Direct Evidence of Podocyte Damage in Cardiorenal Syndrome Type 2: Preliminary Evidence
Background: Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have thera...
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| Published in | Cardiorenal medicine Vol. 5; no. 2; pp. 125 - 134 |
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| Main Authors | , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Basel, Switzerland
S. Karger AG
01.04.2015
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Background: Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have therapeutic implications, as glomerular damage requires tight blood pressure control and renin-angiotensin-aldosterone system (RAAS) inhibition. The present investigation evaluates patients with CRS type 2 (CRS-2) for direct evidence of glomerular damage as evidenced by the presence of urinary podocin. Methods: The presence of glomerular damage was assessed in acutely decompensated patients with CRS-2 and healthy controls. Urinary podocin was determined by quantification of a tryptic peptide of podocin with high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Morning urine samples were collected for podocin, creatinine (Cr), and protein. Urinary podocin was expressed in femtomoles of podocin/milligram of Cr. Results: The urinary podocin/Cr ratio was greater in patients than in controls (0.37 ± 0.77 vs. 0.06 ± 0.05 fmol podocin/mg Cr, p = 0.04). A total of 40% of the patients had a urinary podocin/Cr ratio greater than the upper limit of normal (>0.2 fmol podocin/mg Cr). Patients with an elevated podocin/Cr ratio were more likely to have received ≤50% of the maximum dose of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (p = 0.04) than patients with a podocin/Cr ratio in the normal range. Conclusions: CRS-2 may be associated with glomerular damage as evidenced by an elevated urinary podocin/Cr ratio. Modulators of RAAS may have a protective effect on urinary podocin loss. |
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| AbstractList | Background: Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have therapeutic implications, as glomerular damage requires tight blood pressure control and renin-angiotensin-aldosterone system (RAAS) inhibition. The present investigation evaluates patients with CRS type 2 (CRS-2) for direct evidence of glomerular damage as evidenced by the presence of urinary podocin. Methods: The presence of glomerular damage was assessed in acutely decompensated patients with CRS-2 and healthy controls. Urinary podocin was determined by quantification of a tryptic peptide of podocin with high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Morning urine samples were collected for podocin, creatinine (Cr), and protein. Urinary podocin was expressed in femtomoles of podocin/milligram of Cr. Results: The urinary podocin/Cr ratio was greater in patients than in controls (0.37 ± 0.77 vs. 0.06 ± 0.05 fmol podocin/mg Cr, p = 0.04). A total of 40% of the patients had a urinary podocin/Cr ratio greater than the upper limit of normal (>0.2 fmol podocin/mg Cr). Patients with an elevated podocin/Cr ratio were more likely to have received ≤50% of the maximum dose of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (p = 0.04) than patients with a podocin/Cr ratio in the normal range. Conclusions: CRS-2 may be associated with glomerular damage as evidenced by an elevated urinary podocin/Cr ratio. Modulators of RAAS may have a protective effect on urinary podocin loss. © 2015 S. Karger AG, Basel Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have therapeutic implications, as glomerular damage requires tight blood pressure control and renin-angiotensin-aldosterone system (RAAS) inhibition. The present investigation evaluates patients with CRS type 2 (CRS-2) for direct evidence of glomerular damage as evidenced by the presence of urinary podocin. The presence of glomerular damage was assessed in acutely decompensated patients with CRS-2 and healthy controls. Urinary podocin was determined by quantification of a tryptic peptide of podocin with high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Morning urine samples were collected for podocin, creatinine (Cr), and protein. Urinary podocin was expressed in femtomoles of podocin/milligram of Cr. The urinary podocin/Cr ratio was greater in patients than in controls (0.37 ± 0.77 vs. 0.06 ± 0.05 fmol podocin/mg Cr, p = 0.04). A total of 40% of the patients had a urinary podocin/Cr ratio greater than the upper limit of normal (>0.2 fmol podocin/mg Cr). Patients with an elevated podocin/Cr ratio were more likely to have received ≤50% of the maximum dose of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (p = 0.04) than patients with a podocin/Cr ratio in the normal range. CRS-2 may be associated with glomerular damage as evidenced by an elevated urinary podocin/Cr ratio. Modulators of RAAS may have a protective effect on urinary podocin loss. Background: Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have therapeutic implications, as glomerular damage requires tight blood pressure control and renin-angiotensin-aldosterone system (RAAS) inhibition. The present investigation evaluates patients with CRS type 2 (CRS-2) for direct evidence of glomerular damage as evidenced by the presence of urinary podocin. Methods: The presence of glomerular damage was assessed in acutely decompensated patients with CRS-2 and healthy controls. Urinary podocin was determined by quantification of a tryptic peptide of podocin with high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Morning urine samples were collected for podocin, creatinine (Cr), and protein. Urinary podocin was expressed in femtomoles of podocin/milligram of Cr. Results: The urinary podocin/Cr ratio was greater in patients than in controls (0.37 ± 0.77 vs. 0.06 ± 0.05 fmol podocin/mg Cr, p = 0.04). A total of 40% of the patients had a urinary podocin/Cr ratio greater than the upper limit of normal (>0.2 fmol podocin/mg Cr). Patients with an elevated podocin/Cr ratio were more likely to have received ≤50% of the maximum dose of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (p = 0.04) than patients with a podocin/Cr ratio in the normal range. Conclusions: CRS-2 may be associated with glomerular damage as evidenced by an elevated urinary podocin/Cr ratio. Modulators of RAAS may have a protective effect on urinary podocin loss. BACKGROUNDRenal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of glomerular damage other than proteinuria have not been thoroughly investigated. The nature of renal damage in CRS may have therapeutic implications, as glomerular damage requires tight blood pressure control and renin-angiotensin-aldosterone system (RAAS) inhibition. The present investigation evaluates patients with CRS type 2 (CRS-2) for direct evidence of glomerular damage as evidenced by the presence of urinary podocin.METHODSThe presence of glomerular damage was assessed in acutely decompensated patients with CRS-2 and healthy controls. Urinary podocin was determined by quantification of a tryptic peptide of podocin with high-performance liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Morning urine samples were collected for podocin, creatinine (Cr), and protein. Urinary podocin was expressed in femtomoles of podocin/milligram of Cr.RESULTSThe urinary podocin/Cr ratio was greater in patients than in controls (0.37 ± 0.77 vs. 0.06 ± 0.05 fmol podocin/mg Cr, p = 0.04). A total of 40% of the patients had a urinary podocin/Cr ratio greater than the upper limit of normal (>0.2 fmol podocin/mg Cr). Patients with an elevated podocin/Cr ratio were more likely to have received ≤50% of the maximum dose of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers (p = 0.04) than patients with a podocin/Cr ratio in the normal range.CONCLUSIONSCRS-2 may be associated with glomerular damage as evidenced by an elevated urinary podocin/Cr ratio. Modulators of RAAS may have a protective effect on urinary podocin loss. |
| Author | Rajapreyar, Indranee Garovic, Vesna D. Selby, Michael G. Milic, Natasa Payne, Brian Le Jemtel, Thierry H. Barnidge, David R. |
| AuthorAffiliation | a Division of Cardiology, Tulane University, New Orleans, La., USA c Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minn., USA b Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minn., USA d Department of Medical Statistics and Informatics, University of Belgrade School of Medicine, Belgrade, Serbia |
| AuthorAffiliation_xml | – name: c Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minn., USA – name: d Department of Medical Statistics and Informatics, University of Belgrade School of Medicine, Belgrade, Serbia – name: a Division of Cardiology, Tulane University, New Orleans, La., USA – name: b Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minn., USA |
| Author_xml | – sequence: 1 givenname: Thierry H. surname: Le Jemtel fullname: Le Jemtel, Thierry H. – sequence: 2 givenname: Indranee surname: Rajapreyar fullname: Rajapreyar, Indranee – sequence: 3 givenname: Michael G. surname: Selby fullname: Selby, Michael G. – sequence: 4 givenname: Brian surname: Payne fullname: Payne, Brian – sequence: 5 givenname: David R. surname: Barnidge fullname: Barnidge, David R. – sequence: 6 givenname: Natasa surname: Milic fullname: Milic, Natasa – sequence: 7 givenname: Vesna D. surname: Garovic fullname: Garovic, Vesna D. email: garovic.vesna@mayo.edu |
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| Cites_doi | 10.2174/157339911794273973 10.1056/NEJM199503093321006 10.1161/HYPERTENSIONAHA.113.01504 10.1093/ndt/gfs074 10.2174/157339908783502370 10.1161/CIRCHEARTFAILURE.112.000089 10.1038/ki.2011.306 10.1097/MAJ.0b013e318228aef8 10.1016/j.amjcard.2012.06.035 10.1016/j.ajog.2007.02.007 10.1161/HYPERTENSIONAHA.111.188706 10.1016/j.jacc.2008.07.051 10.7326/0003-4819-130-6-199903160-00002 10.1097/01.CCM.0000296270.41256.5C 10.1681/ASN.2007121328 10.2215/CJN.03150509 10.1016/S0140-6736(09)61378-7 10.1016/j.pcad.2012.04.009 10.1016/j.pcad.2011.01.003 10.1136/hrt.2009.166256 10.1681/ASN.2005020159 10.1161/CIRCULATIONAHA.111.064097 10.1016/j.cardfail.2009.07.003 10.1159/000349968 10.1152/ajprenal.00404.2002 10.1038/sj.ki.5000410 10.1161/HYPERTENSIONAHA.113.01115 |
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| Keywords | Cardiorenal syndrome Podocyturia Proteinuria |
| Language | English |
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| Snippet | Background: Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage,... Renal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but markers of... BACKGROUNDRenal structural alterations have been partially uncovered in cardiorenal syndrome (CRS). Patients with CRS may have evidence of tubular damage, but... |
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| Title | Direct Evidence of Podocyte Damage in Cardiorenal Syndrome Type 2: Preliminary Evidence |
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