blood cell casts but may have blood cell casts The is urine this is not can be of interstitial nephritis is of nephrotic range A renal is necessary to the a patient has a recent history of low and with AKI, one should consider uremic In the appropriate a blood with is In recent years there has been an increase in the recognition of uremic syndrome by infections (eg, or or abnormalities in complement (eg, or a high of is and is a small in the diagnosis of intrinsic renal disease. Kidney by renal can provide the of the disease. kidneys point toward an acute that active that are particularly small for age may suggest a more chronic the kidneys will increased in the of AKI, which is a A evaluation of the renal is an important initial there are concerns of renal artery but the result of the evaluation is negative and concern of renal artery further studies should be in with a pediatric by renal to is the most important initial in the diagnosis of an obstructive and may provide clues to the of the For example, a more distal If an obstructive is one should the obstruction most important for children with AKI is In the and the this can be by children who are at risk for developing AKI. In it is important to and be of medications children may in the term or long term and ACE that increase the risk of AKI. In hospitalized it is also important to be of volume nephrotoxic medications, or nephrotoxic exposures. For patients at risk for developing AKI, it is important that the potentially nephrotoxic medications, and of medications such as and initial in the treatment of children who present with hypotension, or is to volume. An initial of should be necessary in the of that may be used for short-term volume include normal and red blood The of fluid on the clinical but normal is most This treatment should be to the In children with underlying or suspected cardiac disease, initial fluid may be as for this will appropriate the risk of volume which be in the of heart disease. the fluid is necessary for children to for of fluid or and response and urine fluid early of may be may be for a child who with fluid in adults evaluating low renal have at these low not increase or urine output or the of AKI. should be to renal with the of based on the clinical the patient has been fluid one may consider a of the patient remains The literature results for in patients with The literature the use of is and this medication may be associated with effects serum pulmonary and AKI). The use of to urine output is not children who remain oliguric after volume fluid may be In these children, one may fluid to insensible fluid losses with AKI are to a number of electrolyte including acidosis, and Typical sodium in healthy children are 2 to 3 but should be in children with AKI, with made based on frequent sodium should be to prevent and other of sodium and should be from in these patients to the of and will to be replaced as necessary because low of and can have implications in critically ill children. to maintain or fluid in AKI patients represents an for renal remains one of the most of AKI. The symptoms of are frequently including and even For this and of laboratory results in children with AKI are important. The most of is cardiac abnormalities and changes may be noted when are to mEq/L mmol/L), but there can be significant on the clinical In pathophysiologic states of increased release from cells syndrome and changes may occur at The that result in changes with the underlying pathophysiologic mechanisms, and associated electrolyte abnormalities The changes are first by Other changes may include and prolonged may lead to patients with greater than mEq/L mmol/L), one should an If are to mEq/L and the patient has an appropriate urine output without abnormalities on one may consider treatment with a that in the or a with to and the to a more normal If there are changes on a greater than mEq/L mmol/L), or a in a child with high cell states (eg, and should be as and treatment include which to the cardiac potential and the risk of but not This may be by the of sodium and/or with of which cause of and reduction of blood but these not from the may be there is an associated with the evaluating sodium in adults with have not but this has not been in children. sodium may be as part of treatment for it should not be the by as it is for such as can be This has been to by mEq/L and is but may to be in children with cardiac because is a common effect of with drives into cells by sodium and In with these should be made to from the including loop with fluid and sodium should be in neonates or children with underlying disease. If these renal should be seen in AKI is characterized by an which reflects an inability of the kidneys to or the of the treatment of use of should be for and with of with can lead to a of as are on for which can result in of a suboptimal glomerular filtration rate in the of AKI, can particularly with increased cell syndrome and In most can be by In patients with it is important to and because may occur as a result of to children with AKI drug may be evaluation of patient medication is to drug the kidney function to of most drugs will in episodes of AKI, of kidney function can lead to of the glomerular filtration clinical is should evaluate the of nephrotoxic medications on a consider and drug as able when nephrotoxic medications are When children renal medication must be adjusted further episodes of AKI, it is important to medication in a approach that pediatric and AKI is by a state, particularly in critically ill children. The protein in these children may be as high as 3 of with an accompanying of to that of healthy children and should not protein delivery as a to control blood urea nitrogen to protein one may a blood urea nitrogen of to If and be this may be an for renal is when to AKI have or are to be for renal include volume fluid acidosis, blood urea nitrogen or or an inability to provide in patients with renal dysfunction. In recent years the importance of volume in critically ill children has become and the of fluid at the of renal has been to be associated with increased of renal include and renal The of is a of patient and clinical is in critically ill children and relatively to but not provide the same rate of or ability to volume as other during 3 to hours better but is not as in critically ill children or children with fluid during a can be in these patients. has been a shift toward renal as the of in critically ill children. This for volume and control during include increased of fluid and ability to provide and remain for those patients who renal but are not critically literature has that critically ill children who are after an episode of AKI are at increased risk of chronic kidney disease in life. of these patients is important. The for these children is not In more of AKI that renal should be with In one may consider blood pressure and

Acute Kidney Injury

Long-Term Outcomes of Acute Kidney Injury

Characteristics and Outcomes of Survivors of Critical Illness and Acute Kidney Injury Followed in a Pilot Acute Kidney Injury Clinic

e19582 Background: Tumor lysis syndrome (TLS) is a well-known complication of hematological malignancies including leukemia and lymphoma which can occur after chemotherapy or spontaneously, early recognition of TLS can be challenging sometimes. We attempted to evaluate the Weekend effect on TLS outcomes. Methods: Healthcare Cost and Utilization Project National Inpatient Sample (HCUP-NIS) was queried to identify TLS admissions between 2016-2018 in patients with diagnosis of acute leukemia and lymphoma. We studied socio-demographic differences, all-cause mortality, acute renal failure and dialysis. Secondary outcomes included mean length of stay (LOS), mean total hospital charges (THC). Statistics were performed using the t-test, univariate and multinomial logistic regression. Results: A total 1595 TLS admissions were identified (51% in lymphoma and 49% in acute leukemia), weekend admissions were 14.4% of total admissions. There was no significant difference in the baseline characteristics between the 2 groups including mean age, sex, race, median household income national quartile for patient zip code, insurance, region of hospital and location/teaching status of the hospital. Total 195 (12%) patients died in the total study group; Mortality rate among patients with lymphoma was 16% while those with leukemia was 9%. Overall mortality rate among the Weekend group compared to weekday group was insignificantly higher (20% vs 11% with P = 0.11, aOR 1.4 CI 0.56-3.46 p = 0.53). Mortality in the Weekend group was significantly higher in patients with lymphoma (30% vs 13% P = 0.04) while in leukemia patients there was no significant weekend effect (8% vs 9% P = 0.83). Total 1170 patients developed acute renal failure (aOR 1.56 Cl 0.64-3.9 p 0.32) of which 30 required dialysis, none of them was admitted in the weekend group. Mean LOS for the whole cohort was 6.47 days and mean THC was $94,954 with no significant difference between the 2 groups. Conclusions: All-cause mortality was significantly higher in patients with TLS and lymphoma admitted on the weekend (p = 0.04) compared to weekday while no weekend effect was found in TLS admissions in leukemia. Further studies are needed to clarify if this higher mortality may be associated with delay in TLS diagnosis over weekend admissions in lymphoma patients.

Cancer and the Kidney: The Growth of Onco-nephrology

Tumor lysis syndrome (TLS) is a common oncologic emergency among patients with pediatric hematologic malignancies. The mainstay of TLS management is aggressive intravenous hydration. However, the epidemiology of fluid overload (FO) and acute kidney injury (AKI) in this population is understudied. In this study, we aimed to describe the incidence, severity, and complications of FO and AKI among pediatric patients with TLS. We completed a single-center retrospective cohort study of pediatric patients with a new diagnosis of hematologic malignancy over a 10-year period. Patients with TLS were analyzed in two groups based on the severity of AKI and FO. Charts were reviewed for complications associated with AKI and FO including hypoxemia, mechanical ventilation, hyponatremia, pulmonary edema, pediatric intensive care (PICU) admission, and need for renal replacement therapy (RRT). We analyzed 56 patients with TLS for FO and AKI. We found severe FO (≥10%) occurred in 35.7% (n=20). PICU admission occurred in 35% of patients with severe FO compared to 8.3% in those with mild/moderate FO <10% (p=.013). Complications of hypoxemia (30% vs. 5.6%, p=.012) and pulmonary edema (25% vs. 2.8%, p=.010) were more common among those with severe FO. AKI occurred in 37.5% (n=21) patients and resulted in a significant increase in PICU admission and requirement for RRT (p=.001 and <.001, respectively). Our results show FO and AKI are common, and often unrecognized complications of TLS associated with increased morbidity. Prospective, multicenter studies are needed to further dissect the burden of FO and AKI within this vulnerable population.

Michael R. Charlton, William J. Wall, Akinlolu O. Ojo, Pere Gines, Stephen Textor, Fuad S. Shihab, Paul Marotta, Marcelo Cantarovich, James D. Eason, Russell H. Wiesner, Michael A. Ramsay, Juan C. Garcia-Valdecasas, James M. Neuberger, Sandy Feng, Connie L. Davis, Thomas A. Gonwa, and the International Liver Transplantation Society Expert Panel Mayo Clinic, Rochester MN; Department of General Surgery, London Health Science Center, London, Ontario, Canada; Department of Internal Medicine, University of Michigan Health System, Ann Arbor, MI; Liver Unit, Hospital Clinic, University of Barcelona School of Medicine, Barcelona, Spain; Department of Nephrology, University of Utah School of Medicine, Salt Lake City, UT; Medical School, University of Western Ontario, London, Ontario, Canada; Department of Medicine, McGill University Health Center, Montreal, Quebec, Canada; Transplant Institute, University of Tennessee, Memphis, TN; Baylor University Medical Center, Dallas, TX; Hospital Clinic I Provincial, Barcelona, Spain; Queen Elizabeth Hospital, Birmingham, England; Department of Transplant Surgery, University of California San Francisco Medical Center, San Francisco, CA; Department of Medicine, University of Washington Medical Center, Seattle, WA; and Mayo Clinic, Jacksonville, FL

World Kidney Day 2013: Acute Kidney Injury—Global Health Alert

Tumor lysis syndrome (TLS), hyperleukocytosis, and disseminated intravascular coagulation (DIC) are representative oncological emergencies that overlap mutually at the beginning of therapy for aggressive leukemia. Lately recombinant urate oxidase (rUO) enables to control uric acid level and its crystallization, the most frequent risk factor for clinical TLS; therefore, hyperphosphatemia appears to be the main risk in the rUO era. We here report an infantile leukemia patient who developed severe hyperphosphatemia, resulting in acute renal failure and ischemic encephalopathy. A 9-month-old female baby was adynamic with a bulging anterior fontanel, and was diagnosed as infantile acute lymphoblastic leukemia with a mixed lineage leukemia gene rearrangement. A laboratory examination revealed leukocytosis, bicytopenia, hyperuricemia, a prolonged prothrombin time, activated partial thromboplastin time, and elevated lactate dehydrogenase level. Soon after a reduced dose of prednisolone was administered, she developed hypoxia caused by systemic inflammatory response syndrome and heart failure. Her white blood cell count decreased sharply, leading to acute renal failure due to hyperphosphatemia, which required continuous hemodiafiltration for 48 hours. Although renal function subsequently recovered, severe ischemic encephalopathy remained. She achieved morphological remission once, however, relapsed and passed away soon after. We have to pay attention to the progression of hyperphosphatemia, hyperkakemia and DIC, although hyperuricemia was controlled using rUO. Changes in electrolyte levels must be continuously monitored, and TLS, DIC and/or hyperleukocytosis should be promptly managed especially in patients who are sensitive to therapy.

Immunosuppression in liver transplant recipients with renal impairment

CODE ACUTE KIDNEY INJURY-RENAL REPLACEMENT THERAPY, PROGNOSIS AND SURVIVAL IN PATIENTS WITH ACUTE KIDNEY INJURY AFTER IN-HOSPITAL CARDIAC ARREST

Background: Acute kidney injury (AKI) is a common clinical condition with high morbidity and mortality. Early risk stratification by identifying patients at risk for death or dialysis requirement has important therapeutic implications for timely interventions. Objective: The aim of this study was to examine the association of routine blood test parameters, specifically red blood cell distribution width (RDW) and neutrophil-to-lymphocyte ratio (NLR), with the AKI patient outcomes. Methods: All adult patients hospitalized from January 1, 2016, to June 30, 2016, in the Second Xiangya Hospital of Central South University were surveyed. Demographic characteristics, laboratory measurements, comorbidities, and outcomes of a total of 1,188 adult AKI patients were analyzed. Results: The incidence of AKI was 1.8% (1,188/65,329). The all-cause mortality was 16.0% (190/1,188). The multivariable relative risk of AKI mortality comparing high RDW with low RDW was 1.84 and the risk comparing high NLR with low NLR was 2.54. RDW and NLR combination showed additive values in stratifying high-risk patients, and the predictive power was comparable to the use of serum creatinine for staging AKI. In subgroup analyses, high RDW predicted prerenal AKI mortality better than intrinsic AKI. High RDW and NLR also independently predicted renal replacement therapy (RRT) requirement in AKI patients. In contrast, WBC count and platelet-to-lymphocyte ratio did not show obvious correlations with death and RRT requirement in AKI patients. Conclusion: The results support the potential usefulness of RDW and NLR in risk stratification of AKI patients, providing additional prognostic information for treatment and supportive care.