|Year : 2018 | Volume
| Issue : 2 | Page : 18-20
Critical care nephrology - An overview and update guest editorial
Vinayak Patki1, Uma Ali2
1 Chief, Advanced Pediatric Critical Care Centre and Head, Dept. of Pediatrics, Wanless Hospital, Miraj, Maharashtra, India
2 Consultant Pediatric Nephrologist, SRCC-NH Children's Hospital, Mumbai, Lilavati Hospital and Research Centre, Mumbai and Jupiter Hopsital, Thane, India
|Date of Submission||18-Apr-2020|
|Date of Acceptance||18-Apr-2027|
|Date of Web Publication||18-Apr-1930|
Chief, Advanced Pediatric Critical Care Centre & Head, Dept of Pediatrics, Wanless Hospital, Miraj, 416101, Maharashtra
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Patki V, Ali U. Critical care nephrology - An overview and update guest editorial. J Pediatr Crit Care 2018;5:18-20
Acute kidney injury (AKI) is increasingly being recognized in hospitalized patients. In the general hospital setting, approximately 15% of inpatients sustain an episode of acute kidney injury (AKI) and in the critical care centers this can increase to over 25%. It is associated with significant short-term morbidity and mortality, which cannot be completely explained by loss of organ function. There is evidence that reduced renal cytokine clearance as well as increased cytokine production by the acutely injured kidney contribute to a systemic inflammation state, which results in significant effects on other organs. AKI compromises the function of the innate immune system. AKI is an acute systemic disease with serious distant organ effects.
The definition of AKI based on easily available bedside biomarkers such as urine output and serum creatinine has undergone several revisions in the last decade, in order to standardize the diagnostic criteria for early detection as well as staging of severity. Fluid overload has now been recognized as a marker that identifies those at risk for developing AKI in the critical care setting. Considerable research has brought into limelight urinary biomarkers that reflect different molecular mechanisms of renal injury and repair that occur at various stages during the evolution of AKI. The future will see a refinement of the AKI criteria to include both the old and new biomarkers in order to detect AKI early and stage the severity of injury more accurately.
Acute kidney injury (AKI) is a serious yet potentially reversible complication of sepsis. Several molecular mechanisms involved in the development of septic AKI have been identified, which may help in the development of future therapies. After sepsis and hypotension, drugs are the leading cause of acute kidney injury (AKI) in critically ill patients. Susceptibilities and exposures for development of AKI have been identified, of which some are modifiable allowing for the possibility of AKI prevention or diminution of AKI severity. We need to depend on risk- assessment strategies for prevention of AKI as there has been little success for using drug therapies.
Fluid therapy is the most common intervention received by acutely ill hospitalized patients; however, its optimal use remains questionable. Its prescription should be patient and context specific, with clear indications and contradictions, and have the type, dose, and rate specified. Any fluid therapy, if provided inappropriately, can cause unnecessary harm to patients. The quantitative toxicity of fluid therapy contributes to worse outcomes; there should be greater bedside attention to fluid prescription, fluid balance, development of avoidable complications attributable to fluid overload, and for the timely de-escalation of administered fluids in patients whose clinical status and physiology allow active fluid mobilization.
Acute kidney injury is a frequent complication of acute heart failure syndromes, leading to an adverse prognosis. Acute cardiorenal syndrome represents a unique form of acute kidney injury specific to acute heart failure syndromes. Patient phenotyping using biomarkers reflecting different aspects of acute cardiorenal syndrome pathophysiology may help to inform prognosis and treatment. Adjunctive vasoactive, neurohormonal, and diuretic therapies may relieve congestive symptoms and/or improve renal function, but no single therapy has been proved to reduce mortality in acute cardiorenal syndrome.
Acute kidney injury (AKI) is also a frequent complication of end-stage liver disease, especially in those with acute-on-chronic liver failure, occurring in up to 50% of hospitalized patients with cirrhosis. There is no specific blood or urine biomarker that can reliably identify the cause of AKI in cirrhotic patients. The utility of biomarkers to determine irreversible renal dysfunction with liver transplant remains lacking, warranting further investigation, although biomarker development to differentiate the cause of AKI in cirrhosis has promise.
Thrombocytopenia-associated multiple organ failure (TAMOF) is a clinical phenotype characterized by the development of thrombocytopenia and multiorgan dysfunction in the context of critical illness. It encompasses a spectrum of syndromes associated with the development of thrombotic microangiopathy, such as thrombotic thrombocytopenic purpura/ hemolytic uremic syndrome (TTP/HUS) and disseminated intravascular coagulation (DIC). Acute kidney injury (AKI) is a common feature in patients with TAMOF. Nephrology management is essential as these conditions require special focussed therapies.
Contrast-associated acute kidney injury (CAAKI) is a common, iatrogenic condition that may go unrecognized. The principal risk factors for CAAKI are underlying renal impairment, diabetes, and intravascular volume depletion. CAAKI is associated with serious adverse short-term and longterm outcomes, including mortality and more rapidly progressive chronic kidney disease, though the causal nature of these associations is not proved.
Renal replacement therapy (RRT) is central to the clinical management of patients with acute kidney injury. Currently, both the type of RRT as well as the timing of RRT in children that results in the best outcome is unclear. Results from several observational studies suggest that early renal support therapy may reduce mortality and improve outcome. Though it is possible that a timely initiation of RRT may be associated with improved renal and nonrenal outcomes in these patients, there is little evidence in literature to exactly identify the most appropriate timing for RRT.
The risk for both future chronic kidney disease and associated cardiovascular complications is increased by an episode of AKI. The incidence of chronic kidney disease following a single episode of AKI is almost 30% Nephrology follow-up is essential for all survivors of AKI. This increase in health care burden and economic costs needs to be quantified and justifies the need to develop robust quality-improvement projects aimed at AKI prevention, identification, and improved management.
This symposium touches all corners of nephrology in critical care settings. Renowned nephrologists and pediatric intensivists from India have contributed to this symposium with the aim of updating physicians caring for critically ill children about recent advances in various aspects of critical care nephrology. They provide insights drawn from basic science, research findings and personal experience. Along with review of the past, they also provide a glimpse into the future. We hope you will find this collection of articles interesting and thought-provoking.
Source of Funding : Nil
Conflict of Interest: Nil
| References|| |
VA/NIH Acute Renal Failure Trial Network, Palevsky PM, Zhang JH, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med 2008;359(1):7-20.
RENAL Replacement Therapy Study Investigators, Bellomo R, Cass A, et al. Intensity of continuous renal- replacement therapy in critically ill patients. N Engl J Med 2009;361(17):1627-38.
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl 2012; 2:1-138.
Honore PM, Jacobs R, Hendrickx I, Bagshaw SM, Joannes-Boyau O, Willem Boer W et al.Prevention and treatment of sepsis-induced acute kidney injury: an update. Ann. Intensive Care 2015; 5:51. DOI 10.1186/s13613-015- 0095-3
Goldstein SL, Kirkendall E, Nguyen H, et al. Electronic health record identification of nephrotoxin exposure and associated acute kidney injury. Pediatrics 2013; 132(3): e756-67.
Angus DC, Barnato AE, Bell D, et al. A systematic review and meta-analysis of early goal-directed therapy for septic shock: the ARISE, ProCESS and ProMISe Investigators. Intensive Care Med 2015. [Epub ahead of print].
Rhodes A, Evans LE, Alhazzani W, Levy MM, Antonelli M, Ferrer R et al; Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock Critical Care Medicine. 2017; 45(3):486-552.
Ronco C, McCullough P, Anker SD, et al. Cardio-renal syndromes: report from the consensus conference of the acue dialysis quality initiative. Eur Heart J 2010; 31: 703-711.
Acevedo JG, Cramp ME. syndrome: Update on diagnosis and therapy. World J Hepatol. 2017 Feb 28;9(6):293-9.
Moake JL. Thrombotic microangiopathies. N Engl J Med. 2002 Aug 22;347(8):589-600.
De Broe M L, Roch Ramel F. Renal handling of drugs and xenobiotics. In: De Broe ME, Porter GAs (eds). Clinical Nephrotoxins: Renal Injury from Drugs and Chemicals. New York: Springer, 2008, pp. 43-72
Verghese P. Contrast nephropathy in children. J Pediatr Intensive Care . 2015;3(2):045-52.
Sethi SK, Bunchman T, Raina R, Kher V. Unique considerations in renal replacement therapy in children: Core curriculum 2014. Am J Kidney Dis. 2014; 63: 329-45.
Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11: R31.