Non-albumin proteinuria marks tubular involvement and is associated with arterial stiffness in subjects affected by severe obesity.

Obesity is a well-established risk factor for kidney disease, and tubular damage can play a pivotal role in the development of obesity-related kidney damage. This study aimed to investigate the pathophysiological pathways involved in the development of non-albumin proteinuria (NAP), a marker of tubu...

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Publicado en:Obesity Research & Clinical Practice Vol. 17; no. 6; pp. 485 - 492
Autores principales: Moriconi, Diego, Nannipieri, Monica, Armenia, Silvia, Taddei, Stefano, Solini, Anna, Bruno, Rosa Maria
Formato: research Journal Article
Publicado: Elsevier B.V. Nov2023
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Nov2023
      vid: 17
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      pub: Elsevier B.V.
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        10.1016/j.orcp.2023.10.002
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        atl: Non-albumin proteinuria marks tubular involvement and is associated with arterial stiffness in subjects affected by severe obesity.
      aug:
        au:
          Moriconi, Diego
          Nannipieri, Monica
          Armenia, Silvia
          Taddei, Stefano
          Solini, Anna
          Bruno, Rosa Maria
        affil: Department of Clinical and Experimental Medicine, University of Pisa, Italy
      sug:
        subj:
          Albuminuria Etiology
          Proteinuria Complications
          Arterial Stiffness Physiology
          Obesity, Morbid Complications
          Obesity, Morbid Surgery
          Human
          Blood Pressure
          Lipoproteins, LDL Cholesterol Blood
          Obesity
          Pulse Wave Velocity Adverse Effects
          Bariatric Surgery Methods
          Kidney Function Tests Evaluation
          Kidney Physiology
          Glycated Hemoglobin Analysis
          Body Mass Index
          Cardiovascular Risk Factors
          Risk Assessment
          Scales
          Clinical Assessment Tools
          Comparative Studies
      ab: Obesity is a well-established risk factor for kidney disease, and tubular damage can play a pivotal role in the development of obesity-related kidney damage. This study aimed to investigate the pathophysiological pathways involved in the development of non-albumin proteinuria (NAP), a marker of tubular involvement, in a cohort of subjects with severe obesity and preserved kidney function. A total of 106 subjects with BMI ≥ 35 kg/m2 in waiting list for bariatric surgery underwent blood chemistry analysis including metabolic and lipid profile, vascular tests for cardiovascular risk stratification and a comprehensive assessment of kidney function, including renal resistive index (RRI) and NAP measurement. Nineteen patients with ACR ≥ 30 mg/g regardless of NAP values (ALB+), nineteen with NAP≥ 150 mg/g and albuminuria < 30 mg/g (iNAP) and sixty-eight without proteinuria (No-P) were found. Both ALB+ and iNAP groups exhibited a higher prevalence of hypertension and anti-hypertensive treatment compared to No-P, while the prevalence of diabetes was similar between groups. Concerning lipid profile, no differences in total, HDL and LDL cholesterol were found, while ALB+ patients had higher serum triglyceride levels than the other two groups. RRI and carotid-femoral pulse wave velocity (cf-PWV) was significantly higher in ALB+ and iNAP groups compared to No-P. Remarkably, cf-PWV remained still significant after adjustment for age, sex and MBP (p = 0.0004). In overall population, a multiple regression analysis showed that cf-PWV was an independent determinant of NAP in a model including age, sex, glycated hemoglobin, systolic and mean blood pressure (R2 =0.17, p = 0.031). iNAP subjects showed increased arterial stiffness comparable to that observed in ALB+ group, suggesting that they may represent a subgroup at higher cardiovascular risk, often unrecognized in clinical practice.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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