2019
DOI: 10.1007/s00277-019-03813-9
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Non-invasive urinary biomarkers of renal function in sickle cell disease: an overview

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Cited by 9 publications
(4 citation statements)
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“…The identification of biomarkers associated with clinical measures of SCDN and pHTN in blood, an easily accessible tissue, offers great promise for earlier diagnosis. One example is cystatin-C, a cysteine proteinase inhibitor, that was first proposed as a biomarker of glomerular filtration in 1985 and has since been widely utilized for chronic kidney disease (CKD) diagnosis, outperforming traditional measures such as creatinine as it is less dependent on muscle mass and biological factors. Still, CKD diagnosis using cystatin-C is far from perfect, and misclassification errors are common. , In the quest for more accurate predictive and diagnostic parameters, many potential biomarkers for CKD have been studied, including cytokines and chemokines, urinary proteins related to inflammation and tissue repair, as well as efforts to improve GFR estimation using serum metabolites. It is unclear how these biomarkers for CKD will translate to SCDN, as the mechanisms underlying disease pathogenesis are unique given the chronic hemolysis and anemia that exacerbate kidney injury in SCD. Moreover, hyperfiltration and hypersecretion into the renal tubules at early stages of SCDN may make creatinine clearance rates misleading. , Several novel SCDN biomarkers have been proposed, , however many of these studies suffered from small sample size and/or limitations of targeted analysis. Far fewer studies have investigated a role for biomarkers in early detection of pHTN in SCD patients. However, protein biomarkers for cardiovascular disease have been associated with kidney function in the general population, and interestingly, sFLT-1 has been associated with both SCDN and pHTN among SCD patients. , More predictive power may arise from using multiple biomarkers simultaneously or from predicting the co-occurrence of SCDN and pHTN, although this has not previously been considered in the context of SCD.…”
Section: Introductionmentioning
confidence: 99%
“…The identification of biomarkers associated with clinical measures of SCDN and pHTN in blood, an easily accessible tissue, offers great promise for earlier diagnosis. One example is cystatin-C, a cysteine proteinase inhibitor, that was first proposed as a biomarker of glomerular filtration in 1985 and has since been widely utilized for chronic kidney disease (CKD) diagnosis, outperforming traditional measures such as creatinine as it is less dependent on muscle mass and biological factors. Still, CKD diagnosis using cystatin-C is far from perfect, and misclassification errors are common. , In the quest for more accurate predictive and diagnostic parameters, many potential biomarkers for CKD have been studied, including cytokines and chemokines, urinary proteins related to inflammation and tissue repair, as well as efforts to improve GFR estimation using serum metabolites. It is unclear how these biomarkers for CKD will translate to SCDN, as the mechanisms underlying disease pathogenesis are unique given the chronic hemolysis and anemia that exacerbate kidney injury in SCD. Moreover, hyperfiltration and hypersecretion into the renal tubules at early stages of SCDN may make creatinine clearance rates misleading. , Several novel SCDN biomarkers have been proposed, , however many of these studies suffered from small sample size and/or limitations of targeted analysis. Far fewer studies have investigated a role for biomarkers in early detection of pHTN in SCD patients. However, protein biomarkers for cardiovascular disease have been associated with kidney function in the general population, and interestingly, sFLT-1 has been associated with both SCDN and pHTN among SCD patients. , More predictive power may arise from using multiple biomarkers simultaneously or from predicting the co-occurrence of SCDN and pHTN, although this has not previously been considered in the context of SCD.…”
Section: Introductionmentioning
confidence: 99%
“…Some evidence supports an association between CKD, SCN, and acute kidney injury (AKI) including the hypothesis that AKI, especially recurrent AKI, predisposes to long-term CKD. [13][14][15] The proposed mechanism in SCN includes AKI due to recurrent hypoxia, ischemic reperfusion injury, and cumulative kidney damage. [16][17][18][19][20][21] The current measure of AKI utilizes serum creatinine; this measure has known limitations, which are amplified in SCA.…”
mentioning
confidence: 99%
“…The pathophysiologic basis for CKD and SCN is incompletely understood. Some evidence supports an association between CKD, SCN, and acute kidney injury (AKI) including the hypothesis that AKI, especially recurrent AKI, predisposes to long-term CKD 13–15 . The proposed mechanism in SCN includes AKI due to recurrent hypoxia, ischemic reperfusion injury, and cumulative kidney damage 16–21 .…”
mentioning
confidence: 99%
“…A busca por biomarcadores não convencionais para detectar precocemente a LRA tem sido alvo de estudos nos últimos anos. A molécula-1 de lesão renal (KIM-1) é uma proteína transmembrana expressa em células epiteliais tubulares desdiferenciadas após LRA isquêmica ou nefrotóxica, que possui uma forma solúvel detectável na urina cuja expressão não ocorre em rins normais 11,12 . A proteína-1 quimiotática de monócitos (MCP-1) é uma potente quimiocina produzida nos rins, expressa, principalmente, por células glomerulares e epiteliais tubulares em resposta à lesão por isquemiareperfusão 5,13 .…”
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