| First Author | Zhou L | Year | 2012 |
| Journal | BMC Nephrol | Volume | 13 |
| Pages | 6 | PubMed ID | 22289137 |
| Mgi Jnum | J:222350 | Mgi Id | MGI:5644391 |
| Doi | 10.1186/1471-2369-13-6 | Citation | Zhou L, et al. (2012) UT-B-deficient mice develop renal dysfunction and structural damage. BMC Nephrol 13:6 |
| abstractText | BACKGROUND: Urea transporter UT-B is the major urea transporter in erythrocytes and the descending vasa recta in the kidney. In this study, we investigated the effects of long-term UT-B deficiency on functional and structural defect in the kidney of 16-and 52-week-old UT-B-null mice. METHODS: UT-B-knockout mice were generated by targeted gene disruption and lacked UT-B protein expression in all organs. The urinary concentrating ability of mice was studied in terms of daily urine output, urine osmolality, and urine and plasma chemistries. Changes in renal morphology were evaluated by hematoxylin and eosin staining. RESULTS: The UT-B-null mice showed defective urine concentrating ability. The daily urine output in UT-B-null mice (2.5 +/- 0.1 ml) was 60% higher and urine osmolality (985 +/- 151 mosm) was significantly lower than that in wild-type mice (1463 +/- 227 mosm). The 52-week-old UT-B-null mice exhibited polyuria after water deprivation, although urine osmolality was increased. At 52 weeks of age, over 31% of UT-B-null mice exhibited renal medullary atrophy because of severe polyuria and hydronephrosis. CONCLUSIONS: Long-term UT-B deficiency causes severe renal dysfunction and structural damage. These results demonstrate the important role of UT-B in countercurrent exchange and urine concentration. |
