Contributions to nephrology
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Pathophysiological mechanisms of cardiorenal syndromes (CRS) types 1-5 are still sparsely characterized. In an attempt to address this issue, a consensus conference on CRS was held in Venice, Italy, in November 2012 under the auspices of the Acute Dialysis Quality Initiative (ADQI). ⋯ Pre-conference we performed a systematic search and review of the available literature using a modified Delphi analysis. Hereby identified and in this review discussed questions were: (i) What are the predominant pathophysiologic mechanisms of CRS type 1 in acute decompensated heart failure? (ii) Could biomarker profiling identify pathomechanisms or hemodynamic phenotype of patients with CRS type 1? Could predictive biomarkers improve renal safety of therapy in CRS type 1? (iii) How do the timing, severity and duration relate to the mechanisms and outcomes of CRS type 1? In summary, after discussion and appraisal of the best available evidence, working group 1 makes consensus recommendations for future research on pathologic mechanisms of CRS type 1 and recommendations for clinical practice where treatment is in either proof or disproof of a mechanism.
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Acute kidney injury (AKI) is a common but complex clinical syndrome with multiple etiologies. These etiologies target different sites and pathways within the kidney. Novel biomarkers of 'kidney damage' (which can be tubular or glomerular) can be used to diagnose AKI, even in the absence of an increase in serum creatinine or oliguria. ⋯ The presence of underlying CKD or of sepsis poses additional challenges in differential diagnosis, since these conditions alter both baseline biomarker excretion and biomarker performance. We recommend that biomarkers be validated within the clinical context in which they are to be used. Within that context, combinations of biomarkers may, in the future, allow differentiation of the site, mechanism and phase of injury.
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Acute kidney injury (AKI) commonly occurs in hospitalized patients and is independently and strongly associates with morbidity and mortality. The clinical benefits of a timely and definitive diagnosis of AKI have not been fully realized due to limitations imposed by the use of serum creatinine and urine output to fulfill diagnostic criteria. These restrictions often lead to diagnostic delays, potential misclassification of actual injury status, and provide little information regarding underlying cause. ⋯ Promising diagnostic injury markers include neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule 1 (KIM-1), interleukin 18 (IL-18) and liver-type fatty acid binding protein (L-FABP). However, there are currently insufficient data on damage biomarkers to support their use for AKI staging. Rigorous validation studies measuring the association between the novel damage biomarker(s) and clinically relevant outcomes are needed.
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Several new biomarkers of kidney damage have been characterized and are being validated in clinical studies. These damage biomarkers complement existing conventional biomarkers of kidney function (e.g. serum creatinine, serum urea, and urine output) that are currently utilized to diagnose and stage acute kidney injury (AKI). Both functional and damage biomarkers provide an opportunity to identify patients with AKI who are at risk for a less favorable prognosis in terms of worsening damage or further declines in kidney function and likelihood of need for renal replacement. ⋯ Set cut-offs for various biomarkers and their bedside utility are forthcoming and will be in part determined by regulatory intended use guidelines, platform standardization, and inter-laboratory calibration. There remain many unresolved areas of AKI biomarker use in selected syndromes of AKI (e.g. cardiorenal syndrome, hepatorenal syndrome). As clinicians gain experience with AKI biomarkers, clinical care plans that incorporate them into routine care will shortly follow.
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Stroke is a leading cause of mortality and morbidity worldwide. Traditional cardiovascular risk factors - hypertension, diabetes and dyslipidemia - are related to the incidence of stroke. Chronic kidney disease has also been recognized to be a major public health problem as a cardiovascular risk factor. ⋯ Chronic kidney disease may also be associated with an increase in nontraditional risk factors such as hyperhomocysteinemia, inflammation, asymmetric dimethylarginine, oxidative stress, and anemia, and thrombogenic factors such as left ventricular hypertrophy, endothelial dysfunction, and arterial stiffness. Herein, we review the results of meta-analyses of published cohort studies for a better understanding of the precise nature of the relationship between chronic kidney disease and stroke, important to both the clinical and public health fields. Further studies are warranted to determine whether interventions to prevent the progression of kidney impairment are effective at reducing the risk of stroke.