Human | KLB | 152831 | klotho beta | The down-regulation of the renal klotho gene could increase renal damage induced by angiotensin II, while klotho gene induction could have therapeutic possibilities in treating angiotensin II-induced kidney damage |
Human | NOX3 | 50508 | NADPH oxidase 3 | Potential candidate genes in these regions that have been implicated in diabetic nephropathy and/or renal damage in models of hypertension include CYBA (or P22PHOX) (16q24), NOX1 (10q22), and NOX3 (6q25.1-q26) |
Human | AOC3 | 8639 | amine oxidase, copper containing 3 | Serum levels of VAP-1 are associated with the severity of kidney damage or stages of kidney disease |
Human | VCAM1 | 7412 | vascular cell adhesion molecule 1 | persistently elevated, levels of sVCAM-1 throughout the various phases and types of the disease, suggests an important role in the immunopathological lesions of HFRS and is closely correlated to the severity of HFRS and the degree of kidney damage |
Human | TNFAIP3 | 7128 | tumor necrosis factor, alpha-induced protein 3 | A1 and A20 are both required for optimal protection from apoptosis (A1) and inflammation (A20) in conditions leading to renal damage |
Human | CCL5 | 6352 | chemokine (C-C motif) ligand 5 | It is reported that 2 polymorphisms in the RANTES promoter do not correlate with SLE individually; interaction of the polymorphisms probably exerts a risk effect against SLE; and polymorphism at the 403 locus is probably related with renal damage |
Human | CCL2 | 6347 | chemokine (C-C motif) ligand 2 | results suggest that monocyte chemoattractant protein-1 is produced in renal tubular cells and released into urine in proportion to the degree of proteinuria (albuminuria), and its increased expression in renal tubuli contributes to renal tubular damage Title:Association of monocyte chemoattractant protein-1 with renal tubular damage in diabetic nephropathy.|Association:Y|Conclusion:We conclude that heavy proteinuria itself may accelerate the progression of diabetic nephropathy by increasing the MCP-1 expression in renal tubuli. |
Human | NOS3 | 4846 | nitric oxide synthase 3 (endothelial cell) | Endothelial nitric oxide synthase polymorphisms play no role in promoting hypertensive renal damage, and do not influence endothelial-mediated vasodilatation in never-treated men with essential hypertension |
Human | IL12A | 3592 | interleukin 12A (natural killer cell stimulatory factor 1, cytotoxic lymphocyte maturation factor 1, p35) | Renal immune complex deposition can occur in absence of IL-12p35, but structural renal damage requires presence of IL-12p35 or mediators induced by this molecule, such as IFN-gamma |
Human | CFH | 3075 | complement factor H | Complement factor H contributes to the control mechanism of in situ complement activation and prevents renal damage in idiopathic membranous nephropathy |
Human | GJA1 | 2697 | gap junction protein, alpha 1, 43kDa | Cx43 expression and cell-to-cell communication increased in response to high glucose and may protect the collecting duct from renal damage associated with more established diabetic nephropathy |
Human | FCAR | 2204 | Fc fragment of IgA, receptor for | Fc alpha receptor type I activation mediates glomerulonephritis progression by initiating a cytokine/chemokine cascade that promotes leukocyte recruitment and kidney damage in transgenic mice |
Human | FABP1 | 2168 | fatty acid binding protein 1, liver | EPO supplementation may ameliorate renal tubular damage, in part, due to a reduction of oxidative stress in CRF patients with anemia |
Human | FABP4 | 2167 | fatty acid binding protein 4, adipocyte | FABP4 concentrations should be taken into consideration as an early marker of kidney damage in patients with type 2 diabetes |
Human | ACE | 1636 | angiotensin I converting enzyme | Title:Potential risk factors associated with progressive renal damage in childhood urological diseases: the role of angiotensin-converting enzyme gene polymorphism.|Association:Y|Conclusion:Considered together, these studies suggest that there are differences in the distribution of angiotensin-converting enzyme gene polymorphism in patients with congenital urological abnormalities who have evidence of renal parenchymal damage versus those who do not have such damage. Given that this genetic variation activates the renin-angiotensin system and this activation may be particularly robust in the kidney, we propose that the genotype of an individual independent of other factors modifies the likelihood of parenchymal loss in this setting. Based on these observations we conclude that ACE DD genotype implicate a strong possible role in the hypertensive state and in renal damage among north Indians |
Human | BCL2A1 | 597 | BCL2-related protein A1 | A1 and A20 are both required for optimal protection from apoptosis (A1) and inflammation (A20) in conditions leading to renal damage |
Human | AGTR1 | 185 | angiotensin II receptor, type 1 | a maternal autoantibody with the ability to activate AT(1) receptors may account for the development of renal damage seen in preeclamptic patients |