The Impact of Renal Tubular Damage, as Assessed by Urinary β
            <sub>2</sub>
            –Microglobulin–Creatinine Ratio, on Cardiac Prognosis in Patients With Chronic Heart Failure

Otaki, Yoichiro; Watanabe, Tetsu; Shishido, Tetsuro; Takahashi, Hiroki; Funayama, Akira; Narumi, Takatsune; Kadowaki, Shinpei; Hasegawa, Hiromasa; Honda, Shintaro; Netsu, Shunsuke; Ishino, Mitsunori; Arimoto, Takanori; Miyashita, Takehiko; Miyamoto, Takuya; Konta, Tsuneo

doi:10.1161/circheartfailure.112.000089

Cited by 25 publications

(23 citation statements)

References 32 publications

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“…This was a prospective observational study to elucidate the clinical importance of RTD in patients with CHF [11,14]. We included 456 patients who were admitted to our hospital for the diagnosis or treatment of CHF between 2009 and 2013.…”

Section: Study Subjectsmentioning

confidence: 99%

“…RTD-UBCR was defined as a UBCR C 300 lg/g (log 10 UBCR C 2.47 lg/g), as previously reported [11,14]. RTD-NAG was defined as a NAG C 14.2 U/g, according to previous report [13].…”

Section: Biochemical Markersmentioning

confidence: 99%

“…Recently, we and others reported that RTD and glomerular damage are risk factors for poor cardiac prognosis in patients with CHF [11,13,14]. Renal tubule cells play a pivotal role in reabsorbing sodium, water, bicarbonate, and amino acids [15].…”

Section: Introductionmentioning

confidence: 99%

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Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

et al. 2015

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Section: Study Subjectsmentioning

confidence: 99%

“…RTD-UBCR was defined as a UBCR C 300 lg/g (log 10 UBCR C 2.47 lg/g), as previously reported [11,14]. RTD-NAG was defined as a NAG C 14.2 U/g, according to previous report [13].…”

Section: Biochemical Markersmentioning

confidence: 99%

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Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

et al. 2015

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“…During an episode of acute decompensation, increased glomerular pressure may cause proteinuria. In a recent observational study, patients with acute decompensated heart failure were found to have increased urinary albumin excretion that resolved or decreased significantly with standard heart failure treatment [18]. Although diabetes is known to play an important role in the pathogenesis of many glomerular diseases, glomerular damage was not closely related to the presence of diabetes in our patients.…”

Section: Discussionmentioning

confidence: 68%

“…The aim of the present investigation was to assess patients with CRS-2 for the presence of glomerular damage during an episode of acute cardiac decompensation, owing to its temporal association with increased urinary albumin excretion [18]. The presence of glomerular damage was assessed by quantification of urinary podocyte-specific peptides by liquid chromatography (LC) coupled to tandem mass spectrometry (LC-MS/MS).…”

Section: Introductionmentioning

confidence: 99%

Direct Evidence of Podocyte Damage in Cardiorenal Syndrome Type 2: Preliminary Evidence

et al. 2015

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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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Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

et al. 2021

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Aims Urinary liver-type fatty acid-binding protein (L-FABP) is expressed in proximal tubular epithelial cells and excreted into the urine during tubular injury. We hypothesized that high urinary L-FABP is associated with poor prognosis in patients with acute heart failure (AHF). Methods and resultsWe analysed 623 patients (74 ± 13 years old; 60.0% male patients) with AHF. Urinary L-FABP levels were measured at the time of admission and adjusted for the urinary creatinine concentration. The primary endpoint was all-cause mortality. The median value and interquartile range of urinary L-FABP levels were 6.66 and 3.37-21.1 μg/gCr, respectively. Urinary L-FABP levels were significantly correlated with both beta-2 microglobulin and cystatin C levels; the correlation with the former was higher than that with the latter. During the follow-up of 631 (interquartile range: 387-875) days, 142 deaths occurred. A high tertile of urinary L-FABP level was associated with high mortality; this association was retained after adjusting for other covariates (second tertile hazard ratio 1.40, P = 0.152 vs. first tertile; third tertile hazard ratio 1.94, P = 0.005 vs. first tertile). Conclusions Urinary L-FABP is more closely associated with tubular dysfunction than with glomerular dysfunction. Tubular dysfunction, which was evaluated based on urinary L-FABP levels, in patients with AHF is associated with all-cause mortality and is independent of pre-existing risk factors. L-FABP should be considered for use in the prognosis of AHF.

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The Impact of Renal Tubular Damage, as Assessed by Urinary β ₂ –Microglobulin–Creatinine Ratio, on Cardiac Prognosis in Patients With Chronic Heart Failure

Abstract: The online-only Data Supplement is available at http://circheartfailure.ahajournals.org/lookup/suppl

Cited by 25 publications

References 32 publications

Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

Direct Evidence of Podocyte Damage in Cardiorenal Syndrome Type 2: Preliminary Evidence

Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

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The Impact of Renal Tubular Damage, as Assessed by Urinary β 2 –Microglobulin–Creatinine Ratio, on Cardiac Prognosis in Patients With Chronic Heart Failure

Abstract: The online-only Data Supplement is available at http://circheartfailure.ahajournals.org/lookup/suppl

Cited by 25 publications

References 32 publications

Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

Comorbid renal tubular damage and hypoalbuminemia exacerbate cardiac prognosis in patients with chronic heart failure

Direct Evidence of Podocyte Damage in Cardiorenal Syndrome Type 2: Preliminary Evidence

Urinary liver‐type fatty acid‐binding protein as a prognostic marker in patients with acute heart failure

Contact Info

Product

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The Impact of Renal Tubular Damage, as Assessed by Urinary β ₂ –Microglobulin–Creatinine Ratio, on Cardiac Prognosis in Patients With Chronic Heart Failure