Burden of Chronic Hemodialysis on the Ability to Work: Time for Action.

Background Understanding the factors that contribute to unemployment will help in the design of creative resolutions to enable hemodialysis patients to return to a productive life. Methods We examined employment among 625 patients aged 18 to 60 years who were on hemodialysis in 8 dialysis units. Results Overall employment was low among patients on chronic hemodialysis at 49.7%. Unemployment was significantly higher in women than in men (86.6% vs 17.1%, p < 0.0001). The employment rate was 70.5% for those with no diabetes and hypertension, 29.5% for those with diabetes, and 25.9% for those with diabetes and hypertension. Furthermore, the results of the Cox regression showed that the variables of gender, level of education, capability of driving, and diabetes were related to employment of patients. Conclusions The majority of patients on hemodialysis are unemployed or exit paid employment due to early retirement. Patients with diabetes and women are a vulnerable population with a higher unemployment rate.

Requirement of clusterin expression for prosurvival autophagy in hypoxic kidney tubular epithelial cells.

Cellular autophagy is a prosurvival mechanism in the kidney against ischemia-reperfusion injury (IRI), but the molecular pathways that activate the autophagy in ischemic kidneys are not fully understood. Clusterin (CLU) is a chaperone-like protein, and its expression is associated with kidney resistance to IRI. The present study investigated the role of CLU in prosurvival autophagy in the kidney. Renal IRI was induced in mice by clamping renal pedicles at 32°C for 45 min. Hypoxia in renal tubular epithelial cell (TEC) cultures was induced by exposure to a 1% O2 atmosphere. Autophagy was determined by either light chain 3-BII expression with Western blot analysis or light chain 3-green fluorescent protein aggregation with confocal microscopy. Cell apoptosis was determined by flow cytometric analysis. The unfolded protein response was determined by PCR array. Here, we showed that autophagy was significantly activated by IRI in wild-type (WT) but not CLU-deficient kidneys. Similarly, autophagy was activated by hypoxia in human proximal TECs (HKC-8) and WT mouse primary TECs but was impaired in CLU-null TECs. Hypoxia-activated autophagy was CLU dependent and positively correlated with cell survival, and inhibition of autophagy significantly promoted cell death in both HKC-8 and mouse WT/CLU-expressing TECs but not in CLU-null TECs. Further experiments showed that CLU-dependent prosurvival autophagy was associated with activation of the unfolded protein response in hypoxic kidney cells. In conclusion, these data suggest that activation of prosurvival autophagy by hypoxia in kidney cells requires CLU expression and may be a key cytoprotective mechanism of CLU in the protection of the kidney from hypoxia/ischemia-mediated injury.