ABSTRACT
Purpose: Oral valproic acid (VPA) used as an anticonvulsant has been shown to improve contrast threshold sensitivities in patients receiving it on long-term. This study aimed to evaluate the efficacy of oral VPA in improving visual function in eyes with advanced stage glaucoma. Methods: In this prospective randomized study, 31 patients (n = 31 eyes) with advanced stage glaucoma (with an intraocular pressure <16 mmHg) in at least one eye received oral VPA 500 mg once a day for 3 months and 33 patients (n = 33 eyes) continued on glaucoma therapy. Patients were followed up at 3 and 12 months (to evaluate the legacy effect of the drug). Blood VPA concentrations were measured at 3 months. Following parameters were assessed at baseline, 3 months and 12 months: log of the minimum angle of resolution (LogMAR) visual acuity, mean deviation on visual fields, and multifocal electroretinogram (ERG). Results: Median LogMar visual acuity in the VPA group improved from 0.3 at baseline to 0.18 and 0.18 at 3 and 12 months, respectively (P < 0.01). In comparison, the median visual acuity in control group at baseline was 0.18 and showed neither worsening nor improvement over 3 and 12 months (P = 0.56). The improvement in VPA group was significant compared to the control group (P < 0.01; Wilcoxon Signed-rank test). An improvement in one line was experienced in 11 out of 31 eyes in the VPA group compared to 1 out of 33 eyes among controls (P = 0.003). No significant improvement was noted in the mean deviation, and the multifocal ERG (Latency and amplitudes) in the VPA-treated patients. The average blood VPA concentration measured at 3 months of therapy was 26 � 8.9 ?g/ml (range 8� ?g/ml) which is much lower than that achieved during anticonvulsant therapy. None of the patients complained of any adverse effects that required stopping VPA therapy. Conclusion: A 3 months oral VPA therapy results in some improvement in visual acuity in a subgroup of eyes with advanced glaucoma and the effect was seen to persist 9 months after the drug was stopped.
ABSTRACT
Drug-induced Acute Kidney Injury (AKI) constitutes an important cause of acute renal failure and chronic kidney disease in present day clinical practice. Drug-induced acute renal failure (ARF) accounted for 20% of all ARF in an Indian study. The incidence and prevalence of chronic kidney disease (CKD) has dramatically increasing worldwide. Progression of AKI from mild or moderate to end stage may be prevented by selecting potentially effective therapies, if it is detected in very early stage. But early detection of AKI is often difficult due to paucity of early predictive noninvasive biomarkers. Development of omics technology has led to the identification of several urinary protein biomarkers and transcriptional biomarkers, which enable earlier detection of kidney injury. Urinary protein biomarkers have great benefit due to the easy or non-invasive availability of urine and many showing good predictive power. Several urinary protein biomarkers have been identified and have demonstrated superiority in detecting kidney injury in comparison to conventional parameters like serum creatinine (SCr), blood urea nitrogen (BUN) etc. These promising experimental biomarker of kidney damage require further confirmation of its use in routine clinical use.