Special Feature: UT Southwestern Internal Medicine ConferenceAcute Kidney Injury: The Beginning of the End of the Dark Ages
Section snippets
INTRODUCTION AND DEFINITIONS
Early studies of acute renal failure (ARF) were compromised by inconsistent definitions of this disease by different investigators. Although all agreed that a decrease in renal function over the course of hours to days is the hallmark of ARF, there was no agreement on what constituted renal dysfunction. A major step forward was the formation of the Acute Dialysis Quality Initiative and the Acute Kidney Injury Network.1., 2. In 2005, these consensus groups of nephrologists and intensive care
AKI IS ONE MAJOR CAUSE OF ACUTE RENAL DYSFUNCTION
One of the difficulties in treating acute renal dysfunction is making the diagnosis early enough to alter the course of the disease. The problem lies, in part, in differentiating AKI (structural injury to the kidney) from the other etiologies of acute renal dysfunction (increase in serum creatinine and/or decreased urine output). These etiologies have been divided into 3 broad categories and have been discussed in many excellent standard textbooks and review articles.4 We summarize them briefly
Patients With AKI Have a Higher Mortality Than Matched Patients Without AKI
The importance of AKI is often underappreciated. In fact, even mild AKI has profound implications for mortality and progression of chronic kidney disease.
Two multicenter clinical studies, Program to Improve Care in Acute Renal Disease (PICARD) and Beginning and Ending Therapy for the Kidney (BEST Kidney) showed that in-hospital mortality for patients with AKI in participating academic medical centers ranged from as low as 24% to as high as 75%.5
Studies of administrative databases have shown an
TREATMENT OF ISCHEMIC AKI IN 2011—BEFORE DIALYSIS IS NEEDED
The management of patients with ischemic AKI may be divided into 2 different objectives: one is the treatment of the kidney; the other is the treatment of the patient. Confusion in these 2 different objectives will result in serious errors in management and complaications.
Successful management of ischemic AKI rests on a firm understanding of the pathophysiology of renal failure. After the initial precipitous drop in GFR during hypoperfusion, secondary effects such as exposure to nephrotoxins
USE AND MISUSE OF IV FLUIDS—EARLY VERSUS LATE IN THE COURSE OF ISCHEMIC AKI
Optimization of cardiac filling pressures, and thus, improved renal perfusion is the mainstay of treating and preventing ischemic AKI in 2011. This is usually accomplished by a combination of intravenous (IV) fluids and vasopressors. It is becoming increasingly apparent that early, appropriate administration of IV crystalloid solution may prevent AKI, particularly in patients with septic shock.42., 43., 44. Early goal-directed therapy for sepsis as originally described by Rivers, has been shown
USE AND MISUSE OF DIURETICS
Recall our earlier division of the therapy of ischemic AKI into 2 different objectives: treatment of the kidney and treatment of the patient.
EFFECTS OF DIALYSIS ON RENAL RECOVERY
Conventional wisdom states that intermittent hemodialysis impairs recovery of the kidney from ischemic AKI. This is believed to occur because of hemodynamic instability during dialysis, vascular catheter-related infection and/or cytokine release after blood interacts with the dialyzer membrane. On the basis of these issues, continuous renal replacement therapy has been proposed to be a better dialysis modality for AKI. In fact, there is limited data that any of these factors have a negative
CHALLENGES IN MEASURING RENAL FUNCTION AND RENAL INJURY
Because we lack an easy, direct method of measuring renal injury, our current diagnosis of AKI relies on assaying 2 major renal functions and assuming that decreased functions are directly correlated with injury. Unfortunately, this may not be true, particularly early after injury.57., 58.
One function is the GFR. Even if we were able to easily and reliably measure the GFR, this would be a poor indicator of injury because, in many patients, the renal mass must be markedly reduced before the GFR
CONCLUSION
Clinical research during the past decade has advanced our understanding of the implications of AKI and redefined the goals of fluid management. Despite these advances, the mortality rate of patients with AKI remains high. We also appreciate that renal injury is an inflammatory condition that affects multiple organ systems. Basic research in the inflammatory response to AKI has the potential of identifying novel therapeutic targets; however, until we have accurate and sensitive tests that can
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2017, Medical HypothesesCitation Excerpt :Each of these biomarkers has its individual strengths and weaknesses and only if used together and in a panel format, these biomarkers could help the diagnosis or distinguishing the etiology of AKI. Unfortunately, none of these biomarkers have been broadly validated for clinical use and assays for these biomarkers are not widely available [11]. Even if a panel of these biomarkers would be able to detect AKI, it is still the clinician that should identify those who are at risk of AKI, and use the panel to establish or rule out the diagnosis.
Novel biomarkers of acute kidney injury and chronic kidney disease
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Vascular Surgery Kidney Injury Predictive Score: A Historical Cohort Study
2015, Journal of Cardiothoracic and Vascular AnesthesiaCitation Excerpt :In addition, the authors showed the risk of AKI significantly decreased for each 10 mL/min/body surface area increase in eGFR at the baseline (odds ratio 0.8; 95% confidence interval, 0.7-0.8; p<0.001) (Table 3 and Supplementary Figure 1). Emerging data regarding the association between volume overload and poor postsurgical outcomes signify the importance of judicious use of intravenous fluids in postoperative patients.42 In a systematic analysis, early use of inotropic agents in the resuscitation phase was protective against AKI.43
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2023, Journal of Biological Regulators and Homeostatic AgentsAccuracy of Urine Calprotectin in the Diagnosis of Acute Kidney Injury in Neonates: A Cross-Sectional Study
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This study was supported by NIH RO-1 DK069633 grant (to CYL), NIH T32DK07257 (to PDW), NIH DK079328 UT Southwestern O’Brien Kidney Research Core Center and a Beecherl grant (to CYL).