Initially described in 1984, human immunodeficiency virus-associated nephropathy (HIVAN) has now become a common disease within the HIV-seropositive population. It is a focal segmental glomerulosclerosis causing rapid deterioration of renal function. It is the most common cause of chronic renal disease in HIV patients and occurs almost exclusively in blacks. Through murine and human studies, it is now clear that HIVAN is caused by a direct effect of infection of renal cells by HIV-1 and that the virus actively replicates within renal cells. How the virus causes disease within cells is not yet understood, but there is evidence for factors within infected cells causing both proliferation and apoptosis. Steroids, angiotensin converting enzyme (ACE) inhibitors, and highly active antiretroviral therapy (HAART) have been used for the treatment of HIVAN, with HAART, in particular, showing a dramatic improvement in both the pathologic changes and clinical course of HIVAN.
Introduction: Increased serum uric acid (SUA) levels are found in cardiovascular and kidney diseases, associated with the development of vascular injury. Uric acid stimulates the inflammatory pathways, promotes vascular smooth muscle cells proliferation, activates renin-angiotensin system leading to the development and progression of vascular damage. Renal function-normalized uric acid [SUA to serum creatinine ratio (SUA/SCr)] has been suggested to be a better indicator of uric acid.
Diabetic nephropathy is a prevalent complication of diabetes and stands as the primary contributor to end-stage renal disease. The global prevalence of diabetic nephropathy is on the rise, however, due to its intricate pathogenesis, there is currently an absence of efficacious treatments to enhance renal prognosis in affected patients. The mammalian target of rapamycin (mTOR), a serine/threonine protease, assumes a pivotal role in cellular division, survival, apoptosis delay, and angiogenesis.
Purpose: Emerging literature links the role of the renin-angiotensin-aldosterone system (RAAS) to the progression of cancers. However, the function of RAAS has not been verified in Clear-cell renal cell carcinoma (ccRCC).
Methods: ACE expression in ccRCC tissues was determined using RT-PCR, Western blot, and immunohistochemistry staining.
Kidney tissue injury in renal artery stenosis (RAS) involves inflammation, endoplasmic reticulum stress (ERS), and mitochondria damage. Tumor necrosis factor-stimulated gene-6 (TSG-6), an endogenous reparative molecule, may decrease ERS and improve renal function. To assess its impact on the stenotic murine kidney, we injected TSG-6 or vehicle for two weeks in mice with RAS.
Septic acute kidney injury (AKI) is an important risk factor for developing chronic kidney disease (CKD). Hu antigen R (HuR) is recognized as a crucial modulator in inflammation. We hypothesized that elevated HuR contributes to the transition from septic AKI to CKD by promoting persistent inflammation and fibrosis, and inhibition of HuR may reverse septic kidney injury.
