ABSTRACT
AIM: To compare the changes of optic disc parameters, peripapillary retinal nerve fibers layer(pRNFL)thickness and macular ganglion cell layer(mGCL)thickness among patients with early diabetes retinopathy and healthy controls by Cirrus HD-optical coherence tomography(OCT).METHODS: In this cross-sectional comparative study, 45 non-diabetic retinopathy(NDR), 52 mild nonproliferative diabetic retinopathy(NPDR), 55 moderate NPDR with type 2 diabetes mellitus(T2DM)and 64 age-matched healthy controls were included. The fasting blood glucose(FBG), duration of diabetes, glycosylated hemoglobin(HbA1c)and past history of the patients were collected in detail. Optic disc parameters(i.e., binocular RNFL thickness symmetry percentage, rim area, optic disc area, cup-to-disc ratio, cup volume), pRNFL thickness and mGCL thickness were measured by Cirrus HD-OCT. The comparison of different groups was performed by one-way analysis of variance.RESULTS: Compared with the control group, the binocular RNFL thickness symmetry percentage and rim area were significantly decreased, while the average C/D and vertical C/D were significantly increased in the NDR group, mild NPDR group and moderate NPDR group(all P<0.05). Compared with the control group, the peripapillary RNFL thicknesses(superior, temporal, inferior, nasal)and macular GCL thickness(average, minimum, superior, supero-temporal, infero-temporal, inferior, supero-nasal, and infero-nasal)became thinner in the NDR group, mild NPDR group, and moderate NPDR group(all P<0.05).CONCLUSION: Patients with early DR have significantly decreased binocular RNFL thickness asymmetry, rim area, pRNFL and mGCL thickness, while they have significantly increased cup-to-disc ratio when compared to healthy controls. The results support the statement that DM causes inner retinal neurodegenerative changes even in T2DM patients without overt microangiopathy.
ABSTRACT
<p><b>Background:</b>Cyclosporine A (CsA) is a commonly used clinical immunosuppressant. However, CsA exposure in rabbits during the gestation period was shown to cause a postnatal decrease in the number of nephrons, with the effects remaining unknown. In this study, we aimed to explore the effects of CsA on metanephros development in the pregnant BALB/c mice.</p><p><b>Methods:</b>Pregnant mice were randomly divided into two groups, and CsA (10 mg·kg·d) was subcutaneously injected from gestation day 10.5 to day 16.5 in the CsA group, whereas a comparable volume of normal saline was given to the control group. All of the mice were sacrificed on gestation day 17.5 and serum CsA concentration was measured. The fetuses were removed and weighed, and their kidneys were prepared for histological assessment and polymerase chain reaction assay. In an in vitro experiment, embryo kidneys of fetal mice on gestation day 12.5 were used, and CsA (10 μmol/L) was added in the culture of the CsA group. The growth pattern of the ureteric bud and nephrons was assessed by lectin staining.</p><p><b>Results:</b>No significant differences in the weight of embryo (4.54 ± 1.22 vs. 3.26 ± 1.09 mg) were observed between the CsA and control groups, the thickness of the cortical (510.0 ± 30.3 vs. 350.0 ± 29.7 μm, P < 0.05) and nephrogenic zone (272.5 ± 17.2 vs. 173.3 ± 24.0 μm, P < 0.05), and the number of glomeruli (36.5 ± 0.7 vs. 27.5 ± 2.1, P < 0.05) were reduced in the CsA group when compared to the control group. The cell proliferation of Ki-67 positive index between control and CsA group (307.0 ± 20.0 vs. 219.0 ± 25.0, P < 0.05) in the nephrogenic zone was decreased with the increase of apoptotic cells (17.0 ± 2.0 vs. 159.0 ± 33.0, P < 0.05). The mRNA expression of WT-1, Pax2, and Pax8 was downregulated by CsA treatment. As for the in vitro CsA group, the branch number of the ureteric bud was decreased in the CsA-treated group with the nephrons missing in contrast to control after the incubation for 24 h and 72 h (all P < 0.0001).</p><p><b>Conclusion:</b>Treatment of CsA suppressed metanephros development in the pregnant mice; however, the potential action of mechanism needs to be further investigated.</p>
ABSTRACT
<p><b>BACKGROUND</b>Unfractionated heparin is the most commonly used anticoagulant in continuous renal replacement therapy (CRRT), but it can increase the risk of bleeding. Citrate is a promising substitute. Our study was to assess the efficacy and safety of citrate versus unfractionated heparin in CRRT.</p><p><b>METHODS</b>We searched the MEDLINE, the EMBASE, the Cochrane Central Register of Controlled Trials, and the China National Knowledge Infrastructure Database until up to November 2011 for randomized controlled trials comparing citrate with unfractionated heparin in adult patients with acute kidney injury prescribed CRRT. The primary outcome was mortality and the secondary outcomes included circuit survival, control of uremia, risk of bleeding, transfusion rates, acid-base statuses, and disturbance of sodium and calcium homeostasis.</p><p><b>RESULTS</b>Four trials met the inclusion criteria. Meta-analysis found no significant difference between two anticoagulants on mortality. Less bleeding and more hypocalcemic episodes were with citrate. Citrate was superior or comparable to unfractionated heparin in circuit life.</p><p><b>CONCLUSIONS</b>Citrate anticoagulation in CRRT seems to be superior in reducing bleeding risk and with a longer or similar circuit life, although there is more metabolic derangement. Mortality superiority has not been approved.</p>