Objective Secondary care services are struggling to manage demand for induced abortion, but less is known about what scope exists to improve the primary care of women requiring abortion. The study objective was to identify service-related delays and barriers faced by women seeking abortion care. MethodsThe study comprised case note review and cross-sectional surveys conducted in South Durham in the North East of England, UK. We surveyed and reviewed the case notes of women attending two fertility control clinics. We also surveyed general practitioners (GPs) who referred women to these clinics. The outcomes were waiting times within the pathway to induced abortion, women's rating of care, GPs' attitudes and self-reported practice.Results Of 210 women surveyed, 132 (63%) responded. Of 107 referred by GPs, 16 (15%) had to make a second appointment with another GP willing to refer them and 34 (32%) waited two or more days to receive a date for their hospital appointment. The national standard waiting time of 3 weeks from first appointment with the referring doctor to the procedure was achieved for 56/127 women (44%; 95% CI, 35-53). Women rated global satisfaction, provision of information and staff interaction more highly in secondary than primary care. Of 170 GPs surveyed, 140 (82%) responded; 33 (24%) considered themselves 'broadly anti-abortion'.Conclusions Women face delays in accessing induced abortion care, both before and after referral from primary care. Whilst scope exists for improving quality of care and access within present service configurations, alternative approaches that bypass traditional gatekeepers to abortion care should be evaluated. G Women seeking access to abortion services want their general practitioner to treat them with respect, provide information and arrange prompt referral.G Women seeking abortion experience barriers that will require alternative models of care to overcome. Some of these barriers contribute to delay, though their most important effect is on the patient experience.
Chronic kidney disease (CKD) is prevalent worldwide and is associated with significant co-morbidities including cardiovascular disease (CVD). Traditionally, the subtotal nephrectomy (remnant kidney) experimental model has been performed in rats to model progressive renal disease. The model experimentally mimics CKD by reducing nephron number, resulting in renal insufficiency. Presently, there is a lack of translation of pre-clinical findings into successful clinical results. The pre-clinical nephrology field would benefit from reproducible progressive renal disease models in mice in order to avail of more widely available transgenics and experimental tools to dissect mechanisms of disease. Here we evaluate if a simplified single step subtotal nephrectomy (STNx) model performed in the 129S2/SV mouse can recapitulate the renal and cardiac changes observed in patients with CKD in a reproducible and robust way. The single step STNx surgery was well-tolerated and resulted in clinically relevant outcomes including hypertension, increased urinary albumin:creatinine ratio, and significantly increased serum creatinine, phosphate and urea. STNx mice developed significant left ventricular hypertrophy without reduced ejection fraction or cardiac fibrosis. Analysis of intra-renal inflammation revealed persistent recruitment of Ly6Chi monocytes transitioning to pro-fibrotic inflammatory macrophages in STNx kidneys. Unlike 129S2/SV mice, C57BL/6 mice exhibited renal fibrosis without proteinuria, renal dysfunction, or cardiac pathology. Therefore, the 129S2/SV genetic background is susceptible to induction of progressive proteinuric renal disease and cardiac hypertrophy using our refined, single-step flank STNx method. This reproducible model could be used to study the systemic pathophysiological changes induced by CKD in the kidney and the heart, intra-renal inflammation and for testing new therapies for CKD.
Progressive fibrosis is a feature of aging and chronic tissue injury in multiple organs, including the kidney and heart. Glioma-associated oncogene 1 expressing (Gli1 + ) cells are a major source of activated fibroblasts in multiple organs, but the links between injury, inflammation, and Gli1 + cell expansion and tissue fibrosis remain incompletely understood. We demonstrated that leukocyte-derived tumor necrosis factor (TNF) promoted Gli1 + cell proliferation and cardiorenal fibrosis through induction and release of Indian Hedgehog (IHH) from renal epithelial cells. Using single-cell–resolution transcriptomic analysis, we identified an “inflammatory” proximal tubular epithelial (iPT) population contributing to TNF- and nuclear factor κB (NF-κB)–induced IHH production in vivo. TNF-induced Ubiquitin D ( Ubd ) expression was observed in human proximal tubular cells in vitro and during murine and human renal disease and aging. Studies using pharmacological and conditional genetic ablation of TNF-induced IHH signaling revealed that IHH activated canonical Hedgehog signaling in Gli1 + cells, which led to their activation, proliferation, and fibrosis within the injured and aging kidney and heart. These changes were inhibited in mice by Ihh deletion in Pax8 -expressing cells or by pharmacological blockade of TNF, NF-κB, or Gli1 signaling. Increased amounts of circulating IHH were associated with loss of renal function and higher rates of cardiovascular disease in patients with chronic kidney disease. Thus, IHH connects leukocyte activation to Gli1 + cell expansion and represents a potential target for therapies to inhibit inflammation-induced fibrosis.
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