The transcriptional networks that maintain oxidant balance in the mature kidney provide promising entry points for future therapeutic interventions, including for CKD. The use of anti-oxidants targeted to specific pathways that are altered in CKD may prove beneficial, but it is likely that several anti-oxidants will be needed as a multi-drug therapy to target oxidant modifying pathways during the development of CKD. These include lipid peroxidation, which can be improved by α-tocopherol; glutathione redox regulation, which can be restored by NAC; uremic
toxins, which can be reduced by allopurinol; inflammation, which can be attenuated by ω-3 polyunsaturated fatty acids; and finally, mitochondrial dysfunction, which may be improved by CoQ10. Mosca and colleagues86 Talazoparib clinical trial found that healthy individuals taking a combination of α-tocopherol, α-lipoic acid, CoQ10, carnitines
and selenomethionine increased plasma anti-oxidant status, decreased lymphocyte HKI 272 apoptosis and decreased mitochondrial-derived ROS. In the CKD population, identification of patients who would benefit from anti-oxidant therapy is first needed, and then a multifaceted anti-oxidant approach may be necessary for successful treatment of CKD. “
“Aim: There is little data on the prevalence and severity of dyslipidaemia in Asian patients with lupus nephritis (LN). Whether the dyslipidaemia in LN patients differs from subjects with comparable levels of renal impairment also remains undefined. Methods: Lipid profiles of 100 Chinese patients with quiescent LN (age 46.3 ± 9.3 years, 83% female, maintenance prednisolone dose 5.80 ± 2.43 mg/day) were studied and compared with 100 controls who had non-lupus non-diabetic chronic kidney diseases (CKD), matched for sex, age and renal function. Results: LN patients and CKD controls
had Amylase similar renal function and proteinuria, while blood pressure was higher in controls. Twenty-five percent of LN patients and 17% of controls were receiving statin treatment. Despite this, 59% of LN patients and 46% CKD controls showed abnormal lipid parameters (P = 0.066). LN patients showed higher levels of total cholesterol (TC) and triglycerides (TG) than controls (5.28 ± 0.12 vs 4.86 ± 0.08 mmol/L, P = 0.004; and 1.62 ± 0.12 vs 1.20 ± 0.07 mmol/L, P = 0.002, respectively). More LN patients had abnormal TC, TG or low-density lipoprotein cholesterol (LDL-C) (54%, 16% and 38%; P = 0.016, = 0.005 and = 0.021, respectively). Hydroxychloroquine (HCQ) treatment was associated with lower TC, LDL-C and HDL-cholesterol. Conclusion: Dyslipidaemia is prevalent in LN patients and is more severe than controls with a similar degree of CKD despite disease quiescence, low steroid dose and low level of proteinuria. Concomitant corticosteroid and renal impairment are likely contributing factors. HCQ treatment is associated with reduced severity of dyslipidaemia in LN patients.