Stable oxygen isotope variability in two contrasting glacier river catchments in Greenland

Analysis of stable oxygen isotope (δ18O) characteristics is a useful tool to investigate water provenance in glacier river systems. In order to attain knowledge on the diversity of δ18O variations in Greenlandic rivers, we examined two contrasting glacierised catchments disconnected from the Greenland Ice Sheet (GrIS). At the Mittivakkat Gletscher river, a small river draining a local temperate glacier in southeast Greenland, diurnal oscillations in δ18O occurred with a 3 h time lag to the diurnal oscillations in run-off. The mean annual δ18O was −14.68 ± 0.18 ‰ during the peak flow period. A hydrograph separation analysis revealed that the ice melt component constituted 82 ± 5 % of the total run-off and dominated the observed variations during peak flow in August 2004. The snowmelt component peaked between 10:00 and 13:00 local time, reflecting the long travel time and an inefficient distributed subglacial drainage network in the upper part of the glacier. At the Kuannersuit Glacier river on the island Qeqertarsuaq in west Greenland, the δ18O characteristics were examined after the major 1995–1998 glacier surge event. The mean annual δ18O was −19.47 ± 0.55 ‰. Despite large spatial variations in the δ18O values of glacier ice on the newly formed glacier tongue, there were no diurnal oscillations in the bulk meltwater emanating from the glacier in the post-surge years. This is likely a consequence of a tortuous subglacial drainage system consisting of linked cavities, which formed during the surge event. Overall, a comparison of the δ18O compositions from glacial river water in Greenland shows distinct differences between water draining local glaciers and ice caps (between −23.0 and −13.7 ‰) and the GrIS (between −29.9 and −23.2 ‰). This study demonstrates that water isotope analyses can be used to obtain important information on water sources and the subglacial drainage system structure that is highly desired for understanding glacier hydrology

Gender differences in the use of cardiovascular interventions in HIV-positive persons; the D:A:D Study

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Development and Validation of a Risk Score for Chronic Kidney Disease in HIV Infection Using Prospective Cohort Data from the D:A:D Study

Ristola M. on työryhmien DAD Study Grp ; Royal Free Hosp Clin Cohort ; INSIGHT Study Grp ; SMART Study Grp ; ESPRIT Study Grp jäsen.Background Chronic kidney disease (CKD) is a major health issue for HIV-positive individuals, associated with increased morbidity and mortality. Development and implementation of a risk score model for CKD would allow comparison of the risks and benefits of adding potentially nephrotoxic antiretrovirals to a treatment regimen and would identify those at greatest risk of CKD. The aims of this study were to develop a simple, externally validated, and widely applicable long-term risk score model for CKD in HIV-positive individuals that can guide decision making in clinical practice. Methods and Findings A total of 17,954 HIV-positive individuals from the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D) study with >= 3 estimated glomerular filtration rate (eGFR) values after 1 January 2004 were included. Baseline was defined as the first eGFR > 60 ml/min/1.73 m2 after 1 January 2004; individuals with exposure to tenofovir, atazanavir, atazanavir/ritonavir, lopinavir/ritonavir, other boosted protease inhibitors before baseline were excluded. CKD was defined as confirmed (>3 mo apart) eGFR In the D:A:D study, 641 individuals developed CKD during 103,185 person-years of follow-up (PYFU; incidence 6.2/1,000 PYFU, 95% CI 5.7-6.7; median follow-up 6.1 y, range 0.3-9.1 y). Older age, intravenous drug use, hepatitis C coinfection, lower baseline eGFR, female gender, lower CD4 count nadir, hypertension, diabetes, and cardiovascular disease (CVD) predicted CKD. The adjusted incidence rate ratios of these nine categorical variables were scaled and summed to create the risk score. The median risk score at baseline was -2 (interquartile range -4 to 2). There was a 1: 393 chance of developing CKD in the next 5 y in the low risk group (risk score = 5, 505 events), respectively. Number needed to harm (NNTH) at 5 y when starting unboosted atazanavir or lopinavir/ritonavir among those with a low risk score was 1,702 (95% CI 1,166-3,367); NNTH was 202 (95% CI 159-278) and 21 (95% CI 19-23), respectively, for those with a medium and high risk score. NNTH was 739 (95% CI 506-1462), 88 (95% CI 69-121), and 9 (95% CI 8-10) for those with a low, medium, and high risk score, respectively, starting tenofovir, atazanavir/ritonavir, or another boosted protease inhibitor. The Royal Free Hospital Clinic Cohort included 2,548 individuals, of whom 94 individuals developed CKD (3.7%) during 18,376 PYFU (median follow-up 7.4 y, range 0.3-12.7 y). Of 2,013 individuals included from the SMART/ESPRIT control arms, 32 individuals developed CKD (1.6%) during 8,452 PYFU (median follow-up 4.1 y, range 0.6-8.1 y). External validation showed that the risk score predicted well in these cohorts. Limitations of this study included limited data on race and no information on proteinuria. Conclusions Both traditional and HIV-related risk factors were predictive of CKD. These factors were used to develop a risk score for CKD in HIV infection, externally validated, that has direct clinical relevance for patients and clinicians to weigh the benefits of certain antiretrovirals against the risk of CKD and to identify those at greatest risk of CKD.Peer reviewe