Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01034 (cystatin C)
 3,397 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute kidney injury (AKI) and fluid overload are conditions that require an early diagnosis and a prompt intervention. The recognition of these pathologic conditions is possible in the early stages if specific signs and symptoms are taken into account. Among them, oliguria represents an important sign. Reduced urine output for a certain number of hours may be an important sign of kidney dysfunction. This must be evaluated in conjunction with other factors such as hydration status and use of drugs. At the same time, traditional markers of kidney function such as urea nitrogen and creatinine must be evaluated in light of a possible altered balance. Increased levels may be due to reduced kidney function but also increased generation or altered solute distribution space due to non-optimal hydration status. Finally, novel biomarkers for renal tissue damage are becoming popular. Molecules such as NGAL or cystatin C may become altered well before creatinine or oliguria signal a condition of reduced kidney function. Here, the difference between insult and dysfunction becomes evident. Novel biomarkers seem to enable the clinician to make early diagnosis of kidney damage, distinguishing between AKI and acute kidney failure. Reduced glomerular filtration rate is, in fact, a late event in the continuum of the AKI syndrome.
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PMID:Oliguria, creatinine and other biomarkers of acute kidney injury. 2042 98

Acute kidney injury (AKI) comprises several syndromes that are associated with a sudden decrease in renal function. AKI is a common condition especially among critically ill patients. It is typically multifactorial and of great prognostic significance. The incidence of AKI has increased while the associated mortality rate has remained unchanged over the last years. Recent definitions of AKI, namely the Risk, Injury, Failure, Loss of renal function and End-stage kidney disease (RIFLE) classifycation or the Acute Kidney Injury Network (AKIN) criteria, incorporate serum creatinine and urine output as the principal markers to define and detect AKI. However, elevated serum creatinine or oliguria were demonstrated to detect AKI at late stages of renal injury when preventive strategies may be less effective. Therefore, there has recently been a great scientific interest in obtainng valuable markers for early AKI detection. In the last 5 years numerous new markers such as neutrophil-gelatinase associated lipo-calin, interleukin-18, cystatin C and kidney injury molecule 1 in the urine and/or serum have been studied and proposed as early detection markers of AKI. Persistently, these markers performed well in initial pilot trials. However, these promising results could often not be confirmed in later, larger multicentre trials and limitation of these biomarkers in the early diagnosis of renal injury were discovered. Furthermore, as AKI is multi-factorial and heterogeneous in origin, it seems likely that not one single marker but a panel of biomarkers will be required to detect all subtypes of AKI early during their evolution. This has initiated proteomic studies to develop panels of biomarkers which may facilitate early detection of AKI. The present review will focus on the most important clinical studies evaluating the ability of single AKI biomarkers and on those in clinical proteomics that attempted to establish panels of biomarkers in urine for early and accurate AKI diagnosis and prognosis.
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PMID:Proteomic biomarkers for the early detection of acute kidney injury. 2295 93

The incidence of postoperative acute kidney injury (AKI) in patients undergoing cardiac surgery ranges from 7.7% to 28.1% in different studies, probably in relation to the criteria adopted to define AKI. AKI markedly increases mortality risk. However, despite the development of less invasive techniques, cardiac surgery remains the first option in many conditions such as severe coronary artery disease, valve diseases and complex interventions. The risk of postsurgery AKI can be reduced by adopting less invasive approaches, such as off-pump coronary artery bypass grafting or transcatheter aortic valve implantation, but these options cannot be employed in all cases. Thus, since traditional cardiac surgery remains the only option in many cases, it is important to adopt strategies helping the clinician to prevent AKI or diagnose it early. Old age, preprocedural chronic kidney disease, obesity, some comorbidities, wide pulse pressure and some pharmacological regimens represent risk factors for postsurgery AKI and mortality. Important intraoperative factor are use and duration of cardiopulmonary bypass. Postoperative efforts should be aimed toward maximizing cardiac output, avoiding drugs vasoconstricting the renal artery, providing adequate crystalloid infusion and alkalinizing urine. Fluid management should not be based on the measurements for cardiac filling pressures, which are mostly unreliable in these patients. Novel biomarkers such as cystatin C, kidney injury molecule-1 and human neutrophil gelatinase-associated lipocalin have been found to change earlier than creatinine, particularly when measured in combination, so their use in clinical practice can facilitate early diagnosis and treatment of AKI. The occurrence of oliguria despite adequate cardiovascular therapy can be managed with furosemide, possibly using continuous infusion, or renal replacement therapy.
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PMID:Acute kidney injury in patients undergoing cardiac surgery. 2304 36

Traditional diagnosis of acute kidney injury (AKI) depends on detection of oliguria and rise of serum creatinine level, which is an unreliable and delayed marker of kidney damage. Delayed diagnosis of AKI in the critically ill patient is related to increased morbidity and mortality, prolonged length of stay, and cost escalation. The discovery of a reliable biomarker for early diagnosis of AKI would be very helpful in facilitating early intervention, evaluating the effectiveness of therapy, and eventually reducing cost and improving outcome. Innovative technologies such as genomics and proteomics have contributed to the discovery of new biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (Cys C), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and liver-type fatty acid binding protein (L-FABP). The current status of the most promising of these novel AKI biomarkers, including NGAL, Cys C, KIM-1, L-FABP, and IL-18, is reviewed.
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PMID:Role of new biomarkers: functional and structural damage. 2347 55