Background Sudden cardiovascular death is increased in chronic kidney disease (CKD). Experimental CKD models suggest that angiogenesis and nitric oxide (NO) inhibitors induce myocardial fibrosis and microvascular dropout thereby facilitating arrhythmogenesis. We undertook this study to characterize associations of CKD with human myocardial pathology, NO-related circulating angiogenesis inhibitors, and endothelial cell behavior. Methods We compared heart (n=54) and serum (n=162) samples from individuals with and without CKD, and assessed effects of serum on human coronary artery endothelial cells (HCAEC) in vitro. Left ventricular fibrosis and capillary density were quantified in post-mortem samples. Endothelial to mesenchymal transition (EndMT) was assessed by immunostaining of post-mortem samples and RNA expression in heart tissue obtained during cardiac surgery. Circulating asymmetric dimethylarginine (ADMA), endostatin (END), angiopoietin-2 (ANG), and thrombospondin-2 (TSP) were measured, and the effect of these factors and of subject serum on proliferation, apoptosis, and EndMT of HCAEC were analyzed. Results Cardiac fibrosis increased 12% and 77% in stage 3-4 CKD and ESRD and microvascular density decreased 12% and 16% vs. preserved renal function. EndMT-derived fibroblast proportion was 17% higher in stage 3-4 CKD and ESRD (Ptrend=0.02). ADMA, ANG, TSP, and END concentrations increased in CKD. Both individual factors and CKD serum increased HCAEC apoptosis (P=0.02), decreased proliferation (P=0.03), and induced EndMT. Conclusions CKD is associated with an increase in circulating angiogenesis and NO inhibitors, which impact proliferation and apoptosis of cardiac endothelial cells and promote EndMT, leading to cardiac fibrosis and capillary rarefaction. These processes may play key roles in CKD-associated CV disease.

Objectives To determine the relationship between long-term prostate cancer survivors’ symptom burden and information needs. Subjects/patients and methods We used population-based data from the Michigan Prostate Cancer Survivor Study (n=2,499). We examined unadjusted differences in long-term information needs according to symptom burden and performed multivariable logistic regression to examine symptom burden and information needs adjusting for patient characteristics. Results High symptom burden was reported across all domains (sexual 44.4%, urinary 14.4%, vitality 12.7%, bowel 8.4%, emotional 7.6%) with over half of respondents (56%) reporting they needed more information. Top information needs involved recurrence, relationships, and long-term effects. Prostate cancer survivors with high symptom burden more often searched for information regardless of domain (p<0.05). High sexual burden was associated with greater need for information about relationships (OR=2.05; 95% CI 1.54–2.72) and long-term effects (OR=1.60; 95% CI 1.23–2.07). High bowel burden was associated with greater information need for long-term effects (OR=2.28; 95% CI 1.43–3.63). Conclusions Long-term prostate cancer survivors with high symptom burden need more supportive information. Tailoring information to these needs may be an efficient approach to support the growing population of long-term prostate cancer survivors.

Readmission intensity differs widely after discharge following radical cystectomy. As postoperative efforts to minimize the readmission burden increase, a better understanding of the factors that contribute to the highest intensity readmissions will help direct limited resources (eg telephone calls, office visits) toward high yield areas.

Our model improves the detection of concerning symptoms after radical cystectomy by optimizing the timing and number of outpatient encounters. By understanding how to design better outpatient followup care for patients treated with radical cystectomy we can help reduce the readmission burden for this population.

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