Objective: To assess the nature, distribution and expression pattern of CD75, a neuraminidase-sensitive lymphocyte cell surface differentiation antigen, in calcium oxalate (CaOx) stone disease, as cell-surface sialic acid might be involved CaOx crystal binding, and lectin-binding assays suggest that sialic acid in the alpha2,6 position is upregulated in stone-forming kidneys.
Materials And Methods: Human CaOx stone-forming and normal kidneys (13 each) and primary kidney epithelial cells (CAKI-1, three samples) were analysed. The protein pattern, distribution and expression of CD75 were analysed using Western blotting, immunohistology and semi-quantitative confocal laser scanning microscopy (cLSM). Production was investigated by alpha2,6-sialyltransferase specific reverse transcription-polymerase chain reaction.
Results: Western blotting showed one strong band at approximately 43 kDa that reacted with anti-CD75 when renal epithelial and CAKI-1 tumour cell extracts were analysed. However, in renal tissue extracts of CaOx stone formers there were additional bands at 120 and 205 kDa. Image processing after cLSM showed that anti-CD75 reactivity was significantly greater on E-cadherin-positive distal and collecting tubular cells from CaOx stone-forming kidneys, at a mean (sd) intensity of 87 (7), than on those from normal kidneys, at 41 (5) (P = 0.005).
Conclusion: CD75 expression in human kidney was primarily on the luminal surface of distal tubules and collecting ducts. Whether increased epithelial CD75 expression in CaOx stone disease is a cause or result of the disease remains to be clarified.
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http://dx.doi.org/10.1111/j.1464-410x.2003.04751.x | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Urology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, 430060, P. R. China.
The initiation of calcium oxalate (CaOx) kidney stone formation is highly likely to stem from injury to the renal tubular epithelial cells (RTECs) induced by stimulation from an aberrant urinary environment. CHAC1 plays a critical role in stress response mechanisms by regulating glutathione metabolism. Endoplasmic reticulum (ER) stress and ferroptosis are demonstrated to be involved in stone formation.
View Article and Find Full Text PDFKidney Med
January 2025
Department of Neurology, Damascus University-Faculty of Medicine, Damascus, Syria, MA.
A 50-year-old woman with kidney failure complained of back pain and an inability to walk. The medical history included hypothyroidism, nephrolithiasis, and resistant anemia aligned with several transfusions. The examination showed hepatosplenomegaly, lower limb weakness, absence of reflexes, and lack of sensations with a sensory level T6.
View Article and Find Full Text PDFNat Med
January 2025
Department of Nephrology and Hypertension, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.
J Agric Food Chem
January 2025
Institute of Biomineralization and Lithiasis Research, College of Chemistry and Materials Science, Jinan University, Guangzhou 510632, China.
Hyperoxaluria can easily induce calcium oxalate (CaOx) crystals and cause cell damage, thereby increasing the risk of kidney stone formation. In this study, three sulfated polysaccharides (PSPs) were obtained by the sulfur trioxide-pyridine method. The antioxidant activity of PSPs and the inhibitory effects of PSPs on CaOx crystallization, cellular oxidative damage, and cellular inflammation were explored in vitro, and PSPs were used to treat hyperoxaluria-induced crystallization model mice in order to validate the stone-preventive effect of PSPs in vivo.
View Article and Find Full Text PDFUrolithiasis
December 2024
Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, 1, Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya, Japan.
The early stages of kidney crystal formation involve inflammation and hypoxia-induced cell injury; however, the role of the hypoxic response in kidney crystal formation remains unclear. This study investigated the effects of a prolyl hydroxylase domain inhibitor (roxadustat) on renal calcium oxalate (CaOx) crystal formation through in vitro and in vivo approaches. In the in vitro experiment, murine renal tubular cells (RTCs) were exposed to varying roxadustat concentrations and CaOx crystals.
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