Abstract
Purpose To research the distribution and quantitative changes of UT-A1, UT-B1, and AQP5 in uremic skin tissue. Methods 34 cases of uremic patients (UP) and 11 controls were recruited. Immunohistochemistry, immunofluorescence, RT-PCR, and Western Blot were used to identify the proteins in sweat glands. Results AQP5, UT-A1, and UT-B1 were expressed and localized in human skin basal lines, skin sweat glands, and sweat ducts, both in UP and controls. Compared to controls, AQP5 mRNA abundance was significantly decreased in UP (P < 0.01), and, with the decrease of eGFR, the AQP5 expression was significantly decreased (P < 0.05). By contrast, UT-A1 and UT-B1 mRNA abundance was significantly increased in the skin of UP compared with the control (P < 0.01), and, with the decrease of eGFR, the AQP5 expression was significantly increased (P < 0.05). We found that the gene changes were coincident with the corresponding target proteins. The urea transporter subtypes, UT-A1 and UT-B1, were expressed in the skin basal cell layer and exocrine sweat glands. The abundance of UT-A1 and UT-B1 in uremic sweat glands was significantly increased in UP, while the expression of AQP5 was decreased. Conclusion Elimination of urea through the skin by producing sweat is a potential therapeutic strategy for renal failure patients.
Highlights
With the decline of kidney function, the water and metabolic wastes were accumulated in the uremic patients, which results in the injury of multiply organs
By Western Blot, we found that the gene change is coincident with the corresponding target protein (Figure 7). All these findings indicate that the uremic environment results in an altered levels of AQP5, Urea transporters (UTs)-A1, and UT-B1 protein
The structure of human sweat glands has some similarity with the convoluted tubules of the kidney and the composition of sweat is very similar with urine, containing potassium, sodium, urea nitrogen, creatinine, uric acid, and other metabolic waste [1, 2]
Summary
With the decline of kidney function, the water and metabolic wastes were accumulated in the uremic patients, which results in the injury of multiply organs. Human sweat glands have some similarity with the convoluted tubules of the kidney. A series of observations found that the composition of sweat and urine are very similar [1, 2]. Urea concentration in the sweat was much higher than the serum, which indicated that sweat is another way of expelling water and metabolic wastes besides urine. It was found that urea concentration was much higher in the sweat of chronic kidney disease (CKD) patients than that in normal people [3, 4], indicating that the sweat glands play an important role in the water and metabolic wastes excretion in CKD patients. Aquaporin-5 (AQP5), a highly conserved membrane protein, involved in the bidirectional transfer of water and small solutes across cell membranes, plays an important role in water transport throughout the several body systems
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