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Objective To explore the association of urinary level of kidney injury molecule-1 (KIM-1) with renal tubulointerstitial lesions in patients with lupus nephritis (LN). And to find a potential clinical biomarker, which could reflect the specific tubulointerstitial lesions of LN. Methods Sixty cases of biopsy proven new-onset LN patients were enrolled into the study. And 10 normal kidney tissues were collected, which came from 10 patients with kidney trauma or renal tumor nephrectomy. Sixty patients with LN were divided into mild disease group, moderate disease group, severe disease group and the extremely severe disease group according to the criteria of 2000 Hill's morphologic index for the evaluation of renal pathology. Urine and renal tissues specimen were collected. The clinical and pathological data were analyzed retrospectively. Urine level of KIM-1 was detected by enzyme linked immunosorbent assay (-). Immunohistochemical staining was used to observe the expression of KIM-1 in the renal tissue. T-test, One-Way analysis of variance(ANOVA) test or rank sum test and Pearson or Spearman correlation analysis were used for statistical analysis. Results ①With the aggravation of tubulointerstitial lesions, the urinary level of KIM-1 was increased gradually, which was shown in the control group [(0.32 ±0.03) ng/ml], mild group [(2.31 ±0.30) ng/ml], moderate group [(6.12 ±0.51) ng/ml], severe group [(12.51 ±1.83) ng/ml] and the extremely severe group [(15.30 ±2.11) ng/ml] (all P0.05). The expression of KIM-1 in the renal tissue was positively correlated with serum creatinine (SCr), quantity of 24 h UP, SLEDAI, R-SLEDAI, GAI, TLAI and AI (r=0.780, 0.780, 0.812, 0.727, 0.735, 0.910, 0.701, P0.05). Conclusion Urinary KIM-1 enables to assess the tubulointerstitial lesion in LN patients, and it can be a sensitive biomarker to predict the tubulointerstitial damage and to evaluate the degree of tubulointerstitial lesions.
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Objective To investigate the relationship between interleukin (IL)-18 and podocyte injury of lupus nephritis (LN). Methods Sixty cases of biopsy proven LN patients were enrolled into the study. Thirty cases were selected as controls. The clinical and pathological data, blood and urine samples and renal tissues were collected. The Nephrin expression was detected by immunohistochemical method and IL-18 was measured by enzyme linked immunosorbent assay. The relationship between IL-18 and the Nephrin expression, clinical and pathological indicators of LN were analyzed. Results Thirty-eight cases were in active disease and 22 cases were in inactive disease in LN group according to SLE disease activity index (SLEDAI) 2000. One-way ANOVA showed that the level of plasma and urine IL-18 in the LN groups were higher than those in the control group [(200±38) ng/ml, (18±5) ng/ml] (F=110.84, 203.09, P0.05), and was negatively correlated with estimated glomerular filtration rate (eGFR) (r=-0.562, P<0.05). It was positively correlated with serum creatinin, blood urea nitrogen, AI, TLAI and inflammatory cell infiltration (r=0.529, 0.482, 0.665, 0.690, 0.671, P<0.05). Conclusion IL-18 has a very close relationship with podocyte injury in patients with LN, and the uIL-18 can be a potential non-invasive detection method to monitor podocyte injury in LN patients.
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BACKGROUND:Transient receptor potential channel C6 (TRPC6) is a new and important slit diaphragm-associated protein in podocytes involved in regulating glomerular filter function. Glomerular TRPC6 expression is closely associated with proteinuria in diabetic kidney disease. OBJECTIVE: To investigate the expression of canonical TRPC6 in mouse podocytes induced by high glucose, and to explore the possible mechanism of diabetic kidney disease. METHODS:Mouse podocyte cels were cultured and divided into normal glucose group (5.6 mmol/L D-glucose), normal control group (5.6 mmol/L D-glucose+25 mmol/L mannitol) and experimental groups which were in the environment of high glucose (30 mmol/L). The experimental groups included high glucose group, valsartan treatment groups (10-5 mol/L) and U73122 control group (10μmol/L U73122). After 48 hours, the expressions of mRNA and proteins of TRPC6, nephrin and angiotensin II (AngII) were detected respectively by real-time quantitative PCR and western blot analysis. RESULTS AND CONCLUSION:Compared with the normal control group, the expressions of mRNA and proteins of TRPC6 and angiotensin II were markedly elevated in the high glucose group (P 0.05). Angiotensin II-TRPC6 signaling pathway may mediate high glucose-induced podocyte injury, meanwhile it provides a new theoretical basis for the treatment of diabetic kidney disease, by which the angiotensin receptor blockers can protect podocytes in diabetic kidney disease.
