The Clinical Significance of Urinary Retinol-Binding Protein 4: A Review

Ratajczyk, Krzysztof; Konieczny, Andrzej; Czekaj, Adrian; Piotrów, Paweł; Fiutowski, Marek; Krakowska, Kornelia; Kowal, Paweł; Witkiewicz, Wojciech; Marek-Bukowiec, Karolina

doi:10.3390/ijerph19169878

Cited by 8 publications

(3 citation statements)

References 83 publications

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“…The glomerulus freely filters it, and the proximal tubular portion afterwards reabsorbs and catabolizes it. According to a study, urine RBP levels are a highly sensitive predictor of renal tubule failure in people with AKI from a variety of causes [ 70 ]. According to studies, RBP and B2M levels are highly associated when urine pH is more than 6.0.…”

Section: Emerging Novel Biomarkers For Detecting Acute Kidney Injurymentioning

confidence: 99%

Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review

2022

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The definition of acute kidney injury (AKI), despite improvements in criteria, continues to be based on the level of serum creatinine and urinary output that do not specifically indicate tubular function or injury, or glomerular function or injury that is not significant enough to warrant acute hospitalization of the patient. Finding novel biomarkers of AKI has become a major focus nowadays in nephrology to overcome the further complications of end stage renal disease (ESRD). Many compounds, such as KIM 1, IL 18, NGAL, uromodulin, calprotectin, vanin 1, galactin 3, platelet-derived growth factor (PDGF), urinary Na+/H+ exchanger isoform 3 (NHE3), retinol binding protein (RBP) and Cystatin C, are released from the renal tubules and thus any alterations in tubular function can be detected by measuring these parameters in urine. Additionally, glomerular injury can be detected by measuring immunoglobulin G, nephrin, podocalyxin, podocin, transferrin, netrin-1, pyruvate kinase M2, etc. in urine. These novel biomarkers will be useful for timing the initial insult and assessing the duration of AKI. According to available research, these biomarkers could be applied to assess the onset of AKI, distinguishing between kidney injury and dysfunction, directing the management of AKI, and enhancing disease diagnosis. Therefore, we intend to present recent developments in our understanding of significant biomarkers implicated in various aspects of renal damage. Numerous biomarkers are implicated in various pathophysiological processes that follow renal injury, and can improve prognosis and risk classification.

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Section: Emerging Novel Biomarkers For Detecting Acute Kidney Injurymentioning

confidence: 99%

Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review

2022

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“…RBP-4 is a lipocalin that is predominantly synthesized by the liver and adipocytes and freely filtered and catabolized by the tubules. 64 A pilot study in Sri Lanka assessed the diagnostic utility of RBP-4 in CKDu ( n = 406). A panel of RBP-4, osteopontin (OPN), and KIM-1 distinguished patients with CKDu from nonendemic CKD (AUC-ROC, 0.976) but not endemic CKD from nonendemic CKD.…”

Section: Resultsmentioning

confidence: 99%

Systematic Review of Kidney Injury Biomarkers for the Evaluation of CKD of Uncertain Etiology

Claudel,

Waikar,

Amador

et al. 2024

Kidney International Reports

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“…The proteomic analysis also revealed increased expression of RBP4 in kidney tissue. Increased RBP4 has been suggested as a biomarker for renal damage and proteinuria (Ratajczyk et al ., 2022), which has also been suggested for UMOD (Thielemans et al ., 2023). Therefore, further studies need to address whether serum or urinary RBP4 or UMOD levels could be used as a potential biomarker for kidney disease onset and progression in BBS patients (Xun et al ., 2018; Swa et al ., 2022), similar to what has been suggested for UMOD in ADPKD (Cansever et al ., 2021).…”

Section: Discussionmentioning

confidence: 99%

Loss of Bbs8 leads to cystic kidney disease in mice and affects tubulin acetylation through HDAC2

Kieckhöfer,

Matthiessen,

Ebert

et al. 2024

Preprint

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Bardet-Biedl Syndrome (BBS) is a genetic disorder marked by considerable genetic and phenotypic diversity. BBS often presents as a combination of retinitis pigmentosa, obesity, polydactyly, and cystic kidney disease and is considered a model ciliopathy. The syndrome is caused by pathogenic variants in BBS genes, some of which encode components of a ciliary multi-protein complex, known as the BBSome, as well as a chaperonin-like complex, which is required for BBSome assembly. In this study, we describe the occurrence of kidney cysts in a BBS mouse model. Specifically, loss of BBS8 led to the development of cystic kidney disease by the end of the first year of life. In addition to transcriptional changes of key genes involved in regulated cell death and inflammation, proteomic approaches revealed increased expression and altered phosphorylation of histone deacetylase HDAC2 in knockout kidneys. Consistently, loss of Bbs8 resulted in a reduction of acetylated alpha-tubulin in primary cilia. This leads to diminished stability and altered dynamics of primary cilia, potentially contributing to the formation of cystic kidneys and other BBS manifestations previously described in Bbs8 deficient mice.

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The Clinical Significance of Urinary Retinol-Binding Protein 4: A Review

Cited by 8 publications

References 83 publications

Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review

Proficient Novel Biomarkers Guide Early Detection of Acute Kidney Injury: A Review

Systematic Review of Kidney Injury Biomarkers for the Evaluation of CKD of Uncertain Etiology

Loss of Bbs8 leads to cystic kidney disease in mice and affects tubulin acetylation through HDAC2

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