Previous studies have shown a significant increase in monoclonal gammopathy (MG) prevalence in patients with human immunodeficiency virus (HIV). HIV and MG both can cause renal injury and have attracted increasing nephrologists' attention. To date, there has been a lack of relevant studies on the renal pathology of HIV combined with MG. Here, we report a case of a newly diagnosed HIV patient with co-morbid MG and subsequent or concurrent massive proteinuria whose renal biopsy showed minimal change disease (MCD). After a period of administration of highly active antiretroviral therapy (HAART), HIV viral RNA was undetectable in plasma, along with complete remission of the nephropathy. However, there was no significant effect on MG.
Background: miR-140-5p is frequently dysregulated in different types of tumors and has been found to suppress inflammation through TLR4 in lung injury. In the current investigation, we try to decipher the possible function of miR-140-5p in hypoxia-induced nephrotoxicity and renal fibrogenesis in human renal cells. Methods: Hypoxia in HK-2 cells was produced using cobalt chloride (CoCl2). Hypoxia-induced cellular viability and apoptosis were determined by cell viability assay and ELISA-based apoptosis assay, respectively. Western blotting was carried out to measure expression levels of pro-fibrotic and apoptosis-related proteins. Result: The present study observed that upregulation of miR-140-5p significantly decreases apoptosis and increases cell viability in hypoxia challenged HK-2 cells. Furthermore, miR-140-5p over expression decreased expression of pro-apoptotic proteins like Bad and Bax and pro-fibrotic proteins like Collagen I, CTGF and fibronectin. While as, expression of anti-apoptotic protein, namely Bcl-2, was increased in hypoxia-insulted HK-2 cells. Moreover, the luciferase reporter assay confirmed that miR-140-5p targets TLR4. TLR4 knockdown prevents miR-140-5p from performing its suppressive role in hypoxia linked to apoptosis and fibrosis.
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