Histopathology of cocaine hepatotoxicity
Ian R. WanlessSylvain DoréN GopinathJensen C. C. TanRoss CameronE.J. HeathcoteLaurie BlendisGary Levy
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Histopathology
Acetaminophen
Steatosis
Azotemia
Acute tubular necrosis
Azotemia
Acute tubular necrosis
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Introduction: The fractional excretion of sodium (FE Na) in urine has appeared as a helpful way to distinguish prerenal azotemia from acute tubular necrosis (ATN). Objectives: The urinary index of sodium has some limits. Lithium can be an additional careful indicator. The goal of our study was to assess the standards fractional excretion of sodium and lithium, (FE Na and FE Li) in distinguishing pre-renal azotemia (PRA) from ATN. Patients and Methods: Twenty-seven patients with prerenal azotemia, 25 patients with ATN and 20 healthy persons were included in this investigation. The plasma and urine sodium, creatinine and lithium levels were assessed. Additionally, FE Na and FE Li were calculated. To assess the diagnostic usefulness of FE Na and FE Li in discriminating prerenal azotemia from ATN, we created a receiver operating characteristic (ROC) curve. Results: The area under the curves (AUCs) of fractional excretion of Li and Na were 0.84 and 0.83 for distinguishing prerenal azotemia from ATN, respectively. There was a significant direct association between FE Na and FE Li in patients with ATN (P=0.001). No significant association of FE Na and FE Li in patients with prerenal azotemia was detected (p=0.26). By a cutoff point of 2.96%, the sensitivity and specificity for FE Na, were 68% and 75%, respectively for distinguishing PRA from ATN. By a cutoff point of 4.17%, the sensitivity and specificity of FE Li were 80% and 79%, respectively, for distinguishing prerenal azotemia from ATN. Conclusion: This investigation appeared a high AUC and accuracy of fractional excretion of sodium and lithium as a diagnostic method for distinguishing prerenal azotemia from ATN when used simultaneously. However, the discrimination of sensitivity and specificity of fractional excretion of lithium was greater than the fractional excretion of Na.
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Acute kidney injury (AKI) is common in hospitalized patients and its associated mortality is high. The causes of AKI are commonly divided into 3 groups: pre-renal, intra-renal, and post-renal. According to this paradigm, pre-renal azotemia (PRA) represents a separate entity characterized by a rapidly reversible increase in serum creatinine and urea concentration. This rapid reversibility is believed to reflect a functional reduction in glomerular filtration rate as opposed to established structural kidney injury, which leads to acute tubular necrosis (ATN). This PRA vs. ATN paradigm is well established in the medical and renal literature and widely discussed in textbooks. However, there is no consensus definition for PRA or ATN. The typical description for PRA in the literature is 'reversible increase in serum creatinine and urea concentrations', 'characterized by intact renal parenchymal function but renal hypoperfusion'. Therefore, although the term PRA implies that it is defined histopathologically, it also contains a functional aspect (transient azotemia, TA). Early recognition of PRA or ATN is considered important because PRA can be reversed with fluid resuscitation, but such treatment causes edema in lungs as well as other tissues and therefore can be harmful in ATN. However, evidence suggests that PRA cannot be diagnosed prospectively and is clinically the same as TA, that urinary analysis and biochemistries cannot distinguish PRA and ATN in septic AKI, and that ATN is histologically uncommon in septic AKI. Recent observational studies also found that TA cannot be distinguished from ATN epidemiologically and that the existence of TA is related to high hospital mortality. These findings suggest the need for specific and focused investigations directed at identifying effective treatments to decrease the incidence of TA in hospitalized patients.
Azotemia
Acute tubular necrosis
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Azotemia
Acute tubular necrosis
Interstitial nephritis
Renal pathology
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Azotemia
Acute tubular necrosis
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Acute kidney injury (AKI) is defined as a fall in glomerular filtration rate (GFR) leading to the accumulation of nitrogenous wastes. Two major causes, prerenal azotemia and acute tubular necrosis (ATN), account for nearly 75% of AKI.
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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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This patient had severe dehydration and renal failure presumed to be extrarenal. After volume replacement, the course was not typical for simple extrarenal azotemia or acute tubular necrosis. Tubular handling of salt and water may not provide adequate criteria to evaluate the cause of reduced glomerular filtration rate.
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We report a 66-year-old man with minimal change nephrotic syndrome (MCNS) that was associated with reversible acute renal failure (ARF) caused by acute tubular necrosis (ATN). He had a subacute onset of proteinuria and progressive azotemia. Hemodialysis (HD) was required to improved azotemia. Renal biopsy revealed minor glomerular abnormalities associated with ATN. While continuing HD, steroid therapy was started, which subsequently allowed the patient to be weaned from HD and relieved from NS. In this patient, histological examination and clinical course suggested that ATN was probably induced by hypovolemia due to MCNS.
Azotemia
Acute tubular necrosis
Nephrosis
Hypovolemia
Minimal change disease
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