We studied kidneys of rats intoxicated with uranylnitrate (UN) or subjected to 5/6 nephrectomy (NX) or after a combination of both procedures (NX-UN). Our observations indicate that UN causes impressive changes of ultrastructure (partial loss of brush border, appearance of intercellular clefts in the epithelial barrier) and altered protein expression (α-SMA, collagen I and III) in proximal tubule cells. Renal parameters (creatinine clearance, proteinuria) seemed to be unaffected. Blood pressure recovered to normal values within 12 months. However ultrastructural and functional restoration of modified proximal tubules was not complete. We conclude that changed proximal tubules may induce progression of interstitial fibrosis causing renal failure. NX animals and more pronounced NX-UN animals showed dramatic changes in renal function. We observed increased levels of proteinuria, blood pressure and decreased creatinine clearance. Progressive glomerular reorganization includes loss of filtration gaps and enhanced thickness of glomerular basement membranes (GBM) with increased immunoreactivity for collagen IV. Cells in vicinity of Bowman's capsule contained high amounts of immunoreactive α-smooth muscle actin. The NX-UN group showed more dramatic changes in ultrastructure of proximal tubules including apoptosis. Enhanced expression and secretion of extracellular matrix proteins (ECM e.g. collagens I, III, fibronectin) indicate progressive epithelial-mesenchymal transition (EMT) leading to permanent impairment of renal function.
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http://dx.doi.org/10.1016/j.etp.2012.01.002 | DOI Listing |
Cell Commun Signal
January 2025
Centre of Postgraduate Medical Education, Centre of Translation Research, Department of Biochemistry and Molecular Biology, ul. Marymoncka 99/103, Warsaw, 01-813, Poland.
Background: Renal cell cancer (RCC) is the most common and highly malignant subtype of kidney cancer. Mesenchymal stromal cells (MSCs) are components of tumor microenvironment (TME) that influence RCC progression. The impact of RCC-secreted small non-coding RNAs (sncRNAs) on TME is largely underexplored.
View Article and Find Full Text PDFDiabetes
January 2025
Centre de recherche, Centre hospitalier de l'Université de Montréal (CRCHUM) and Département de médecine, Université de Montréal, 900 Saint Denis Street, Montréal, QC Canada H2X 0A9.
The role of the intrarenal renin-angiotensin system (iRAS) in diabetic kidney disease (DKD) progression remains unclear. In this study, we generated mice with renal tubule-specific deletion of angiotensinogen (Agt; RT-Agt-/-) in both Akita and streptozotocin (STZ)-induced mouse model of diabetes. Both Akita RT-Agt-/- and STZ-RT-Agt-/- mice exhibited significant attenuation of glomerular hyperfiltration, urinary albumin/creatinine ratio, glomerulomegaly and tubular injury.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Endocrinology, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, 230022, People's Republic of China.
Background: Tubular injury triggered by hyperglycemia is an important pathological characteristic in diabetic nephropathy (DN). Accumulated advanced glycation end products and their precursor methylglyoxal (MGO), contribute to the development of DN. Carnosine has been shown to prevent the development of DN but the underlying mechanism still needs to be studied in depth.
View Article and Find Full Text PDFSci Rep
January 2025
Medical Imaging Center, First Affiliated Hospital, Jiamusi University, Jiamusi, Heilongjiang, China.
Chronic hyperglycemia, a hallmark of diabetes, can trigger inflammatory responses in the kidney, leading to diabetic nephropathy (DN). Follistatin-like protein 1 (FSTL1) has emerged as a potential therapeutic target in various kidney diseases. This study investigated the effect of high glucose on FSTL1 expression and its role in oxidative stress and cellular transdifferentiation injury in HK-2 human proximal tubule epithelial cells, a model of DN.
View Article and Find Full Text PDFRen Fail
December 2025
Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, People's Republic of China.
Background: Diabetic kidney disease (DKD) is the leading cause of end-stage renal disease. Sodium-glucose cotransporter protein 2 inhibitors (SGLT2i) are antihyperglycemic agents that provide additional renal-protective effects in patients with DKD, independent of their glucose-lowering effects. However, the underlying mechanism remains unclear.
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