Objectives The use of combination antiretroviral therapy (cART) increases clinical uncertainty about changes in renal function. Specifically, little is known regarding the interaction of the effects of aging, baseline renal impairment, and stages of HIV infection on post‐treatment changes in renal function. Methods This analysis included 5533 HIV‐infected patients on cART in 2004–2016. Progression to chronic kidney disease (CKD) was defined as either two consecutive estimated glomerular filtration rate (eGFR) measurements < 60 mL/min/1.73 m2 for baseline eGFR ≥ 60 mL/min/1.73 m2 (mild renal impairment or normal renal function) or a 25% decline for baseline eGFR < 60 mL/min/1.73 m2 (moderate renal impairment). Results During follow‐up (median 4.8 years), 130 (2.3%) of the patients progressed to CKD. A total of 20.1% of patients with baseline normal renal function progressed to mild renal impairment, while 74.0% of patients with baseline mild or moderate renal impairment improved to normal renal function. In multivariable analysis, a significant positive baseline‐eGFR‐by‐World Health Organization (WHO)‐stage interaction effect on progression to CKD in all patients was identified, indicating a cross‐over effect from a reduced risk to an increased risk. A significant negative baseline‐age‐by‐WHO‐stage interaction effect on progression to mild renal impairment in patients with baseline normal renal function was identified, with adjusted hazard ratios progressively lower at older ages. In addition, there were significant associations with older age, lower baseline eGFR, Dai ethnic minority, and anaemia for both outcomes, hyperglycaemia for CKD only, and higher CD4 count, tenofovir and ritonavir‐boosted lopinavir use for mild renal impairment only. Conclusions Our data suggest a complex pattern of renal function dynamics in patients on cART, which requires precise management with systematic monitoring of the interaction of the effects of sociodemographic, nephrological and HIV‐specific clinical characteristics.
Background: It is unclear if the complex relationship between physical frailty and cognition variesacross the severity of cognitive impairment. Objectives:We therefore aimed to explore if there are stage-specificdifferences in the relationship between frailty and cognitive impairment. Design:Cross-sectional study. Setting:A specialist Memory Clinic setting. Participants: Mild cognitive impairment (MCI) and mild-moderateAlzheimer’s disease (AD) community-dwelling subjects. Measurements: We obtained data on demographics,multimorbidity, cognition-related measures, nutrition, neuroimaging measures, muscle mass, Vitamin D level,apolipoprotein – e (APOE) status and physical performance measures. Frailty measures of gait speed, hand gripstrength, question on exhausation and weight loss, classified subjects according to the Buchmann criteria intonon-frail and frail categories. Results: Forty-five MCI, 64 mild AD and 13 moderate AD subjects (total n=122)were studied. The prevalence of frailty for MCI, mild AD and moderate AD was 35.6%, 21.9% and 46.2%respectively, indicating a u-shaped trend. Significant differences were noted in fatigue, grip strength and gaitspeed frailty sub-items. Significant correlation of frailty with cognition were noted in mild-moderate AD(Spearman’s coefficient 0.26, p<0.05) but not in MCI (0.01, p=0.6). No other differences in multimorbidity,Vitamin D, APOE, nutritional measures, white matter lesions were observed. Sarcopenia interestingly had aninverse stage-specific relationship unlike frailty. Conclusions:Our results suggest a U-shaped relationshipbetween frailty and cognition, characterized by initial dissociation with cognitive impairment and subsequentconvergence at later stages. Future studies incorporating immune markers and endocrine pathways withlongitudinal follow-up could potentially elucidate intermediary mechanisms in the frailty cascade.
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