Ling Wang1, Jian Wu2, Jia-Fen Cheng3, Xin-Ying Liu4, Fang Ma5, Le-Hang Guo6, Jun-Mei Xu7, Tianfu Wu8, Chandra Mohan9, Ai Peng10, Hui-Xiong Xu11, Ya-Xiang Song12. 1. Department of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. nowax@126.com. 2. Department of Ultrasound in Medicine, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. apagar@126.com. 3. Department of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. 034379@tongji.edu.cn. 4. Department of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. singing_l@163.com. 5. Department of Ultrasound, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai, China. mafang59@126.com. 6. Department of Ultrasound in Medicine, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. gopp1314@hotmail.com. 7. Department of Ultrasound in Medicine, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. Junmei_510@hotmail.com. 8. Department of Biomedical Engineering, University of Houston, 3605 Cullen Blvd, Houston, TX, 77204, USA. tianfu.wu@gmail.com. 9. Department of Biomedical Engineering, University of Houston, 3605 Cullen Blvd, Houston, TX, 77204, USA. cmohan@central.uh.edu. 10. Department of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. pengai@tongji.edu.cn. 11. Department of Ultrasound in Medicine, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. xuhuixiong@hotmail.com. 12. Department of Nephrology and Rheumatology, Shanghai Tenth People's Hospital, Tongji University, No. 301 Yanchangzhong Road, District of Zhabei, Shanghai, 200072, China. yaxiangs@126.com.
Abstract
PURPOSE: To investigate the diagnostic value of quantitative contrast-enhanced ultrasound (CEUS) for early detection of renal hyperperfusion in diabetic kidney disease (DKD). MATERIALS AND METHODS: 55 DKD patients with estimated glomerular filtration rate (eGFR) >30 ml/min/1.73 m(2) and 26 normal controls (NCs) were enrolled. Clinical data was well documented. Blood samples were drawn for evaluation of renal function including blood urea nitrogen (BUN), serum creatinine (SCr) and serum uric acid (SUA), and urine samples were assayed for total protein quantification, and various microprotein markers. According to eGFR level, DKD patients were divided into early-stage DKD (eGFR ≥90 ml/min/1.73 m(2), n = 18) and middle-stage DKD (eGFR 30-90 ml/min/1.73 m(2), n = 37). Based on urinary microalbumin/creatinine ratio (MALB/UCR), early-stage DKD patients were further classified into two groups: MALB/UCR <10 g/mol (n = 11) and MALB/UCR ≥10 g/mol (n = 7). Then, CEUS was performed to observe the real-time renal perfusion, and low acoustic power contrast-specific imaging was used for quantitative analysis. RESULTS: The renal perfusion images of CEUS were well developed successively. The corresponding perfusion curves based on echo-power signals in time series were constructed. Quantitative analysis showed that area under the descending curve (AUC2) was significantly increased in early-stage DKD compared to middle-stage DKD (p < 0.05), but AUC showed no significant difference. Further comparison between different MALB/UCR levels of early-stage DKD showed that patients with MALB/UCR ≥10 g/mol had significantly increased levels of AUC, AUC2 and proteinuria than patients with low MALB/UCR (p < 0.05). Also, high MALB/UCR DKD patients had increased proteinuria but similar eGFR compared to low MALB/UCR patients. CONCLUSION: Renal microvascular hyperperfusion may be responsible for overt proteinuria until decline of renal filtration in DKD. AUC2 could be an early and sensitive marker for early renal injury and renal microvascular hyperperfusion in DKD.
PURPOSE: To investigate the diagnostic value of quantitative contrast-enhanced ultrasound (CEUS) for early detection of renal hyperperfusion in diabetic kidney disease (DKD). MATERIALS AND METHODS: 55 DKD patients with estimated glomerular filtration rate (eGFR) >30 ml/min/1.73 m(2) and 26 normal controls (NCs) were enrolled. Clinical data was well documented. Blood samples were drawn for evaluation of renal function including blood ureanitrogen (BUN), serum creatinine (SCr) and serum uric acid (SUA), and urine samples were assayed for total protein quantification, and various microprotein markers. According to eGFR level, DKD patients were divided into early-stage DKD (eGFR ≥90 ml/min/1.73 m(2), n = 18) and middle-stage DKD (eGFR 30-90 ml/min/1.73 m(2), n = 37). Based on urinary microalbumin/creatinine ratio (MALB/UCR), early-stage DKD patients were further classified into two groups: MALB/UCR <10 g/mol (n = 11) and MALB/UCR ≥10 g/mol (n = 7). Then, CEUS was performed to observe the real-time renal perfusion, and low acoustic power contrast-specific imaging was used for quantitative analysis. RESULTS: The renal perfusion images of CEUS were well developed successively. The corresponding perfusion curves based on echo-power signals in time series were constructed. Quantitative analysis showed that area under the descending curve (AUC2) was significantly increased in early-stage DKD compared to middle-stage DKD (p < 0.05), but AUC showed no significant difference. Further comparison between different MALB/UCR levels of early-stage DKD showed that patients with MALB/UCR ≥10 g/mol had significantly increased levels of AUC, AUC2 and proteinuria than patients with low MALB/UCR (p < 0.05). Also, high MALB/UCR DKD patients had increased proteinuria but similar eGFR compared to low MALB/UCR patients. CONCLUSION: Renal microvascular hyperperfusion may be responsible for overt proteinuria until decline of renal filtration in DKD. AUC2 could be an early and sensitive marker for early renal injury and renal microvascular hyperperfusion in DKD.
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