Background: The pathology of diabetic nephropathy (DN) broadly involves the injury of glomeruli, tubulointerstitium and endothelium. Cells from these compartments can release increased numbers of microvesicles (MVs) into urine when stressed or damaged. Currently whether urinary MVs from these three parts can help diagnose DN and reflect pathological features remain unclear.
Methods: Forty-nine patients with histologically proven DN and 29 proteinuric controls with membranous nephropathy or minimal change disease were enrolled. Urinary podocyte, proximal tubular and endothelial cell-derived MVs were quantified by flow cytometry. Renal glomerular, tubulointerstitial and vascular lesions were semi-quantitatively scored and their relevance to urinary MVs were analyzed.
Results: DN patients had greater numbers of urinary MVs from podocytes, proximal tubular and endothelial cells compared with proteinuric controls. The combination of podocyte nephrin+ MVs and diabetic retinopathy optimally diagnose DN with 89.7% specificity and 88.9% sensitivity. Moreover, positive correlations were observed between urinary levels of proximal tubular MVs and the severity of tubular injury and between urinary levels of endothelial MVs and the degree of vascular injury. Using urinary proximal tubular MVs as the indicators for tubular injury, the differences between DN patients and proteinuric controls diminished after matching the degree of renal vascular injury or when proteinuria >8 g/24 h.
Conclusions: Urinary kidney-specific cell-derived MVs might serve as noninvasive biomarkers for the diagnosis of DN in diabetic proteinuric patients. Their elevated levels could reflect corresponding renal pathological lesions, helping physicians look into the heterogeneity of DN.
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http://dx.doi.org/10.21037/atm-20-441 | DOI Listing |
BMC Nephrol
January 2025
Department of Oral Function & Anatomy, Dentistry and Pharmaceutical Sciences, Okayama University Graduate School of Medicine, 2-5-1 Shikata-cho, Kita- ku, Okayama, 700-0914, Japan.
Background: Diabetes treatments by the control of sodium-glucose cotransporter 2 (SGLT2) is commonly conducted while there are still uncertainties about the mechanisms for the SGLT2 overexpression in kidneys with diabetes. Previously, we have reported that glomeruli and proximal tubules with diabetic nephropathy express toll-like receptor TLR2/4, and that the TLR ligand lipopolysaccharide (LPS) of periodontal pathogens have caused nephropathy in diabetic model mice. Recently, many researchers suggested that the periodontal pathogenic bacteria Fusobacterium (F.
View Article and Find Full Text PDFNephrology (Carlton)
February 2025
Department of Quality Management, Tianjin Blood Center, Tianjin, China.
Aim: To study the effect and elucidate the underlying mechanisms of VDAC1-ΔC on autophagy in renal tubular epithelial cells injured by hypoxia/reoxygenation.
Methods: C57/BL6 mice were randomly divided into groups: sham operation group, IRI 1d group and IRI 2d group. The inner canthal blood of mice was collected to detect the levels of serum creatinine and urea nitrogen and kidney tissues were sampled, and sections were stained with Periodic acid-Schiff for morphological evaluation.
Diseases
January 2025
Department of Urology, Kanazawa Medical University, Uchinada 920-0293, Ishikawa, Japan.
Urinary stones (urolithiasis) have been categorized as kidney stones (renal calculus), ureteric stones (ureteral calculus and ureterolith), bladder stones (bladder calculus), and urethral stones (urethral calculus); however, the mechanisms underlying their promotion and related injuries in glomerular and tubular cells remain unclear. Although lifestyle-related diseases (LSRDs) such as hyperglycemia, type 2 diabetic mellitus, non-alcoholic fatty liver disease/non-alcoholic steatohepatitis, and cardiovascular disease are risk factors for urolithiasis, the underlying mechanisms remain unclear. Recently, heat shock protein 90 (HSP90) on the membrane of HK-2 human proximal tubular epithelium cells has been associated with the adhesion of urinary stones and cytotoxicity.
View Article and Find Full Text PDFBackground And Aim: Phosphate dysregulation is often associated with chronic kidney disease (CKD), and recent studies suggest that it may also be present in non-CKD patients with systemic conditions including iron deficiency anemia. This study aimed to evaluate the relationship between iron deficiency parameters (total iron-binding capacity {TIBC}, hemoglobin, and serum ferritin) and markers of proximal tubular dysfunction (the maximal tubular reabsorption of phosphate normalized to glomerular filtration rate {TmP/GFR} and tubular reabsorption of phosphate {TRP}) in non-CKD patients with iron deficiency anemia.
Methods: This was a hospital-based analytical cross-sectional study conducted in the outpatient department and/or inpatient wards of the Department of Internal Medicine, Swaroop Rani Nehru (SRN) Hospital associated with Moti Lal Nehru (MLN) Medical College, Prayagraj, Uttar Pradesh, India, between July 2023 and August 2024.
Diabetes Metab J
January 2025
Diabetes Department of Integrated Chinese and Western Medicine, China National Center for Integrated Traditional Chinese and Western Medicine, China- Japan Friendship Hospital, Beijing, China.
Background: Diabetic kidney disease (DKD) is recognized as a significant complication of diabetes mellitus and categorized into glomerular DKDs and tubular DKDs, each governed by distinct pathological mechanisms and biomarkers.
Methods: Through the identification of common features observed in glomerular and tubular lesions in DKD, numerous differentially expressed gene were identified by the machine learning, single-cell transcriptome and mendelian randomization.
Results: The diagnostic markers versican (VCAN) was identified, offering supplementary options for clinical diagnosis.
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