scholarly journals Relationship between patients’ outcomes and the changes in serum creatinine and urine output and RIFLE classification in a large critical care cohort database

2015 ◽  
Vol 88 (2) ◽  
pp. 369-377 ◽  
Author(s):  
Steve K. Harris ◽  
Andrew J.P. Lewington ◽  
David A. Harrison ◽  
Kathy M. Rowan
2019 ◽  
Vol 4 (1) ◽  
pp. 671-674
Author(s):  
Chandra Bhushan Jha ◽  
Akhil Tamrakar

Introduction: Birth asphyxia is an eventuality having far reaching consequences in the neonatal period. Hypoxia and ischemia can cause damage to almost every tissue and organ in the body and various target organs involved. Renal insult is a recognized complication of birth asphyxia and carries a poor prognosis. Timely detection of renal dysfunction and appropriate management may favorably alter the prognosis in many neonates with birth asphyxia. Objective: The present study was done to find out the incidence of acute renal failure in the full term neonates with birth asphyxia. Methodology: A cross sectional study was conducted at Birat Medical College Teaching Hospital, Morang, Nepal from 1st September 2017 to 28th February 2018. Fifty full term neonates born with Apgar score of <6 at 5 minutes and fulfilling inclusion criteria were enrolled in the study. Asphyxiated neonates having Serum creatinine >1.5gm/dl or urine output<1ml/kg/hr were labeled as cases of Acute Renal Failure. Blood sample for serum creatinine was collected at 24hrs, 48 hrs and 72 hrs of life. Results A total of 50 term asphyxiated neonates were enrolled in the present study. Among them 54% and 46% were males and females respectively with male to female ratio of 1.2:1. In the present study 62% of cases developed acute renal failure in either of the first three days of life with mean urine output 1.02±0.27ml/kg/hr and mean serum creatinine of 1.49±0.32 mg/dL. The incidence of oliguric renal failure was 52% and non oliguric renal failure was 48%.The association between serum creatinine and urine output was statistically significant. Conclusion: In the present study birth asphyxia has been an important cause of neonatal acute renal injury, revealing 31 (62%) cases. Monitoring urine output and serum creatinine has helped in detecting the asphyxiated neonates with acute renal injury in the early stage.


2015 ◽  
Vol 26 (9) ◽  
pp. 2231-2238 ◽  
Author(s):  
John A. Kellum ◽  
Florentina E. Sileanu ◽  
Raghavan Murugan ◽  
Nicole Lucko ◽  
Andrew D. Shaw ◽  
...  

2015 ◽  
Vol 309 (5) ◽  
pp. F406-F413 ◽  
Author(s):  
Sarah C. Huen ◽  
Chirag R. Parikh

Acute kidney injury (AKI) is a common hospital complication. There are no effective treatments to minimize kidney injury or limit associated morbidity and mortality. Currently, serum creatinine and urine output remain the gold standard used clinically in the diagnosis of AKI. Several novel biomarkers can diagnose AKI earlier than elevations of serum creatinine and changes in urine output. Recent long-term observational studies have elucidated a subgroup of patients who have positive biomarkers of AKI but do not meet criteria for AKI by serum creatinine or urine output, termed subclinical AKI. These patients with subclinical AKI have increased risk of both short- and long-term mortality. In this review, we will highlight the implications of what these patients may represent and the need for better phenotyping of AKI by etiology, severity of injury, and ability to recover. We will discuss two AKI biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and breast regression protein-39 (BRP-39)/YKL-40, that exemplify the need to characterize the complexity of the biological meaning behind the biomarker, beyond elevated levels reporting on tissue injury. Ultimately, careful phenotyping of AKI will lead to identification of therapeutic targets and appropriate patient populations for clinical trials.


2015 ◽  
Vol 33 (4) ◽  
pp. 539-547 ◽  
Author(s):  
Florence Wong

Background: Acute kidney injury (AKI) is a common complication of advanced cirrhosis. Type 1 hepatorenal syndrome is the best-known and most severe form of AKI, and it has a precise definition and a set of specific diagnostic criteria. More recently, it has become recognized that milder degrees of renal dysfunction also have a negative impact on patient outcome in various patient populations. Key Messages: Several definitions and criteria for staging the severity of AKI have been proposed, including the RIFLE (Risk, Injury, Failure, Loss of Function and End-Stage Renal Disease) group, the Acute Kidney Injury Network (AKIN), and the Kidney Disease: Improving Global Outcome (KDIGO) group. All of them incorporate some changes of serum creatinine and urine output in the definition and staging of AKI. The hepatology community has mostly embraced the AKIN diagnostic and staging criteria and has applied them in the prognostication of patients with advanced cirrhosis. However, the AKIN criteria have not been strictly applied in all studies on cirrhosis. This is partly related to the fact that changes in urine output are difficult to assess in advanced cirrhosis, and partly related to the difficulty in defining the baseline serum creatinine from which the change in serum creatinine is calculated. This has led to some confusion in the interpretation of results of the various studies on AKI in cirrhosis. More recently, some investigators have suggested incorporating the AKIN criteria with setting a lower limit of serum creatinine of 1.5 mg/dl in determining the diagnosis and prognosis of AKI in cirrhosis. Conclusions: This is an ongoing debate as to how best to define AKI in cirrhosis. In the near future there should be prospective clinical trials that will clarify which diagnostic and staging criteria of AKI will best serve the cirrhotic population.


Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4021-4021 ◽  
Author(s):  
Shelonitda S. Rose ◽  
Simi George ◽  
Serena Wong ◽  
Grace Tenorino ◽  
Mercy Kuriyan

Abstract Acute hemolytic transfusion reaction (AHTR) is a potentially serious complication associated with the transfusion of ABO incompatible blood. It results in disseminated intravascular coagulation (DIC), shock, renal failure and death. Patient misidentification, sample mislabeling are some of the causes of an AHTR. To-date there is no data available on the use of RBCET in the management of an AHTR. We report the clinical course and successful management of an AHTR following massive ABO incompatible blood transfusion. The patient is a 68-year-old female with known coronary artery disease and type O Rh negative blood, who presented to the emergency room with unstable angina. She was taken emergently to the operating room for a quadruple coronary artery bypass graft. Due to sample mislabeling, she received 7 units of incompatible type A Rh negative packed red blood cells (PRBC) intra-operatively. During the immediate post-operative period, she was noted to have increased drainage from the surgical site, decreased urine output, hematuria and a precipitous drop in hemoglobin to 6.5 g/dL. She underwent re-exploration and received an additional 2 units of incompatible type A Rh negative PRBC and other blood products including fresh frozen plasma (FFP), platelets and cryoprecipitate that were ABO incompatible. In the recovery room, family members confirmed her blood type as type O Rh negative. Immediate re-typing utilizing pre-transfusion blood samples collected for CBC and chemistry, and obtaining blood bank records from her previous admission from another hospital a diagnosis of ABO incompatible AHTR was established. Further work-up revealed a strong positive DAT (3+ IgG) with a positive eluate (patient’s anti-A antibodies coating the transfused type A RBC’s). Hemolysis parameters showed elevated LDH 753 IU, bilirubin 2.1 mg/dL, and decreased haptoglobin 29.4 mg/dL. Her urine output continued to decrease with increase in serum creatinine to 2.4mg/dL. A continuous veno-venous hemodialysis (CVVHD) was started along with fluid resuscitation and urine alkalinization. A RBCET was performed within 11 hours after the transfusion of the last incompatible unit, which was followed by a second RBCET 24 hours later. Each RBCET consisted of 8 units of type O Rh negative blood. Following the two RBCET her blood type became type O Rh negative. Hemolysis parameters improved over the next several days and became normal. Serum creatinine progressively improved with increasing urine output. Dialysis was discontinued on day 13. Patient continued to do well and was discharged home in good condition with a normal renal function three weeks after her initial admission. The severity and course of an AHTR is dictated by the load of incompatible blood cells in the circulation. The high mortality rate associated with an AHTR warrants an aggressive approach in addition to supportive care. RBCET is used in the management of severe hemolytic disease of the new born, complications of sickle cell disease, and to lower the parasite load in malaria and babesiosis. The role of RBCET in AHTR is not established. There are two case reports in the Japanese literature where a RBCET was performed in the management of an AHTR with successful outcome. The course of this patient suggests that aggressive management including supportive care, timely RBCET, and renal replacement treatment may prevent DIC, organ damage and alter the grave prognosis associated with AHTR following incompatible blood transfusion.


2012 ◽  
Vol 40 (5) ◽  
pp. 1692-1693
Author(s):  
Kent Doi ◽  
Eisei Noiri

Sensors ◽  
2010 ◽  
Vol 10 (1) ◽  
pp. 934-951 ◽  
Author(s):  
Abraham Otero ◽  
Francisco Palacios ◽  
Teodor Akinfiev ◽  
Roemi Fernández
Keyword(s):  

Sign in / Sign up

Export Citation Format

Share Document