Acute kidney injury

TEXILA INTERNATIONAL JOURNAL OF CLINICAL RESEARCH, 2016

Introduction: Acute Kidney injury (AKI), is defined as an abrupt reduction in kidney function measured by a rapid decline in glomerular filtration rate resulting in the retention of metabolic waste products and dysregulation of fluid, electrolyte, and acid-base homeostasis. AKI is also defined in terms of a rise in serum creatinine concentration or by azotemia (a rise in blood urea nitrogen [BUN] concentration). The causes of acute renal disease can be related to the factors that interfere with structure and function of renal arteries, glomerular, renal tubules and urinary tracts. The current treatment for AKI is mainly supportive in nature; no therapeutic modalities to date have shown efficacy in treating the condition. Maintenance of volume homeostasis and correction of biochemical abnormalities remain the primary goals of treatment. Methods: I undertook a systemic review different books and journals and came up with summary statement. Accordingly supporting evidence and general recommendation was generated for the future research. Result: using the literature review the definition, causes and treatment algorithm of acute kidney injury was jotted down. Conclusion: Acute kidney injury (formerly known as acute renal failure) is a syndrome characterised by the rapid loss of the kidney's excretory function and is typically diagnosed by the accumulation of end products of nitrogen metabolism (urea and creatinine) or decreased urine output, or both.

Advances in Chronic Kidney Disease, 2008

Changes in terminology and new consensus definitions of acute kidney injury (AKI) and stages of severity have simplified some of the problems in the clinical approach to this complex syndrome. Nevertheless, new proactive approaches to the diagnosis of kidney injury instead of kidney failure are required to allow clinical translation of successful therapies developed for experimental AKI. The recent development of novel urinary and plasma biomarkers, which predict kidney failure, has allowed the development of new paradigms for detection, prevention, and stage-specific treatment.

Acute kidney injury (AKI) is an independent risk factor for morbidity and mortality. This review provides essential information for the diagnosis and management of AKI. Blood urea nitrogen and serum creatinine are used for the diagnosis of AKI. The review also focuses on recent studies on the diagnosis of AKI using the RIFLE (R-renal risk, I-injury, F-failure, L-loss of kidney function, E-end stage kidney disease) and Acute Kidney Injury Network criteria, and serum and urine AKI biomarkers. Dialysis is the only Food and Drug Administration-approved therapy for AKI. Recent studies on the dose of dialysis in AKI are reviewed.

Serbian Journal of Experimental and Clinical Research, 2017

Acute damage to the kidney is a serious complication in patients in intensive care units. Th e causes of acute kidney damage in these patients may be prerenal, renal and postrenal. Sepsis is the most common cause of the development of acute kidney damage in intensive care units. For the defi nition and classifi cation of acute kidney damage in clinical practice, the RIFLE, AKIN and KDIGO classifi cations are used. Th ere is a complex link between acute kidney damage and other organs. Acute kidney damage is induced by complex pathophysiological mechanisms that cause acute damage and functional disorders of the heart (acute heart failure, acute coronary syndrome and cardiac arrhythmias), brain (whole body cramps, ischaemic stroke and coma), lung (acute damage to the lung and acute respiratory distress syndrome) and liver (hypoxic hepatitis and acute hepatic insuffi ciency). New biomarkers, colour Doppler ultrasound diagnosis and kidney biopsy have signifi cant roles in the diagnosis o...

Anaesthesia Critical Care & Pain Medicine, 2016

Acute kidney injury (AKI) is a syndrome that has progressed a great deal over the last 20 years. The decrease in urine output and the increase in classical renal biomarkers, such as blood urea nitrogen and serum creatinine, have largely been used as surrogate markers for decreased glomerular filtration rate (GFR), which defines AKI. However, using such markers of GFR as criteria for diagnosing AKI has several limits including the difficult diagnosis of non-organic AKI, also called "functional renal insufficiency" or "pre-renal insufficiency". This situation is characterized by an oliguria and an increase in creatininemia as a consequence of a reduction in renal blood flow related to systemic haemodynamic abnormalities. In this situation, "renal insufficiency" seems rather inappropriate as kidney function is not impaired. On the contrary, the kidney delivers an appropriate response aiming to recover optimal systemic physiological haemodynamic conditions. Considering the kidney as insufficient is erroneous because this suggests that it does not work correctly, whereas the opposite is occurring, because the kidney is healthy even in a threatening situation. With current definitions of AKI, normalization of volaemia is needed before defining AKI in order to avoid this pitfall.

Clinical biochemist reviews, 2016

Acute kidney injury (AKI) is a clinical syndrome that complicates the course and worsens the outcome in a significant number of hospitalised patients. Recent advances in clinical and basic research will help with a more accurate definition of this syndrome and in the elucidation of its pathogenesis. With this knowledge we will be able to conduct more accurate epidemiologic studies in an effort to gain a better understanding of the impact of this syndrome. AKI is a syndrome that rarely has a sole and distinct pathophysiology. Recent evidence, in both basic science and clinical research, is beginning to change our view for AKI from a single organ failure syndrome to a syndrome where the kidney plays an active role in the progress of multi-organ dysfunction. Accurate and prompt recognition of AKI and better understanding of the pathophysiologic mechanisms underlying the various clinical phenotypes are of great importance to research for effective therapeutic interventions. In this revi...

Comprehensive Physiology, 2011

The term "acute renal failure" (ARF) has traditionally been used to describe a syndrome with a rapid decline in glomerular filtration rate (GFR) occurring over a period of hours to weeks as the key feature. Recently, a consortium of nephrologists and intensivists, the Acute Kidney Injury Network (AKIN), representing many of the professional societies involved in the care of critically ill patients, recommended that the term "acute kidney injury" (AKI) replace ARF. This term includes the entire spectrum of ARF and recognizes that minor changes in kidney function (reflected by a change in serum creatinine [SCr] of 0.3 mg/dL) can portend worse patient outcome, 1 whereas the term "failure" is reserved for those patients whose renal functional impairment is so severe that replacement therapy is indicated, or at least considered. The previous issue of Nephrology Rounds reviewed the epidemiology, diagnosis, and treatment of AKI in various settings. This issue of Nephrology Rounds examines the pathophysiological underpinnings of AKI.

Acute kidney injury (AKI) is characterized by a rapid decline in glomerular filtration rate (GFR) over hours to days that results in the retention of urea and other nitrogenous waste products normally cleared by the kidneys.

Journal of Clinical Medicine

Acute kidney injury (AKI) is a common clinical syndrome characterized by a sudden decline in or loss of kidney function. AKI is not only associated with substantial morbidity and mortality but also with increased risk of chronic kidney disease (CKD). AKI is classically defined and staged based on serum creatinine concentration and urine output rates. The etiology of AKI is conceptually classified into three general categories: prerenal, intrarenal, and postrenal. Although this classification may be useful for establishing a differential diagnosis, AKI has mostly multifactorial, and pathophysiologic features that can be divided into different categories. Acute tubular necrosis, caused by either ischemia or nephrotoxicity, is common in the setting of AKI. The timely and accurate identification of AKI and a better understanding of the pathophysiological mechanisms that cause kidney dysfunction are essential. In this review, we consider various medical causes of AKI and summarize the mo...