10327558ec9c8441132e927f7ebeea73 302122.pdf b589dd659ed429b9b0a68bff88db88be28e7acb4 302122.pdf 937f0a6bef3cb6fa493d4fc4c62d1a2122fe80eb15d83c207785245bdaf74ca0 302122.pdf Title: Albuminuria, Forgotten No More: Underlining the Emerging Role in CardioRenal Crosstalk Subject: Kidneys have an amazing ability to adapt to adverse situations, both acute and chronic. In the presence of injury, the kidney is able to activate mechanisms such as autoregulation or glomerular hyperfiltration to maintain the glomerular filtration rate (GFR). While these adaptive mechanisms can occur in physiological situations such as pregnancy or high protein intake, they can also occur as an early manifestation of diseases such as diabetes mellitus or as an adaptive response to nephron loss. Although over-activation of these mechanisms can lead to intraglomerular hypertension and albuminuria, other associated mechanisms related to the activation of inflammasome pathways, including endothelial and tubular damage, and the hemodynamic effects of increased activity of the renin–angiotensin–aldosterone system, among others, are recognized pathways for the development of albuminuria. While the role of albuminuria in the progression of chronic kidney disease (CKD) is well known, there is increasing evidence of its negative association with cardiovascular events. For example, the presence of albuminuria is associated with an increased likelihood of developing heart failure (HF), even in patients with normal GFR, and the role of albuminuria in atherosclerosis has recently been described. Albuminuria is associated with adverse outcomes such as mortality and HF hospitalization. On the other hand, it is increasingly known that the systemic effects of congestion are mainly preceded by increased central venous pressure and transmitted retrogradely to organs such as the liver or kidney. With regard to the latter, a new entity called congestive nephropathy is emerging, in which increased renal venous pressure can lead to albuminuria. Fortunately, the presence of albuminuria is modifiable and new treatments are now available to reverse this common risk factor in the cardiorenal interaction. Keywords: albuminuria; cardiorenal disease; chronic kidney disease; cardiovascular disease; heart failure Author: Gregorio Romero-González, Néstor Rodríguez-Chitiva, Carles Cañameras, Javier Paúl-Martínez, Marina Urrutia-Jou, Maribel Troya, Jordi Soler-Majoral, Fredzzia Graterol Torres, Maya Sánchez-Bayá, Jordi Calabia and Jordi Bover Creator: LaTeX with hyperref Producer: pdfTeX-1.40.25 CreationDate: Mon Jan 29 11:49:15 2024 CET ModDate: Tue Jan 30 10:14:28 2024 CET Custom Metadata: no Metadata Stream: no Tagged: no UserProperties: no Suspects: no Form: none JavaScript: no Pages: 15 Encrypted: no Page size: 595.276 x 841.89 pts (A4) Page rot: 0 File size: 1172258 bytes Optimized: no PDF version: 1.7 name type encoding emb sub uni object ID ------------------------------------ ----------------- ---------------- --- --- --- --------- OSMCID+VnURWPalladioL-Bold Type 1 Custom yes yes yes 10 0 SIUOJY+URWPalladioL-Bold Type 1 Custom yes yes yes 16 0 JNKGVX+URWPalladioL-Roma Type 1 Custom yes yes yes 22 0 JVFHZW+URWPalladioL-Ital Type 1 Custom yes yes yes 27 0 XPUSBJ+TimesNewRomanPS-BoldItalicMT Type 1C WinAnsi yes yes no 43 0 BSDWLC+TimesNewRomanPSMT Type 1C WinAnsi yes yes no 46 0 EILUJF+CMSY10 Type 1 Builtin yes yes yes 66 0 BCDEEE+PalatinoLinotype-Bold TrueType WinAnsi yes yes no 79 0 BCDFEE+PalatinoLinotype-Roman TrueType WinAnsi yes yes no 83 0 BCDGEE+PalatinoLinotype-Italic TrueType WinAnsi yes yes no 87 0 BCDIEE+PalatinoLinotype-Roman CID TrueType Identity-H yes yes yes 91 0 BCDJEE+PalatinoLinotype-Bold CID TrueType Identity-H yes yes yes 98 0 BCDEEE+PalatinoLinotype-Bold TrueType WinAnsi yes yes no 115 0 BCDFEE+PalatinoLinotype-Roman TrueType WinAnsi yes yes no 119 0 BCDGEE+PalatinoLinotype-Italic TrueType WinAnsi yes yes no 123 0 BCDHEE+PalatinoLinotype-Italic CID TrueType Identity-H yes yes yes 127 0 BCDIEE+PalatinoLinotype-Roman CID TrueType Identity-H yes yes yes 134 0 BCDJEE+PalatinoLinotype-Bold CID TrueType Identity-H yes yes yes 141 0 EXVEHZ+VnURWPalladioL Type 1 Custom yes yes yes 165 0 CRUZTT+VnURWPalladioL-Italic Type 1 Custom yes yes yes 173 0 Jhove (Rel. 1.28.0, 2023-05-18) Date: 2024-11-07 02:43:57 CET RepresentationInformation: 302122.pdf ReportingModule: PDF-hul, Rel. 1.12.4 (2023-03-16) LastModified: 2024-11-06 14:03:44 CET Size: 1172258 Format: PDF Version: 1.7 Status: Well-Formed and valid SignatureMatches: PDF-hul MIMEtype: application/pdf PDFMetadata: Objects: 570 FreeObjects: 1 IncrementalUpdates: 0 DocumentCatalog: PageLayout: SinglePage PageMode: UseNone Outlines: Item: Title: Introduction Destination: section.1 Item: Title: Conceptual Evolution of Albuminuria as a Cardiac and Renal Biomarker Destination: section.2 Children: Item: Title: Redefining Albuminuria Destination: subsection.2.1 Item: Title: Understanding the Pathophysiology of Albuminuria Destination: subsection.2.2 Item: Title: Albuminuria: The Neglected Biomarker Destination: subsection.2.3 Item: Title: Albuminuria in the Continuum of Cardiorenal Disease Destination: section.3 Children: Item: Title: Albuminuria and Acute Kidney Injury Destination: subsection.3.1 Item: Title: Albuminuria and Chronic Kidney Disease Destination: subsection.3.2 Item: Title: Albuminuria and Congestive Acute Heart Failure Destination: subsection.3.3 Item: Title: Albuminuria and Heart Failure Destination: subsection.3.4 Item: Title: Minimizing Albuminuria: Old and New Approaches Destination: section.4 Children: Item: Title: RAS Inhibitors Destination: subsection.4.1 Item: Title: Sodium Glucose Cotrasporter-2 Inhibitors Destination: subsection.4.2 Item: Title: Glucagon-Like Peptide 1 Receptor Agonist Destination: subsection.4.3 Item: Title: Mineralocorticoid Receptor Antagonist Destination: subsection.4.4 Item: Title: Conclusions Destination: section.5 Item: Title: References Destination: section.6 Info: Title: Albuminuria, Forgotten No More: Underlining the Emerging Role in CardioRenal Crosstalk Author: Gregorio Romero-González, Néstor Rodríguez-Chitiva, Carles Cañameras, Javier Paúl-Martínez, Marina Urrutia-Jou, Maribel Troya, Jordi Soler-Majoral, Fredzzia Graterol Torres, Maya Sánchez-Bayá, Jordi Calabia and Jordi Bover Subject: Kidneys have an amazing ability to adapt to adverse situations, both acute and chronic. In the presence of injury, the kidney is able to activate mechanisms such as autoregulation or glomerular hyperfiltration to maintain the glomerular filtration rate (GFR). While these adaptive mechanisms can occur in physiological situations such as pregnancy or high protein intake, they can also occur as an early manifestation of diseases such as diabetes mellitus or as an adaptive response to nephron loss. Although over-activation of these mechanisms can lead to intraglomerular hypertension and albuminuria, other associated mechanisms related to the activation of inflammasome pathways, including endothelial and tubular damage, and the hemodynamic effects of increased activity of the renin angiotensin aldosterone system, among others, are recognized pathways for the development of albuminuria. While the role of albuminuria in the progression of chronic kidney disease (CKD) is well known, there is increasing evidence of its negative association with cardiovascular events. For example, the presence of albuminuria is associated with an increased likelihood of developing heart failure (HF), even in patients with normal GFR, and the role of albuminuria in atherosclerosis has recently been described. Albuminuria is associated with adverse outcomes such as mortality and HF hospitalization. On the other hand, it is increasingly known that the systemic effects of congestion are mainly preceded by increased central venous pressure and transmitted retrogradely to organs such as the liver or kidney. With regard to the latter, a new entity called congestive nephropathy is emerging, in which increased renal venous pressure can lead to albuminuria. Fortunately, the presence of albuminuria is modifiable and new treatments are now available to reverse this common risk factor in the cardiorenal interaction. 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