Jianjiang Zhang1, Huiqin Zeng2, Na Wang3, Xiyan Tian4, Wenjie Dou5, Peipei Shi6. 1. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. zhangjianjiang10@163.com. 2. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. huihaodezhq34@163.com. 3. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. wang126na@163.com. 4. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. tianxiyan2007@163.com. 5. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. douwenjie89@163.com. 6. Department of Pediatrics, The First Affiliated Hospital/Zhengzhou University, Zhengzhou, 450052, China. shipeipei1108@163.com.
Abstract
Henoch-Schönlein purpura (HSP) is a small-vessel disease in children that is often accompanied by kidney damage. Despite many efforts to improve the early assessment of renal injury in HSP patients, effective markers are still lacking. In recent years, the relationship between kidney injury molecule-1 (KIM-1) and tubulointerstitial injury has drawn much attention, especially regarding the diagnostic potential of serum and urinary KIM-1 levels. However, the diagnostic value of KIM-1 for detecting urinary kidney injury in HSP patients is still elusive. Furthermore, the treatment of Henoch-Schönlein purpura nephritis (HSPN) relies on the clinician's experience without performing renal biopsy, so it is important to find an effective biomarker and therapy. In the present study, we investigated the diagnostic value of urinary KIM-1 for early renal injury in HSP patients enrolled in a prospective, single-center study. Urinary KIM-1 levels were measured in 27 patients with HSP, 32 patients with HSPN (21 HSPN patients had undergone renal biopsy), and 16 healthy donors, as normal controls. The HSPN patients were randomly divided to receive either routine therapy (n = 13) or routine treatment combined with creatine phosphate sodium (CP) (n = 19). Urinary KIM-1 levels were significantly greater in the HSP and HSPN groups than those in the healthy control group (P < 0.01), and were significantly greater in the HSPN group than in the HSP group (P < 0.01). The urinary KIM-1 levels decreased significantly after 10-14 days of treatment with CP compared with conventional therapy (P < 0.05). CONCLUSION: Our results demonstrate the diagnostic value of KIM-1 and the therapeutic potential of CP for early renal damage in HSP patients. WHAT IS KNOWN: Urine kidney injury molecule-1 (KIM-1) is a sensitive biomarker for tubulointerstitial injury. Henoch-Schonlein purpura (HSP) usually presents with renal damage. WHAT IS NEW: Our results suggest that the urinary KIM-1 level is a sensitive and specific biomarker for the detection of early renal damage in HSP and may predict the severity of HSP and HSPN. The administration of creatine phosphate sodium (CP) may reduce urinary KIM-1 levels and thus correct the hypoxic condition of the kidney. Preconditioning with CP may also be a useful adjunct for preventing early renal damage in HSPN patients.
Henoch-Schönlein purpura (HSP) is a small-vessel disease in children that is often accompanied by kidney damage. Despite many efforts to improve the early assessment of renal injury in HSP patients, effective markers are still lacking. In recent years, the relationship between kidney injury molecule-1 (KIM-1) and tubulointerstitial injury has drawn much attention, especially regarding the diagnostic potential of serum and urinary KIM-1 levels. However, the diagnostic value of KIM-1 for detecting urinary kidney injury in HSP patients is still elusive. Furthermore, the treatment of Henoch-Schönlein purpura nephritis (HSPN) relies on the clinician's experience without performing renal biopsy, so it is important to find an effective biomarker and therapy. In the present study, we investigated the diagnostic value of urinary KIM-1 for early renal injury in HSP patients enrolled in a prospective, single-center study. Urinary KIM-1 levels were measured in 27 patients with HSP, 32 patients with HSPN (21 HSPN patients had undergone renal biopsy), and 16 healthy donors, as normal controls. The HSPN patients were randomly divided to receive either routine therapy (n = 13) or routine treatment combined with creatine phosphate sodium (CP) (n = 19). Urinary KIM-1 levels were significantly greater in the HSP and HSPN groups than those in the healthy control group (P < 0.01), and were significantly greater in the HSPN group than in the HSP group (P < 0.01). The urinary KIM-1 levels decreased significantly after 10-14 days of treatment with CP compared with conventional therapy (P < 0.05). CONCLUSION: Our results demonstrate the diagnostic value of KIM-1 and the therapeutic potential of CP for early renal damage in HSP patients. WHAT IS KNOWN: Urine kidney injury molecule-1 (KIM-1) is a sensitive biomarker for tubulointerstitial injury. Henoch-Schonlein purpura (HSP) usually presents with renal damage. WHAT IS NEW: Our results suggest that the urinary KIM-1 level is a sensitive and specific biomarker for the detection of early renal damage in HSP and may predict the severity of HSP and HSPN. The administration of creatine phosphate sodium (CP) may reduce urinary KIM-1 levels and thus correct the hypoxic condition of the kidney. Preconditioning with CP may also be a useful adjunct for preventing early renal damage in HSPN patients.
Authors: Hui Li; Ramon F Thali; Christy Smolak; Fan Gong; Rodrigo Alzamora; Theo Wallimann; Roland Scholz; Núria M Pastor-Soler; Dietbert Neumann; Kenneth R Hallows Journal: Am J Physiol Renal Physiol Date: 2010-05-12
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