How do patient feedback systems work in low-income and middle-income countries? Insights from a realist evaluation in Bangladesh.

BACKGROUND: Well-functioning patient feedback systems can contribute to improved quality of healthcare and systems accountability. We used realist evaluation to examine patient feedback systems at health facilities in Bangladesh, informed by theories of citizenship and principal-agent relationships. METHODS: We collected and analysed data in two stages, using: document review; secondary analysis of data from publicly available web-portals; in-depth interviews with patients, health workers and managers; non-participant observations of feedback environments; and stakeholder workshops. Stage 1 focused on identifying and articulating the initial programme theory (PT) of patient feedback systems. In stage 2, we iteratively tested and refined this initial theory, through analysing data and grounding emerging findings within substantive theories and empirical literature, to arrive at a refined PT. RESULTS: Multiple patient feedback systems operate in Bangladesh, essentially comprising stages of collection, analysis and actions on feedback. Key contextual enablers include political commitment to accountability, whereas key constraints include limited patient awareness of feedback channels, lack of guidelines and documented processes, local political dynamics and priorities, institutional hierarchies and accountability relationships. Findings highlight that relational trust may be important for many people to exercise citizenship and providing feedback, and that appropriate policy and regulatory frameworks with clear lines of accountability are critical for ensuring effective patient feedback management within frontline healthcare facilities. CONCLUSION: Theories of citizenship and principal-agent relationships can help understand how feedback systems work through spotlighting the citizenship identity and agency, shared or competing interests, and information asymmetries. We extend the understanding of these theories by highlighting how patients, health workers and managers act as both principals and agents, and how information asymmetry and possible agency loss can be addressed. We highlight the importance of awareness raising and non-threatening environment to provide feedback, adequate support to staff to document and analyse feedback and timely actions on the information.

Clindamycin: An Unusual Cause of Acute Kidney Injury.

BACKGROUND Medications are one of the most common causes of acute kidney injury (AKI). Elderly patients with diabetes mellitus and chronic kidney disease seem to be at particularly high risk for development of medication-induced AKI. Among antibiotics, the most commonly implicated agents are aminoglycosides, cephalosporins, trimethoprim-sulfamethoxazole, acyclovir, and amphotericin. Despite its widespread use, clindamycin has been rarely associated with AKI. CASE REPORT A 52-year-old male patient with type II insulin dependent diabetes mellitus without diabetic nephropathy was treated with clindamycin for chronic osteomyelitis. Five days following initiation of therapy, he developed nausea, poor appetite, decrease in urine output, and profound generalized weakness. His symptoms were initially attributed to gastrointestinal side effects of clindamycin and he was advised to take it with food and to hydrate himself vigorously. Despite this change, his symptoms progressed and he developed hematuria and AKI which prompted hospital admission. Extensive workup for AKI that included evaluation for pre-renal, intrinsic renal, and post-renal etiologies failed to point to other etiologies apart from clindamycin-induced AKI. Following cessation of medication and temporary renal replacement therapy (RRT), his renal function returned to baseline. CONCLUSIONS We present a case of clindamycin-induced AKI that was diagnosed after a delay due to uremia symptoms being mistakenly attributed to gastrointestinal side effects of clindamycin. Although rare, clindamycin can be a cause of AKI and clinician should be aware of this association in order to recognize and treat it in timely manner.

Non-canonical activation of CREB mediates neuroprotection in a Caenorhabditis elegans model of excitotoxic necrosis.

Excitotoxicity, caused by exaggerated neuronal stimulation by Glutamate (Glu), is a major cause of neurodegeneration in brain ischemia. While we know that neurodegeneration is triggered by overstimulation of Glu-receptors (GluRs), the subsequent mechanisms that lead to cellular demise remain controversial. Surprisingly, signaling downstream of GluRs can also activate neuroprotective pathways. The strongest evidence involves activation of the transcription factor cAMP response element-binding protein (CREB), widely recognized for its importance in synaptic plasticity. Canonical views describe CREB as a phosphorylation-triggered transcription factor, where transcriptional activation involves CREB phosphorylation and association with CREB-binding protein. However, given CREB's ubiquitous cross-tissue expression, the multitude of cascades leading to CREB phosphorylation, and its ability to regulate thousands of genes, it remains unclear how CREB exerts closely tailored, differential neuroprotective responses in excitotoxicity. A non-canonical, alternative cascade for activation of CREB-mediated transcription involves the CREB co-factor cAMP-regulated transcriptional co-activator (CRTC), and may be independent of CREB phosphorylation. To identify cascades that activate CREB in excitotoxicity we used a Caenorhabditis elegans model of neurodegeneration by excitotoxic necrosis. We demonstrated that CREB's neuroprotective effect was conserved, and seemed most effective in neurons with moderate Glu exposure. We found that factors mediating canonical CREB activation were not involved. Instead, phosphorylation-independent CREB activation in nematode excitotoxic necrosis hinged on CRTC. CREB-mediated transcription that depends on CRTC, but not on CREB phosphorylation, might lead to expression of a specific subset of neuroprotective genes. Elucidating conserved mechanisms of excitotoxicity-specific CREB activation can help us focus on core neuroprotective programs in excitotoxicity. Cover Image for this issue: doi: 10.1111/jnc.14494.