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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article focuses on the epidemiology, pathogenesis, and prevention of the most common forms of acute renal failure encountered in the critically ill. These include pre-renal azotemia and acute tubular necrosis that occurs postoperatively, in patients with rhabdomyolysis, or as a complication of sepsis. In addition, some unusual causes of acute renal failure that occur predominantly in the intensive care unit are briefly discussed.
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PMID:Acute renal failure in the critically ill patient. 1205 31

The evaluation and management of acute renal failure in the ICU patient remains a formidable task because of the complexity of this condition. Clinical and physiologic assessment and complementing laboratory and imaging tests are currently insufficient to differ between true renal parenchymal damage (acute tubular necrosis; it is important to realize that this term does not necessarily imply widespread injury, because whole organ dysfunction in humans has often been associated with very limited parenchymal cellular necrosis) and prerenal azotemia (decreased renal blood flow with altered glomerular hemodynamics and subsequently diminished glomerular filtration, without significant epithelial cell injury). Moreover, tubular damage and altered glomerular hemodynamics may coexist or lead to each other, and their relative contribution to the evolving renal dysfunction has not been unequivocally established. The limited data regarding the renal pathology of such patients and the scant information about human morphologic and functional correlates further undermine our knowledge about diagnostic and therapeutic approaches to these patients. Advanced techniques are critically needed to establish noninvasively the dynamic status of renal parenchymal microcirculation and the distribution of intrarenal oxygenation and to identify evolving cellular energy depletion and tubular cell damage. A few technologies are potentially promising, such as blood oxygen level dependent magnetic resonance imaging, positron emission tomography, and kidney injury molecule-1 detection in patients' urine. Because of the difficulties in analyzing the pathophysiology in humans, clinicians continue to rely largely on animal models to guide understanding and rationale for the identification of therapeutic targets. Data from such animal studies are complemented by studies in isolated perfused kidneys, isolated tubules, and tubular epithelial cell cultures. In this report, we summarize some concepts of acute tubular necrosis that have evolved as a result of these studies, evaluate available animal models, and underscore controversies regarding experimental acute tubular necrosis.
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PMID:Animal models of acute tubular necrosis. 1245 37

Dysfunction of a transplanted kidney may develop at any time in the post-transplant period. The aim of this study was to differentiate levels of early dysfunction of a transplanted kidney. The study included 45 examinees undergoing kidney transplantation. They were divided into four groups, in regard to length of hospitalization and post-transplant complications: group I (up to 15 days, complication-free); group II (up to 15 days, with complications); group III (up to 30 days); group IV (up to 60 days). The control group included patients undergoing abdominal surgery, without uropoetic system disorders. The following parameters were examined on a daily basis a month after transplantation on average: creatinine clearance, creatinine and urea. Statistical analysis of these parameters revealed the following levels of renal dysfunction: control group--circulatory tubular dysfunction without azotemia; group I--polyuric acute tubular necrosis; group II and group III--severe or moderately severe polyuric acute tubular necrosis and group IV--polyuric acute tubular necrosis.
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PMID:Tubulointerstitial dysfunction in early post-transplant period. 1289 73

Renal failure in cirrhosis has multiple etiologies and numerous aggravating factors with evidence of worsening of prognosis. Our study was performed on 130 cirrhotic patients hospitalized in HDF between January 1st, 1994, and December 31st, 1999. We have evaluated the causes of renal failure and the relation of different aggravating factors with the onset of renal failure. Causes of renal failure included drug-induced renal failure, organic nephropathy, pre-renal azotemia, acute tubular necrosis and hepato-renal syndrome. Among the aggravating factors, lactulose was found to alter renal function (p = 0.0175). We studied the survival with respect to the serum creatinine levels and to the severity of liver disease. Three-year survival was respectively 59% and 42% in case of Child A and Child B patients with creatinine lower than 90 micromol/L. No three-year survivors were noted in these subsets of patients when creatinine level was higher than 90 micromol/L (p = 0.0247 and p = 0.0121 respectively). No difference in survival was noted in Child C cirrhosis. The occurrence of renal failure is a factor of bad prognosis in cirrhotic patients irrespective of Child's classification. In patients with Child A and Child B cirrhosis, a serum creatinine level higher than 90 micromol/L is a bad prognostic factor with a significantly decreased survival rate. This factor does not affect survival in Child C cirrhosis because of mortality related to cirrhosis complications.
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PMID:[Cirrhosis and renal failure: the influence of creatinine value on prognosis]. 1518 56

Medications cause renal disease by promoting various types of injury in the kidney. Several drugs reduce renal perfusion and cause prerenal azotemia. Vascular disease can develop following exposure to various medications through direct and indirect effects. A number of glomerular lesions have been described with therapeutic agents and illicit drugs. Acute interstitial nephritis occurs from a drug-induced allergic reaction, which promotes interstitial inflammation and tubular damage. Acute tubular necrosis is a dose-dependent process that occurs from direct drug toxicity on tubular epithelia. Other less common patterns of drug-induced tubular injury include osmotic nephropathy, crystal nephropathy and acute nephrocalcinosis. Finally, postrenal azotemia from structural or functional obstruction of the urinary tract also complicates therapy with a number of medications.
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PMID:Drug-induced nephropathy: an update. 1601 48

Differentiating acute tubular necrosis (ATN) from prerenal azotemia is critical for selecting the appropriate treatment. This study was conducted to evaluate the diagnostic value of Doppler ultrasonography in differentiating ATN from prerenal azotemia in children. A total of 50 oliguric or anuric children with previous normal renal laboratory data were included. Doppler examination and calculation of resistive index (RI) was performed within 24 hours of admission and in the recovery phase of ARF. The sensitivity and specificity of RI in differentiating ATN from prerenal azotemia were assessed. At the cut-off point of RI = 0.75, the sensitivity and specificity of RI in differentiating prerenal failure and ATN was 91.3% and 85.2%, respectively. We conclude that Doppler ultrasonography is helpful in differentiating ATN from prerenal azotemia in children. The cut-off value of 0.75 has the highest accuracy for this purpose.
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PMID:Diagnostic value of Doppler ultrasound in differentiating prerenal azotemia from acute tubular necrosis in children. 1690 22

Elderly individuals comprise the faster growing patient population group and acute renal failure (ARF) is quite common among them, although exact numbers are not known. We reviewed the literature with regards to the characteristics of ARF in elderly patients and describe some useful guidelines. The ageing kidney is characterized by many structural and functional changes, which are mainly due to various chronic disorders, such as hypertension, diabetes and atherosclerosis, which are highly prevalent in these patients. A number of structural and functional changes characteristic of the ageing kidney make elderly people especially prone to renal damage. ARF in the elderly is frequently of multifactorial origin and often with an atypical presentation, like the "intermediate syndrome", which combines characteristics of pre-renal azotemia and acute tubular necrosis. Physical examination and laboratory blood and urine indices may sometimes be misleading occasionally leading to misdiagnosis. Prophylaxis remains the preferred approach to therapy: one should avoid nephrotoxic drugs and poly-pharmacy, adjust drug doses and achieve adequate hydration of the patient as cautiously as possible. Dialysis therapies can be used for treatment of ARF irrespective of age and carry a good prognosis.
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PMID:Acute renal failure in the elderly: particular characteristics. 1716 Jun 31

The term pre-renal azotemia (or on occasion 'pre-renal renal failure') is frequently used in textbooks and in the literature to indicate an acute syndrome characterized by the presence of an increase in the blood concentration of nitrogen waste products (urea and creatinine). This syndrome is assumed to be due to loss of glomerular filtration rate but is not considered to be associated with histopathological renal injury. Thus, the term is used to differentiate 'functional' from 'structural' acute kidney injury (AKI) where structural renal injury is taken to indicate the presence of so-called acute tubular necrosis (ATN). This paradigm is well entrenched in nephrology and medicine. However, growing evidence from experimental animal models, systematic analysis of the human and experimental literature shows that this paradigm is not sustained by sufficient evidence when applied to the syndrome of septic AKI, especially in critically ill patients. In such patients, several assumptions associated with the 'pre-renal azotemia paradigm' are violated. In particular, there is no evidence that ATN is the histopathological substrate of septic AKI, there is no evidence that urine tests can discriminate 'functional' from 'structural' AKI, there is no evidence that any proposed differentiation leads or should lead to different treatments, and there is no evidence that relevant experimentation can resolve these uncertainties. Given that septic AKI of critical illness now accounts for close to 50% of cases of severe AKI in developed countries, these observations call into question the validity and usefulness of the 'pre-renal azotemia paradigm' in AKI in general.
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PMID:Pre-renal azotemia: a flawed paradigm in critically ill septic patients? 1746 9

The L1 cell adhesion molecule (CD171) is a multidomain membrane glycoprotein of the immunoglobulin superfamily. We evaluated its expression in human acute kidney injury and assessed its use as a tissue and urinary marker of acute tubular injury. Using immunohistochemical studies with antibodies to the extracellular or cytoplasmic domains, we compared L1 expression in normal kidneys in 24 biopsies taken from patients with acute tubular necrosis. L1 was found at the basolateral and the lateral membrane in all epithelial cells of the collecting duct in the normal kidney except for intercalated cells. In acute tubular necrosis, L1 lost its polarized distribution being found in both the basolateral and apical domains of the collecting duct. Further, it was induced in thick ascending limb and distal tubule cells. Apically expressed L1 found only when the cytoplasmic domain antibody was used in biopsy specimens of patients with acute tubular necrosis. The levels of urinary L1, normalized for creatinine, were significantly higher in all 24 patients with acute tubular necrosis compared to five patients with prerenal azotemia or to six patients with other causes of acute kidney injury. Our study shows that a soluble form of human L1 can be detected in the urine of patients with acute tubular necrosis and that this may be a marker of distal nephron injury.
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PMID:The L1 cell adhesion molecule is a potential biomarker of human distal nephron injury in acute tubular necrosis. 1805 59

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


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