Acute kidney injury

2020 ◽  
pp. 4807-4829
Author(s):  
John D. Firth
Keyword(s):  
Acute Kidney Injury ◽  
Specific Treatment ◽  
Kidney Injury ◽  
Initial Assessment ◽  
Volume Depletion ◽  
Excretory Function ◽  
Tubular Necrosis ◽  
Life Threatening ◽  
Common Precipitant ◽  
General Aspects

Definition—for practical clinical purposes, acute kidney injury (AKI) is defined as a significant decline in renal excretory function occurring over hours or days, detected by either a fall in urinary output or a rise in the serum concentration of creatinine. Oliguria—defined (arbitrarily) as a urinary volume of less than 400 ml/day—is usually present, but not always. Clinical approach: diagnosis—all patients admitted to hospital with acute illness, but particularly older people and those with pre-existing chronic kidney disease, should be considered at risk of developing AKI. The most common precipitant is volume depletion. Serum creatinine and electrolytes should be measured on admission in all acutely ill patients, and repeated daily or on alternate days in those who remain so. Assessment—after treatment of life-threatening complications, the initial assessment of a patient who appears to have AKI must answer three questions: (1) is the kidney injury really acute? (2) Is urinary obstruction a possibility? And (3) is there a renal inflammatory cause? General aspects of management—the immediate management of a patient with renal impairment is directed towards three goals: (1) recognition and treatment of any life-threatening complications of AKI, (2) prompt diagnosis and treatment of hypovolaemia, and (3) specific treatment of the underlying condition—if this persists untreated then renal function will not improve. Specific causes of acute kidney injury—there are many possible causes of AKI, but in any given clinical context few of these are likely to require consideration. By far the most frequent are prerenal failure and acute tubular necrosis, which together account for 80 to 90% of cases of AKI seen by physicians.

scholarly journals Prevalence of Acute Kidney Injury in Patients with Liver Cirrhosis

2020 ◽  
Vol 58 (228) ◽  
Author(s):  
Pukar Thapa ◽  
Sudhamshu KC ◽  
Achyut Bikram Hamal ◽  
Dilip Sharma ◽  
Sandip Khadka ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Liver Cirrhosis ◽  
Hospital Stay ◽  
Hepatorenal Syndrome ◽  
Kidney Injury ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Tubular Necrosis ◽  
Advanced Liver Cirrhosis ◽  
Life Threatening

Introduction: Acute kidney injury is a common and life-threatening event in patients with liver cirrhosis occurring in approximately 20-50% of hospitalized patients of liver cirrhosis. Pre-renal acute kidney injury, the hepatorenal syndrome type of acute kidney injury and acute tubular necrosis represent the common causes. The aim of this study was to study the profile of acute kidney injury in patients with liver cirrhosis. Methods: Consecutive patients of liver cirrhosis admitted in Liver unit of Bir Hospital were studied to see the presence of acute kidney injury in this hospital based descriptive cross-sectional study. Clinical and laboratory parameters along with various clinical outcome were compared between different groups categorized by the severity of liver disease and renal dysfunction. Results: Out of 302 liver cirrhosis patients, 56 (18.5%) had acute kidney injury among which 23 (46%) were found to have pre-renal acute kidney injury, 15 (30%) with hepatorenal syndrome– acute kidney injury and 12 (24%) with intrinsic renal disease. Patients with higher stages of acute kidney injury had longer duration of hospital stay and hepatorenal syndrome-acute kidney injury was seen in patients with higher grade of ascites and with hyponatremia. Conclusions: Acute kidney injury is a common occurrence in patients with advanced liver cirrhosis with pre-renal acute kidney injury being the commonest cause. Median hospital stay is directly affected by the severity of acute kidney injury and hepatorenal syndrome–acute kidney injury was seen in patients with higher grade of ascites and hyponatremia. Early identification of patients at high risk for acute kidney injury may help to reduce mortality and contain costs.  

Pathophysiology of Acute Kidney Injury

2017 ◽  
Author(s):  
Shalini Bumb ◽  
Andrew Malone ◽  
Matthew A. Sparks
Keyword(s):  
Acute Kidney Injury ◽  
Fluid Overload ◽  
Kidney Injury ◽  
Tissue Perfusion ◽  
Urinary Flow ◽  
Cellular Injury ◽  
Waste Products ◽  
Excretory Function ◽  
Tubular Necrosis ◽  
Vascular Compromise

Acute kidney injury (AKI) is defined as the abrupt loss of kidney excretory function with the accumulation of nitrogenous waste products and fluid overload. The etiologies of AKI are numerous and can largely be classified as prerenal, intrinsic, or postrenal. Complex pathways involving inflammatory mediators, vascular compromise, and direct cellular injury are triggered, and equally as complex pathways, including autophagy and fibrosis, are involved in the recovery. Prerenal azotemia is caused by a reduction in tissue perfusion with resulting AKI. Although acute tubular necrosis is the most common intrinsic etiology, other nephrotoxins and exposures can result in intrinsic injury as well. Postrenal AKI is due to obstruction of urinary flow. Herein, in further detail, the mechanisms, pathophysiology, and manifestations of these causes of AKI are discussed. Research into the mechanisms and development of markers and techniques to advance clinical practice is ongoing.

Diagnosis of oliguria and acute kidney injury

2016 ◽  
Author(s):  
John A. Kellum
Keyword(s):  
Acute Kidney Injury ◽  
Renal Function ◽  
Extracellular Volume ◽  
Kidney Injury ◽  
Clinical Problem ◽  
Clinical Syndrome ◽  
Volume Depletion ◽  
International Consensus ◽  
Tubular Necrosis ◽  
Diagnosis And Classification

Diagnosis and classification of acute pathology in the kidney is major clinical problem. Azotemia and oliguria represent not only disease, but also normal responses of the kidney to extracellular volume depletion or a decreased renal blood flow. Clinicians routinely make inferences about both the presence of renal dysfunction and its cause. Pure prerenal physiology is unusual in hospitalized patients and its effects are not necessary benign. Sepsismay alter renal function without the characteristic changes in urine indices. The clinical syndrome known as acute tubular necrosis does not actually manifest the histological changes that the name implies. Acute kidney injury (AKI) is a term proposed to encompass the entire spectrum of the syndrome from minor changes in renal function to a requirement for renal replacement therapy. Criteria based on both changes in serum creatinine and urine output represent a broad international consensus for diagnosing and staging AKI.

Acute kidney injury in polytrauma and rhabdomyolysis

2018 ◽  
Author(s):  
Mehmet Şükrü Sever ◽  
Raymond Vanholder
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Crush Syndrome ◽  
Medical Complications ◽  
Tubular Necrosis ◽  
Number Of Patients ◽  
Life Threatening ◽  
Ultimate Outcome ◽  
Special Mention ◽  
Mass Disasters

The term ‘polytrauma’ refers to blunt (or crush) trauma that involves multiple body regions or cavities, and compromises physiology to potentially cause dysfunction of uninjured organs. Polytrauma frequently affects muscles resulting in rhabdomyolysis. In daily life, it mostly occurs after motor vehicle accidents, influencing a limited number of patients; after mass disasters, however, thousands of polytrauma victims may present at once with only surgical features or with additional medical complications (crush syndrome). Among the medical complications, acute kidney injury (AKI) deserves special mention, since it is frequent and has a substantial impact on the ultimate outcome.Several factors play a role in the pathogenesis of polytrauma (or crush)-induced AKI: (1) hypoperfusion of the kidneys, (2) myoglobin-induced direct nephrotoxicity, and intratubular obstruction, and also (3) several other mechanisms (i.e. iron and free radical-induced damage, disseminated intravascular coagulation, and ischaemia reperfusion injury). Crush-related AKI is prerenal at the beginning; however, acute tubular necrosis may develop eventually. In patients with crush syndrome, apart from findings of trauma, clinical features may include (but are not limited to) hypotension, oliguria, brownish discoloration of urine, and other symptoms and findings, such as sepsis, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, cardiac failure, arrhythmias, electrolyte disturbances, and also psychological trauma.In the biochemical evaluation, life-threatening hyperkalaemia, retention of uraemic toxins, high anion gap metabolic acidosis, elevated serum levels of myoglobin, and muscle enzymes are noted; creatine phosphokinase is very useful for diagnosing rhabdomyolysis.Early fluid administration is vital to prevent crush-related AKI; the rate of initial fluid volume should be 1000 mL/hour. Overall, 3–6 L are administered within a 6-hour period considering environmental, demographic and clinical features, and urinary response to fluids. In disaster circumstances, the preferred fluid formulation is isotonic saline because of its ready availability. Alkaline (bicarbonate-added) hypotonic saline may be more useful, especially in isolated cases not related to disaster, as it may prevent intratubular myoglobin, and uric acid plugs, metabolic acidosis, and also life-threatening hyperkalaemia.In the case of established acute tubular necrosis, dialysis support is life-saving. Although all types of dialysis techniques may be used, intermittent haemodialysis is the preferred modality because of medical and logistic advantages. Close follow-up and appropriate treatment improve mortality rates, which may be as low as 15–20% even in disaster circumstances. Polytrauma victims after mass disasters deserve special mention, because crush syndrome is the second most frequent cause of death after trauma. Chaos, overwhelming number of patients, and logistical drawbacks often result in delayed, and sometimes incorrect treatment. Medical and logistical disaster preparedness is useful to improve the ultimate outcome of disaster victims.

scholarly journals Timing of Initiation of Renal Replacement Therapy in Sepsis-Associated Acute Kidney Injury

2020 ◽  
Vol 9 (5) ◽  
pp. 1413 ◽  
Author(s):  
José Agapito Fonseca ◽  
Joana Gameiro ◽  
Filipe Marques ◽  
José António Lopes
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Replacement Therapy ◽  
Specific Treatment ◽  
Supportive Therapy ◽  
Kidney Injury ◽  
Hospital Length ◽  
Hospital Length Of Stay ◽  
Tubular Necrosis ◽  
Timing Of Initiation

Sepsis-associated acute kidney injury (SA-AKI) is a major issue in medical, surgical and intensive care settings and is an independent risk factor for increased mortality, as well as hospital length of stay and cost. SA-AKI encompasses a proper pathophysiology where renal and systemic inflammation play an essential role, surpassing the classic concept of acute tubular necrosis. No specific treatment has been defined yet, and renal replacement therapy (RRT) remains the cornerstone supportive therapy for the most severe cases. The timing to start RRT, however, remains controversial, with early and late strategies providing conflicting results. This article provides a comprehensive review on the available evidence on the timing to start RRT in patients with SA-AKI.

Pathophysiology of oliguria and acute kidney injury

2016 ◽  
Author(s):  
Rinaldo Bellomo ◽  
John R. Prowle
Keyword(s):  
Acute Kidney Injury ◽  
Critically Ill ◽  
Critically Ill Patients ◽  
Kidney Injury ◽  
Experimental Models ◽  
Volume Depletion ◽  
Icu Patients ◽  
Tubular Necrosis ◽  
Inflammatory Processes ◽  
Extravascular Volume

Oliguria and acute kidney injury (AKI) are common in critically-ill patients with studies reporting AKI affecting more than 50% of critically-ill patients. AKI is independently associated with increased mortality and is a potentially modifiable aspect of critical illness. The pathogenesis of AKI is complex and varies according to aetiology. The most common trigger in ICU patients is sepsis—the pathophysiology of septic AKI is poorly understood and probably involves intrarenal haemodynamic and inflammatory processes. In the setting of septic AKI, the classic acute tubular necrosis described in experimental models does not occur and histological changes are only minor. Activation of neurohormonal mechanisms is also important, particularly in the hepatorenal syndrome, where activation of the remain-angiotensin system appears to play a major role. The treatment of oliguria and AKI in ICU patients has traditionally relied on the administration of intravenous fluids. While such therapy is warranted in patients with a clear history, and physical examination suggestive of intravascular and extravascular volume depletion, its usefulness in other patients (e.g. septic patients) remains controversial. Removal of nephrotoxins, rapid treatment of the triggering factors, and attention to cardiac output and mean arterial pressure remain the cornerstones of the prevention and treatment of AKI in ICU.

The association between neutrophil-to-lymphocyte ratio and contrast-induced acute kidney injury in patients with carotid artery stenting

Vascular ◽  
2021 ◽  
pp. 170853812110125
Author(s):  
Altuğ Ösken ◽  
Ahmet Öz ◽  
Muhammed Keskin ◽  
Evliya Akdeniz ◽  
Hasan Şahan ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Carotid Artery ◽  
Carotid Artery Stenting ◽  
Kidney Injury ◽  
Fold Increase ◽  
Multivariate Regression Analysis ◽  
Neutrophil To Lymphocyte Ratio ◽  
Lymphocyte Ratio ◽  
Life Threatening ◽  
Prolonged Hospital

Objectives Contrast-induced acute kidney injury (CI-AKI) is a life-threatening complication that leads to comorbidities and prolonged hospital stay lengths in the setting of peripheral interventions. The presence of some CI-AKI risk factors has already been investigated. In this study, we evaluated the predictors of CI-AKI after carotid artery stenting. Methods A total of 389 patients with 50% to 99% carotid artery stenosis who underwent carotid artery stenting were included in this study. Patients were grouped according to CI-AKI status. Results CI-AKI developed in 26 (6.6%) patients. Age, baseline creatinine level, neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio were higher and estimated glomerular filtration rate, haemoglobin and lymphocyte count were lower in CI-AKI patients. In the multivariate regression analysis, the neutrophil-to-lymphocyte ratio triggered a 1.39- to 2.63-fold increase in the risk of CI-AKI onset ( p < 0.001). Conclusions The neutrophil-to-lymphocyte ratio may be a significant predictor of CI-AKI in patients with carotid artery stenting and higher neutrophil-to-lymphocyte ratio values may be independently associated with CI-AKI.

scholarly journals Incidence and risk predictors of acute kidney injury among HIV-positive patients presenting with sepsis in a low resource setting

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Davis Kimweri ◽  
Julian Ategeka ◽  
Faustine Ceasor ◽  
Winnie Muyindike ◽  
Edwin Nuwagira ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Significant Risk ◽  
Kidney Injury ◽  
Significant Risk Factor ◽  
Hiv Positive ◽  
Volume Depletion ◽  
Adjusted Risk ◽  
Adjusted Analysis ◽  
Resource Setting ◽  
Risk Predictors

Abstract Background Acute kidney injury (AKI) is a frequently encountered clinical condition in critically ill patients and is associated with increased morbidity and mortality. In our resource-limited setting (RLS), the most common cause of AKI is sepsis and volume depletion. Sepsis alone, accounts for up to 62 % of the AKI cases in HIV-positive patients. Objective The major goal of this study was to determine the incidence and risk predictors of AKI among HIV-infected patients admitted with sepsis at a tertiary hospital in Uganda. Methods In a prospective cohort study, we enrolled adult patients presenting with sepsis at Mbarara Regional Referral Hospital (MRRH) in southwestern Uganda between March and July 2020. Sepsis was determined using the qSOFA criteria. Patients presenting with CKD or AKI were excluded. Sociodemographic characteristics, physical examination findings, and baseline laboratory values were recorded in a data collection tool. The serum creatinine and urea were done at admission (0-hour) and at the 48-hour mark to determine the presence of AKI. We performed crude and multivariable binomial regression to establish the factors that predicted developing AKI in the first 48 h of admission. Variables with a p < 0.01 in the adjusted analysis were considered as significant predictors of AKI. Results Out of 384 patients screened, 73 (19 %) met our inclusion criteria. Their median age was 38 (IQR 29–46) years and 44 (60.3 %) were male. The median CD4 T-cell count was 67 (IQR 35–200) cells, median MUAC was 23 (IQR 21–27) cm and 54 (74.0 %) participants were on a regimen containing Tenofovir Disoproxil Fumarate (TDF). The incidence of AKI in 48 h was 19.2 % and in the adjusted analysis, thrombocytopenia (Platelet count < 150) (adjusted risk ratio 8.21: 95 % CI: 2.0–33.8, p = 0.004) was an independent predictor of AKI. Conclusions There is a high incidence of AKI among HIV-positive patients admitted with sepsis in Uganda. Thrombocytopenia at admission may be a significant risk factor for developing AKI. The association of thrombocytopenia in sepsis and AKI needs to be investigated.

scholarly journals Significance of Crescentic Glomeruli in Acute Kidney Injury with Rheumatoid Arthritis

2019 ◽  
Vol 9 (1) ◽  
pp. 42-48
Author(s):  
Ali Ayaash ◽  
Dipesh Maan ◽  
Anastasios Kapetanos ◽  
Mark Bunker ◽  
Mary Chester Wasko ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Renal Outcome ◽  
Primary Role ◽  
Tubular Necrosis ◽  
Immune Mediated ◽  
Autoimmune Conditions ◽  
Spontaneous Improvement

Crescentic glomerulonephritis (GN) without immune reactants or deposits (referred to as pauci-immune) is typically characterized by the presence of anti-neutrophilic cytoplasmic antibodies (ANCA). While ANCA-negative patients might be expected to have a more benign course, they often have poor renal outcomes, especially without treatment with steroids and immune-modulating therapy. Pauci-immune crescentic GN can also co-exist with other autoimmune conditions, including rheumatoid arthritis (RA). Here, we describe an ANCA-negative patient with RA who developed dialysis-requiring acute kidney injury (AKI) with findings consistent with focal pauci-immune crescentic GN (i.e., no IgG or immune complex on kidney biopsy). Coexistent conditions included Klebsiella sepsis attributed to pneumonia, rhabdomyolysis, leukocytoclastic immune-mediated skin vasculitis, and positive ANA. He had spontaneous improvement in renal function without immunosuppressive therapy. This crescentic GN was not associated with poor renal outcome as AKI resolved with supportive care and treatment of his infection. The AKI was likely multifactorial with co-existing acute tubular necrosis in the setting of Kebsiella sepsis and rhabdomyolysis, and the crescentic GN was felt more likely to be related to the infection rather than having a primary role. This case highlights the importance of viewing crescentic GN in the context of the clinical picture, as it may not always lead to the need of aggressive immune suppression and is not a universally poor prognostic kidney finding. However, these cases do warrant close follow-up as our patient had recurrent RA disease manifestations over the next 2 years that eventually led to his death from severe pulmonary hypertension.

scholarly journals Acute Kidney Injury Recognition and Management: A Review of the Literature and Current Evidence

2015 ◽  
Vol 8 (5) ◽  
pp. 120 ◽  
Author(s):  
Syed Raza Shah ◽  
Sameer Altaf Tunio ◽  
Mohammad Hussham Arshad ◽  
Zorays Moazzam ◽  
Komal Noorani ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Damage Control ◽  
Kidney Injury ◽  
Control Measures ◽  
Current Evidence ◽  
Disease Treatment ◽  
Complex Disorder ◽  
Electrolyte Homeostasis ◽  
Life Threatening ◽  
Life Threatening Event

<p>Acute renal failure is defined as a rapid decrease in the glomerular filtration rate, occurring over a period of hours to days and by the inability of the kidney to regulate fluid and electrolyte homeostasis appropriately. AKI is a catastrophic, life-threatening event in critically ill patients. AKI can be divided into pre-renal injury, intrinsic kidney disease (including vascular insults) and obstructive uropathies. The prognosis of AKI is highly dependent on the underlying cause of the injury. Children who have AKI as a component of multisystem failure have a much higher mortality rate than children with intrinsic renal disease. Treatment of AKI is subjected to risk stratification and ongoing damage control measures, such as patients with sepsis, exposure to nephrotoxic agents, ischemia, bloody diarrhea, or volume loss, could be helped by optimizing the fluid administrations, antibiotics possessing least nephrotoxic potential, blood transfusion where hemoglobin is dangerously low, limiting the use of nephrotoxic agents including radio contrast use, while maximize the nutrition. Acute kidney injury remains a complex disorder with an apparent differentiation in pathology between septic and nonseptic forms of the disease. Although more studies are still required, progress in this area has been steady over the last decade with purposeful international collaboration.</p>

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