Effect of post-voiding urine volume on progression of renal function decline in patients with type 2 diabetes

Cho, Ajin; Kim, Soo Jin; Lee, Young-Ki; Song, Young Rim; Oh, Jieun; Kim, Sung Gyun; Seo, Jungpil; Yoon, Jong‐Woo; Koo, Ja‐Ryong; Kim, Hyung Jik; Noh, Jung Woo

doi:10.1016/j.diabres.2015.04.014

Cited by 4 publications

(2 citation statements)

References 30 publications

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“…Diabetic bladder dysfunction is a common feature of T2DM that occurs as a result of a sensory disturbance and abnormal detrusor reflex in its early stage, which then develops into bladder detrusor contraction and decreased bladder emptying in the later stage. 24,25 A prior study showed that the excessive activity of the detrusor continues to increase without detrusor decompensation in patients with diabetic bladder dysfunction. 26 Furthermore, bladder detrusor tissues of rats with STZ-induced T2DM presented with decreased miR-363 expression and increased expressions of Col1a2 and Col3a1.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: miR-363 Alleviates Detrusor Fibrosis via the TGF-Î²1/Smad Signaling Pathway by Targeting Col1a2 in Rat Models of STZ-Induced T2DM

Zhang

2020

Molecular Therapy - Nucleic Acids

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Dysregulated expression of microRNAs (miRNAs or miRs) has been implicated in the pathophysiology of type 2 diabetes mellitus (T2DM). However, their underlying role in the complication of detrusor fibrosis remains poorly understood. Therefore, this study aimed to examine the potential functional relevance of miR-363 in detrusor fibrosis of rats with streptozotocin (STZ)-induced T2DM through the predicted target gene collagen type I alpha 2 (Col1a2). Immunohistochemical analysis found an increase in the positive expression of collagen type III alpha 1 (Col3a1) and Col1a2 in detrusor tissues, where miR-363 expression was decreased. Next, gain- and loss-of-function experiments were performed to clarify the effects of miR-363 and Col1a2 on the activities of bladder detrusor cells. Of note, binding affinity between miR-363 and Col1a2 was verified by a dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay. Upregulated miR-363 inhibited Col1a2 expression, which led to increased expression of B-cell lymphoma 2 (Bcl-2) and Smad7 and accelerated cell viability, along with decreases in cell apoptosis and Col3a1, Bcl-2-associated X protein (Bax), transforming growth factor (TGF)-β1, and Smad4 expressions. In conclusion, miR-363 upregulation reduces detrusor fibrosis in rats with STZ-induced T2DM through suppression of the TGF-β1/Smad signaling pathway by targeting Col1a2. Therefore, our study provided further insights for the development of new therapeutic targets for T2DM.

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Section: Discussionmentioning

confidence: 99%

RETRACTED: miR-363 Alleviates Detrusor Fibrosis via the TGF-Î²1/Smad Signaling Pathway by Targeting Col1a2 in Rat Models of STZ-Induced T2DM

Zhang

2020

Molecular Therapy - Nucleic Acids

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“…Their results showed that only Q max and PVR urine volume were identified as independent predictors of CKD, even if a decreased Q max , with a history of hypertension and/or diabetes mellitus, were significantly associated with CKD. Also Cho et al [23] showed that increased PVR was independently associated with a more rapid decline in renal function in patients with Type 2 diabetes. The pressure–flow relationship to diagnose obstruction is much better defined in men, though recently it is used in both genders.…”

Section: Discussionmentioning

confidence: 99%

Chronic kidney disease and urological disorders: systematic use of uroflowmetry in nephropathic patients

Lai

Pastore

Piloni

et al. 2018

Clinical Kidney Journal

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Background Chronic kidney disease (CKD) is a highly prevalent condition. Urologic disorders are known causes of CKD, but often remain undiagnosed and underestimated also for their insidious onset and slow progression. We aimed to evaluate the prevalence of urological unrecognized diseases in CKD patients by uroflowmetry. Methods We enrolled consecutive stable CKD outpatients. The patients carried out two questionnaires, the International Prostate Symptom Score and Incontinence Questionnaire-Short Form, and they also underwent uroflowmetry, evaluating max flow rate ( Q max ), voiding time and voided volume values. Results A total of 83 patients (43 males, mean age of 59.8 ± 13.3 years) were enrolled. Our study showed 28 males and 10 females with a significant reduction of Q max (P < 0.001) while 21 females reported a significant increase of Q max (P < 0.001) with a prevalence of 49.5% of functional urological disease. Moreover, we showed a significant association between Q max and creatinine (P = 0.013), estimated glomerular filtration rate (P = 0.029) and voiding volume (P = 0.05). We have not shown significant associations with age (P = 0.215), body mass index (P = 0.793), systolic blood pressure (P = 0.642) or diastolic blood pressure (P = 0.305). Moreover, Pearson’s chi-squared test showed a significant association between Q max altered with CKD (χ 2 = 1.885, P = 0.170) and recurrent infection (χ 2 = 8.886, P = 0.012), while we have not shown an association with proteinuria (χ 2 = 0.484, P = 0.785), diabetes (χ 2 = 0.334, P = 0.563) or hypertension (χ 2 = 1.885, P = 0.170). Conclusions We showed an elevated prevalence of urological diseases in nephropathic patients; therefore, we suggest to include uroflowmetry in CKD patient assessment, considering the non-invasiveness, repeatability and low cost of examination. Uroflowmetry could be used to identify previously unrecognized urological diseases, which may prevent the onset of CKD or progression to end-stage renal disease and reduce the costs of management.

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Predicting Upper Urinary Tract Risk in the Neurogenic Bladder Patient

Kovacevic

Lopes

Raffee

et al. 2020

Curr Bladder Dysfunct Rep

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Effect of post-voiding urine volume on progression of renal function decline in patients with type 2 diabetes

Cited by 4 publications

References 30 publications

RETRACTED: miR-363 Alleviates Detrusor Fibrosis via the TGF-Î²1/Smad Signaling Pathway by Targeting Col1a2 in Rat Models of STZ-Induced T2DM

RETRACTED: miR-363 Alleviates Detrusor Fibrosis via the TGF-Î²1/Smad Signaling Pathway by Targeting Col1a2 in Rat Models of STZ-Induced T2DM

Chronic kidney disease and urological disorders: systematic use of uroflowmetry in nephropathic patients

Predicting Upper Urinary Tract Risk in the Neurogenic Bladder Patient

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