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BackgroundMulti-morbidity due to diabetes and chronic kidney disease (CKD) remains challenging for current health-systems, which focus on single diseases. As a first step toward health-care improvement, we explored the perspectives of patients and their carers on factors influencing the health-care of those with co-morbid diabetes and CKD.MethodsIn this qualitative study participants with co-morbid diabetes and CKD were purposively recruited using maximal variation sampling from 4 major tertiary health-services from 2 of Australia’s largest cities. Separate focus groups were conducted for patients with CKD stages 3, 4 and 5. Findings were triangulated with semi-structured interviews of carers of patients. Discussions were transcribed verbatim and thematically analysed.ResultsTwelve focus groups with 58 participants and 8 semi-structured interviews of carers were conducted. Factors influencing health-care of co-morbid diabetes and CKD grouped into patient and health service level factors. Key patient level factors identified were patient self-management, socio-economic situation, and adverse experiences related to co-morbid diabetes and CKD and its treatment. Key health service level factors were prevention and awareness of co-morbid diabetes and CKD, poor continuity and coordination of care, patient and carer empowerment, access and poor recognition of psychological co-morbidity. Health-service level factors varied according to CKD stage with poor continuity and coordination of care and patient and carer empowerment emphasized by participants with CKD stage 4 and 5, and access and poor recognition of psychological co-morbidity emphasised by participants with CKD stage 5 and carers.ConclusionsAccording to patients and their carers the health-care of co-morbid diabetes and CKD may be improved via a preventive, patient-centred health-care model which promotes self-management and that has good access, continuity and coordination of care and identifies and manages psychological morbidity.

Generation of distinct cortical projection neuron subtypes during development relies in part on repression of alternative neuron identities. It was reported that the special AT-rich sequencebinding protein 2 (Satb2) is required for proper development of callosal neuron identity and represses expression of genes that are essential for subcerebral axon development. Surprisingly, Satb2 has recently been shown to be necessary for subcerebral axon development. Here, we unravel a previously unidentified mechanism underlying this paradox. We show that SATB2 directly activates transcription of forebrain embryonic zinc finger 2 (Fezf2) and SRY-box 5 (Sox5), genes essential for subcerebral neuron development. We find that the mutual regulation between Satb2 and Fezf2 enables Satb2 to promote subcerebral neuron identity in layer 5 neurons, and to repress subcerebral characters in callosal neurons. Thus, Satb2 promotes the development of callosal and subcerebral neurons in a cell context-dependent manner.Satb2 | Fezf2 | subcerebral neurons | cerebral cortex | cell fate P rojection neurons in the six-layered neocortex can be classified based on axonal projections. The corticocortical neurons send axons to other areas in the ipsilateral cortex or through the corpus callosum and into the contralateral cortex (i.e., callosal projection neurons). The callosal neurons are distributed throughout layers 2-6, but are most abundant in layers 2 and 3. The corticofugal neurons consist of corticothalamic and subcerebral neurons. The corticothalamic neurons are most abundant in layer 6, and send axons into the thalamus. The subcerebral neurons are located in layer 5, and project axons into the spinal cord, superior colliculus, pons, and other brain areas (1-4).

Objective: To estimate the frequency of chronic kidney disease (CKD) in a clinic‐based sample of patients with type 2 diabetes in the setting of Australian primary care. Design, setting and participants: Expressions of interest were invited from all registered general practitioners in Australia: 500 GP investigators were randomly selected from each stratum (state and urban versus rural location), proportional to the census population, and asked to recruit and provide data for 10–15 consecutively presenting adults with type 2 diabetes between April and September 2005. Main outcome measures: Estimated glomerular filtration rate (eGFR) less than 60 mL/min/1.73 m2 and evidence of kidney damage on urinalysis (eg, microalbuminuria). Results: 348 GP investigators submitted data for 3893 individuals with type 2 diabetes (52% men; median age, 66 years). Almost one in every four patients consulting their GPs had an eGFR < 60 mL/min/1.73 m2 (23.1%; 95% CI, 21.8%–24.5%). More than one in three had an elevated urinary albumin–creatinine ratio (ACR) (34.6%; 95% CI, 33.3%–35.9%). There was an overlap of 10.4% of patients with both an eGFR < 60 mL/min/1.73 m2 and an elevated urinary ACR, meaning that almost one in two patients with type 2 diabetes consulting their GPs (47.1%; 95% CI, 45.8%–48.4%) had CKD. CKD was significantly more common in women, in older people, and in individuals with established macrovascular disease. Conclusion: CKD is a common complication of type 2 diabetes, found in about half of all patients with type 2 diabetes consulting their GPs. Efforts to increase the recognition of CKD will lead to improved care, and possibly survival, of patients with type 2 diabetes.