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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is no consensus in the literature on the best renal replacement therapy (RRT) in acute kidney injury (AKI), with both hemodialysis (HD) and peritoneal dialysis (PD) being used as AKI therapy. However, there are concerns about the inadequacy of PD as well as about the intermittency of HD complicated by hemodynamic instability. Recently, continuous replacement renal therapy (CRRT) have become the most commonly used dialysis method for AKI around the world. A prospective randomized controlled trial was performed to compare the effect of high volume peritoneal dialysis (HVPD) with daily hemodialysis (DHD) on AKI patient survival. A total of 120 patients with acute tubular necrosis (ATN) were assigned to HVPD or DHD in a tertiary-care university hospital. The primary end points were hospital survival rate and renal function recovery, with metabolic control as the secondary end point. Sixty patients were treated with HVPD and 60 with DHD. The HVPD and DHD groups were similar for age (64.2+/-19.8 and 62.5+/-21.2 years), gender (male: 72 and 66%), sepsis (42 and 47%), hemodynamic instability (61 and 63%), severity of AKI (Acute Tubular Necrosis-Index Specific Score (ATN-ISS): 0.68+/-0.2 and 0.66+/-0.2), Acute Physiology, Age, and Chronic Health Evaluation Score (APACHE II) (26.9+/-8.9 and 24.1+/-8.2), pre-dialysis BUN (116.4+/-33.6 and 112.6+/-36.8 mg per 100 ml), and creatinine (5.8+/-1.9 and 5.9+/-1.4 mg per 100 ml). Weekly delivered Kt/V was 3.6+/-0.6 in HVPD and 4.7+/-0.6 in DHD (P<0.01). Metabolic control, mortality rate (58 and 53%), and renal function recovery (28 and 26%) were similar in both groups, whereas HVPD was associated with a significantly shorter time to the recovery of renal function. In conclusion, HVPD and DHD can be considered as alternative forms of RRT in AKI.
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PMID:High volume peritoneal dialysis vs daily hemodialysis: a randomized, controlled trial in patients with acute kidney injury. 1940 96

Diagnosis and classification of acute pathology in the kidney are major clinical problems. Azotemia and oliguria represent not only disease but normal responses of the kidney to extracellular volume depletion or decreased renal blood flow. Changes in urine output and glomerular filtration rate are therefore neither necessary nor sufficient for the diagnosis of renal pathology. However, no simple alternative for the diagnosis currently exists. By examining both glomerular and tubular function, clinicians routinely make inferences not only on the presence of renal dysfunction but also on its cause. However, pure prerenal physiology is unusual in hospitalized patients, and its effects are not necessary benign. Sepsis, the most common condition associated with acute renal failure in the intensive care unit, may alter renal function without any characteristic changes in urine indices, and classification of these abnormalities as prerenal will undoubtedly lead to incorrect management decisions. The clinical syndrome known as acute tubular necrosis does not actually manifest the morphologic changes that the name implies. A precise biochemical definition of acute renal failure has never been proposed, and until recently, there has been no consensus on the diagnostic criteria or clinical definition. Depending on the definition used, acute renal failure has been reported to affect from 1% to 25% of intensive care unit patients and has led to mortality rates ranging from 15% to 60%. From this chaos, two principles emerged: first, the need for a standard definition and, second, the need to classify the severity of the syndrome rather than only consider its most severe form. The RIFLE criteria were developed to achieve these goals, and the term acute kidney injury has been proposed to encompass the entire spectrum of the syndrome, from minor changes in renal function to requirement for renal replacement therapy. Thus, acute kidney injury is not acute tubular necrosis, nor is it renal failure. Small changes in kidney function in hospitalized patients are important and are associated with significant changes in short-term and possibly long-term outcomes. The RIFLE criteria provide a uniform definition of acute kidney injury and have now been validated in numerous studies.
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PMID:Acute kidney injury. 1838 85

Septic acute kidney injury accounts for close to 50% of all cases of acute kidney injury in the intensive care unit and, in its various forms, affects between 15% and 20% of intensive care unit patients. However, there is little we really know about its pathophysiology. Although hemodynamic factors might play a role in the loss of glomerular filtration rate, they may not act through the induction of renal ischemia. Septic acute renal failure may, at least in patients with a hyperdynamic circulation, represent a unique form of acute renal failure: hyperemic acute renal failure. Measurements of renal blood flow in septic humans are now needed to resolve this pivotal pathophysiological question. Whatever may happen to renal blood flow during septic acute kidney injury in humans, the evidence available suggests that urinalysis fails to provide useful diagnostic or prognostic information in this setting. In addition, nonhemodynamic mechanisms of cell injury are likely to be at work. These mechanisms are likely due to a combination of immunologic, toxic, and inflammatory factors that may affect the microvasculature and the tubular cells. Among these mechanisms, apoptosis may turn out to be important. It is possible that, as evidence accumulates, the paradigms currently used to explain acute renal failure in sepsis will shift from ischemia and vasoconstriction to hyperemia and vasodilation and from acute tubular necrosis to acute tubular apoptosis or simply tubular cell dysfunction or exfoliation. If this were to happen, our therapeutic approaches would also be profoundly altered.
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PMID:Pathophysiology of septic acute kidney injury: what do we really know? 1838 94

Numerous anatomical and functional changes occurring in the aging kidney lead to reduced glomerular filtration rate, lower renal blood flow and impaired renal autoregulation. The elderly are especially vulnerable to the development of renal dysfunction and in this population acute renal failure (ARF) is a common problem. ARF is often iatrogenic and multifactorial; common iatrogenic combinations include pre-existing renal dysfunction and exposure to nephrotoxins such as radiocontrast agents or aminoglycosides, use of NSAIDs in patients with congestive cardiac failure and use of ACE inhibitors and diuretics in patients with underlying atherosclerotic renal artery stenosis. The aetiology of ARF is classically grouped into three categories: prerenal, intrinsic and postrenal. Prerenal ARF is the second most common cause of ARF in the elderly, accounting for nearly one-third of all hospitalized cases. Common causes can be grouped into true volume depletion (e.g. decreased fluid intake), decreased effective blood volume (e.g. systemic vasodilation) and haemodynamic (e.g. renal artery stenosis, NSAID use). Acute tubular necrosis (ATN) is the most common cause of intrinsic ARF and is responsible for over 50% of ARF in hospitalized patients, and up to 76% of cases in patients in intensive care units. ATN usually occurs after an acute ischaemic or toxic event. The pathogenesis of ATN involves an interplay of processes that include endothelial injury, microvascular flow disruption, tubular hypoxia, dysfunction and apoptosis, tubular obstruction and trans-tubular back-leak. Vasculitis causing ARF should not be missed as this condition is potentially life threatening. The likelihood of a postrenal cause for ARF increases with age. Benign prostatic hypertrophy, prostatic carcinoma and pelvic malignancies are all important causes. Early identification of ARF secondary to obstruction with renal imaging is essential, and complete or partial renal recovery usually ensues following relief of the obstruction.A comprehensive medical and drug history and physical examination are all invaluable. Particular attention should be paid to the fluid status of the patient (skin turgor, jugular venous pressure, lying and standing blood pressure, urine output). Urinalysis should be performed to detect evidence of proteinuria and haematuria, which will aid diagnosis. Fractional excretion of sodium and urine osmolality may be measured but the widespread use of diuretics in the elderly gives rise to unreliable results. Renal imaging, usually ultrasound scanning, is routinely performed for assessment of renal size and to exclude urinary obstruction. In some cases, renal biopsy is necessary to provide specific diagnostic information. The general principles of managing ARF include treatment of life-threatening features such as shock, respiratory failure, hyperkalaemia, pulmonary oedema, metabolic acidosis and sepsis; stopping and avoiding administration of nephrotoxins; optimization of haemodynamic and fluid status; adjustment of drug dosage appropriate to glomerular filtration rate; early nutritional support; and early referral to nephrologists for diagnosis of ARF cause, timely initiation of dialysis and initiation of specific treatment. The treatment of prerenal and ATN ARF is largely supportive with little evidence of benefit from current pharmacological therapies. Despite advances in critical care medicine and renal replacement therapy, the mortality of ARF has not changed significantly over the last 40 years, with current mortality rates being up to 75%.
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PMID:Management of acute renal failure in the elderly patient: a clinician's guide. 1854 Jun 87

The development of recent standardized definitions of acute kidney injury (AKI) has allowed us to begin understanding pediatric AKI epidemiology and risk factors and to stratify outcome by AKI severity. AKI incidence will vary with illness severity of the population studied and definition type, ranging from less than 1% when need for dialysis is used to 82% when less conservative definitions (such as > or =1.5 times baseline serum creatinine) are used to define AKI. The most common AKI causes are secondary, such as sepsis, nephrotoxic medication, and ischemia, each leading to acute tubular necrosis (ATN). Children undergoing cardiopulmonary bypass surgery, stem cell transplantation, or with multiple organ dysfunction syndrome are at high risk for these events. A key feature in diagnosis and management includes identifying the presence of ATN versus a reversible hypovolemic state because patients with ATN may quickly develop fluid overload with overaggressive fluid therapy, requiring dialytic removal. Despite advances in acute pediatric dialysis therapy and in overall care of critically ill children, severe AKI still is associated with a high mortality rate, necessitating more research in early AKI identification and therapeutic trials.
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PMID:Epidemiology and diagnosis of acute kidney injury. 1879 Mar 63

The prognostic of uremic syndrome had been improved by the development of renal replacement therapy. Uremic syndrome remains a dramatic medical concern in African sub-saharan countries. Nephrology practice has been introduced recently in Burkina Faso and epidemiological data on acute renal failure is not available. We conducted this study with the aim to describe the clinical profile of hospitalized patients. One hundred and twenty-one patients (18.4% of all admissions) with acute renal failure (creatinine>240micromol/L, abrupt onset) were included (age: 38.6+/-16.3y; creatinine: 1246.1+/-870.5micromol/L; urea: 40.2+/-18.3micromol/L), 75 men (age: 41.2+/-16.4) and 46 women (age: 34.2+/-15.2y). Acute renal failure was of medical cause in 91 cases, surgical cause in 16 cases and gyneco-obstetrical in 14 cases. Many pathophysiological factors have been identified like volume depletion, infections and obstruction. Acute renal failure was renal in 57 cases (age: 38.2+/-14.6y), prerenal in 43 cases (age: 36.8+/-16.7y) counting acute tubular necrosis in 21 cases, obstructive in 15 cases (age: 50.5+/-15.6y) and unclassified in six cases. Comorbidities have been identified: heart failure (13 cases), hepatocellular failure (eight cases), tumours (four cases) and severe hypertension (13 cases). Dialysis was justified in 84 cases but only accomplished in 14 cases. Hospital length of stay was 20.4+/-14.9 days. Twenty-nine patients died and causes were uraemia in 13 cases, hepatic in three cases, sepsis in 10 cases, malignant tumour in two cases and associated in one case.
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PMID:[Acute renal failure in Burkina Faso]. 1983 24

Dengue virus infection can clinically manifest as dengue fever, dengue shock syndrome and dengue hemorrhagic fever. Acute kidney injury as a result of dengue virus infection can occur due to various reasons including hypotension, rhabdomyolysis, sepsis and rarely immune complex mediated glomerular injury. However, glomerulonephritis associated with IgA Nephropathy in dengue virus infection has not been reported previously. We report a case of 15-year-old boy who was admitted with dengue fever and dialysis dependant acute kidney injury. Urine examination showed microscopic glomerular hematuria and proteinuria. Kidney biopsy showed mesangial proliferation with mesangial IgA dominant immune complex deposits and acute tubular necrosis. A repeated kidney biopsy 6 weeks after clinical recovery showed reversal of glomerular changes as well as resolution of mesangial IgA deposits.
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PMID:Transient IgA nephropathy with acute kidney injury in a patient with dengue fever. 2042 82

Coccidioidomycosis is a fungal disease with a wide variety of manifestations. The systemic infection is a product of airborne spore inhalation released from the soil. This once-endemic disease is steadily increasing in incidence, geographic location, and severity. The rare coccidioidomycosis cases requiring surgical intervention present unique challenges to anesthesia providers. This case report describes a 45-year-old woman with no relevant medical history admitted for lobec-occidi tomy with decortication because of aggressive coccidioidomycosis. Anesthetic considerations included attention to fungal sepsis, acute tubular necrosis related to amphotericin B therapy, and airway challenges. Careful attention to perioperative fungal therapies, invasive monitoring, and electrolyte stabilization remain pivotal concerns offering the best outcomes for patients with coccidioidomycosis.
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PMID:Anesthetic management for lobectomy in a patient with coccidioidomycosis: a case report. 2087 33

Improved mechanistic understanding of renal cell death in acute kidney injury (AKI) has generated new therapeutic targets. Clearly, the classic lesion of acute tubular necrosis is not adequate to describe the consequences of renal ischemia, nephrotoxin exposure, or sepsis on glomerular filtration rate. Experimental evidence supports a pathogenic role for apoptosis in AKI. Interestingly, proximal tubule epithelial cells are highly susceptible to apoptosis, and injury at this site contributes to organ failure. During apoptosis, well-orchestrated events converge at the mitochondrion, the organelle that integrates life and death signals generated by the BCL2 (B-cell lymphoma 2) protein family. Death requires the 'perfect storm' for outer mitochondrial membrane injury to release its cellular 'executioners'. The complexity of this process affords new targets for effective interventions, both before and after renal insults. Inhibiting apoptosis appears to be critical, because circulating factors released by the injured kidney induce apoptosis and inflammation in distant organs including the heart, lung, liver, and brain, potentially contributing to the high morbidity and mortality associated with AKI. Manipulation of known stress kinases upstream of mitochondrial injury, induction of endogenous, anti-apoptotic proteins, and improved understanding of the timing and consequences of renal cell apoptosis will inevitably improve the outcome of human AKI.
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PMID:Apoptosis and acute kidney injury. 2204 34

Necrotizing fasciitis can present with concomitant acute kidney injury. The etiology of acute kidney injury is often multifactorial; potential sources include volume depletion, abdominal compartment syndrome, rhabdomyolysis, and acute tubular necrosis (which may be related to hemodynamic instability, medications, or sepsis/infection). Kidney injury, defined via changes in serum creatinine, portends increased morbidity and mortality. Thus, it is crucial to accurately diagnose and assess the severity of kidney injury. We present the case of a patient with necrotizing fasciitis who endured 31 consecutive days of complete anuria. His serum creatinine decreased over this interval without the use of extracorporeal hemofiltration or dialysis. The explanation for this novel phenomenon lies in massive daily sero-sanguineous discharge and insensible losses with subsequent volume resuscitation. The patient's own convective clearance was substantial enough to maintain a modest creatinine clearance of 15 ml/min during sustained anuria. Our case emphasizes the importance of employing the creatinine, estimated glomerular filtration rate, and urine output portions of the Acute Kidney Injury Network (AKIN) or Risk Injury Failure Loss End stage (RIFLE) criteria in assessing the severity of kidney injury. It further reinforces the imperfection in using serum creatinine as a primary measure of glomerular filtration rate.
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PMID:Autologous creatinine clearance in a case of necrotizing fasciitis and anuria. 2234 4


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