中国医师杂志
中國醫師雜誌
중국의사잡지
JOURNAL OF CHINESE PHYSICIAN
2011年
8期
1009-1013
,共5页
邱剑辉%谭红%何小解%党西强%易著文
邱劍輝%譚紅%何小解%黨西彊%易著文
구검휘%담홍%하소해%당서강%역저문
肾病综合征/病理学/代谢%毛细血管%受体,钙敏感/代谢%药物耐受性%糖皮质激素类
腎病綜閤徵/病理學/代謝%毛細血管%受體,鈣敏感/代謝%藥物耐受性%糖皮質激素類
신병종합정/병이학/대사%모세혈관%수체,개민감/대사%약물내수성%당피질격소류
Nephrotic syndrome/PA/ME%Capillaries%Receptors,calcium-sensing/ME%Drug tolerance%Glucocorticoids
目的 探讨糖皮质激素(GC)耐药原发性肾病综合征(PNS)患儿肾小管上皮细胞钙敏感受体(CaSR)表达与肾小管间质损害、钙磷代谢紊乱、肾小管间质周围微血管密度之间的关系。方法将入选的36例PNS患儿按是否糖皮质激素耐药分两组，激素敏感组(16例)，激素耐药组(20例)，采用半定量评分法对肾小管间质病理损害程度进行评价，利用全自动生化仪测定血清钙(Ca)、磷(P)浓度，免疫组化法检测肾小管上皮CaSR表达与肾小管间质周围微血管密度。结果激素耐药组患儿血清P水平[(2.26±0.15) mmol/L]高于激素敏感组[(1.90±0.12) mmol/L，P＜0.05];激素敏感组患儿肾小管上皮细胞CaSR表达(4.63±0.78)低于激素耐药组(6.56±1.22，P＜0.05)，微血管密度高于激素耐药组(2.98±0.35 vs 2.02±0.24，P＜0.05);肾小管间质轻度损害时，激素敏感组肾小管上皮细胞CaSR表达(4.15±0.58)低于耐药组(4.26±0.61)，但差异无统计学意义(P＞0.05)，微血管密度则高于耐药组(3.12±0.33,3.01±0.21)，但差异无统计学意义(P＞0.05);肾小管间质中度损害时，激素敏感组(5.35±0.64)肾小管上皮细胞CaSR表达低于耐药组(7.37±0.81，P＜0.01)，微血管密度则明显高于耐药组(2.81±0.16,2.02±0.14，P＜0.05);与轻、中度肾小管间质损害的激素耐药患儿相比，重度肾小管间质损害的激素耐药患儿肾小管上皮细胞CaSR表达(11.46±1.38)显著增高，微血管密度(1.15±0.11)显著降低(均P＜0.01)。结论糖皮质激素耐药型PNS患儿肾小管上皮细胞CaSR表达增高与肾小管周围微血管密度下降，可能是由于GC的细胞毒作用损害肾小管上皮细胞后，继发钙磷代谢异常与血管内皮损害所致。
目的 探討糖皮質激素(GC)耐藥原髮性腎病綜閤徵(PNS)患兒腎小管上皮細胞鈣敏感受體(CaSR)錶達與腎小管間質損害、鈣燐代謝紊亂、腎小管間質週圍微血管密度之間的關繫。方法將入選的36例PNS患兒按是否糖皮質激素耐藥分兩組，激素敏感組(16例)，激素耐藥組(20例)，採用半定量評分法對腎小管間質病理損害程度進行評價，利用全自動生化儀測定血清鈣(Ca)、燐(P)濃度，免疫組化法檢測腎小管上皮CaSR錶達與腎小管間質週圍微血管密度。結果激素耐藥組患兒血清P水平[(2.26±0.15) mmol/L]高于激素敏感組[(1.90±0.12) mmol/L，P＜0.05];激素敏感組患兒腎小管上皮細胞CaSR錶達(4.63±0.78)低于激素耐藥組(6.56±1.22，P＜0.05)，微血管密度高于激素耐藥組(2.98±0.35 vs 2.02±0.24，P＜0.05);腎小管間質輕度損害時，激素敏感組腎小管上皮細胞CaSR錶達(4.15±0.58)低于耐藥組(4.26±0.61)，但差異無統計學意義(P＞0.05)，微血管密度則高于耐藥組(3.12±0.33,3.01±0.21)，但差異無統計學意義(P＞0.05);腎小管間質中度損害時，激素敏感組(5.35±0.64)腎小管上皮細胞CaSR錶達低于耐藥組(7.37±0.81，P＜0.01)，微血管密度則明顯高于耐藥組(2.81±0.16,2.02±0.14，P＜0.05);與輕、中度腎小管間質損害的激素耐藥患兒相比，重度腎小管間質損害的激素耐藥患兒腎小管上皮細胞CaSR錶達(11.46±1.38)顯著增高，微血管密度(1.15±0.11)顯著降低(均P＜0.01)。結論糖皮質激素耐藥型PNS患兒腎小管上皮細胞CaSR錶達增高與腎小管週圍微血管密度下降，可能是由于GC的細胞毒作用損害腎小管上皮細胞後，繼髮鈣燐代謝異常與血管內皮損害所緻。
목적 탐토당피질격소(GC)내약원발성신병종합정(PNS)환인신소관상피세포개민감수체(CaSR)표체여신소관간질손해、개린대사문란、신소관간질주위미혈관밀도지간적관계。방법장입선적36례PNS환인안시부당피질격소내약분량조，격소민감조(16례)，격소내약조(20례)，채용반정량평분법대신소관간질병리손해정도진행평개，이용전자동생화의측정혈청개(Ca)、린(P)농도，면역조화법검측신소관상피CaSR표체여신소관간질주위미혈관밀도。결과격소내약조환인혈청P수평[(2.26±0.15) mmol/L]고우격소민감조[(1.90±0.12) mmol/L，P＜0.05];격소민감조환인신소관상피세포CaSR표체(4.63±0.78)저우격소내약조(6.56±1.22，P＜0.05)，미혈관밀도고우격소내약조(2.98±0.35 vs 2.02±0.24，P＜0.05);신소관간질경도손해시，격소민감조신소관상피세포CaSR표체(4.15±0.58)저우내약조(4.26±0.61)，단차이무통계학의의(P＞0.05)，미혈관밀도칙고우내약조(3.12±0.33,3.01±0.21)，단차이무통계학의의(P＞0.05);신소관간질중도손해시，격소민감조(5.35±0.64)신소관상피세포CaSR표체저우내약조(7.37±0.81，P＜0.01)，미혈관밀도칙명현고우내약조(2.81±0.16,2.02±0.14，P＜0.05);여경、중도신소관간질손해적격소내약환인상비，중도신소관간질손해적격소내약환인신소관상피세포CaSR표체(11.46±1.38)현저증고，미혈관밀도(1.15±0.11)현저강저(균P＜0.01)。결론당피질격소내약형PNS환인신소관상피세포CaSR표체증고여신소관주위미혈관밀도하강，가능시유우GC적세포독작용손해신소관상피세포후，계발개린대사이상여혈관내피손해소치。
Objective Study the relationship among CaSR expression, tubulointerstitial damage,metabolic disturbance of calcium and phosphorus and microvascular density around the tubulointerstitium in children with steroid-resistant nephrotic syndrome.Methods 36 cases of children with primary nephrotic syndrome were divided into hormone-sensitive group and steroid-resistant group.Semi-quantitative scores for tubulointerstitial pathological evaluation of the extent of damage, automatic biochemical analyzer for the determination of serum calcium (Ca), phosphorus (P) concentration of renal tubular epithelial CaSR expression and microvessel microvascular density around the tubulointerstitium were determined by immunohistochemical assay.Results More severe the tubulointerstitial damage, lower level of serum Ca and higher level of serum P were observed [(2.26 ± 0.15) mmol/L]in children of the steroid-resistant group and the steroid-sensitive group [(1.90 + 0.12) mmol/L, P ＜ 0.05].CaSR expression (4.63 + 0.78) of renal tubular epithelial cells in the steroid- sensitive group was significantly lower than that in the steroid-resistant group (6.56 + 1.22, P ＜ 0.05), but microvascular density was significantly higher in the steroid- sensitive group(2.98 +0.35 vs 2.02 +0.24, P ＜0.05).When the tubulointerstitial damage was mild, CaSR expression (4.15 +0.58) in renal tubular epithelial cells in the steroid- sensitive group (4.26 ±0.61) was lower than the steroid-resistant group(3.12 ± 0.33; 3.01 ± 0.21), and microvascular density was higher,but the difference was not significant(P ＞0.05).In the moderate tubulointerstitial damage, CaSR expression in renal tubular epithelial cells in the steroid- sensitive group (5.35 ± 0.64) was significantly lower than the resistant group (7.37 +0.81, P ＜0.01), and microvascular density was significantly higher than the resistant group (2.81 ±0.16, 2.02 ±0.14, P ＜0.05).Compared by mild and moderate tubulointerstitial damage in children with the steroid-resistant, CaSR expression (11.46 ± 1.38) in children with severe tubulointerstitial damage was significantly increased, and microvascular density (1.15 ± 0.11) was significantly decreased (all P ＜ 0.01).Conclusions CaSR expression was increased and microvascular density around the tubulointerstitium was decreased in children with steroid-resistant nephrotic syndrome.Dut to steroid resistance, the cytotoxic of steroid damaged the renal tubular epithelial cells, the metabolic disturbance of calcium and phosphorus and the damage of blood vessel endothelium finally resulted in severe tubulointerstitial damage.
