【摘要翻译】枸橼酸钙改善慢性肾损伤的进展
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枸橼酸钙改善慢性肾损伤的进展
背景：慢性肾衰竭的结果之一就是代谢性酸中毒，它可引起骨质去矿化、肌蛋白水解，促进慢性肾衰竭进展。本研究旨在利用肾大部分切除实验模型评价枸橼酸钙纠正代谢性酸中毒的效果。
方法：将Wistar大鼠进行5/6肾大部分切除术，然后随机分成非治疗组（NFX）、枸橼酸钙治疗组(NFX-CIT)、卡托普利治疗组(NFX-CAP)与枸橼酸钙和卡托普利联合治疗组(NFX-CAP-CIT)。每100g饲料含枸橼酸钙1.45g，每1升水含卡托普利500mg。于第1、10和20周时，测定体重、收缩压、蛋白尿、动脉血碳酸氢盐浓度、尿枸橼酸排泄、血浆钙水平和菊粉清除率，并计算肾小球和肾小管间质损害得分。在第1周和第10周采用免疫组织化学方法观察肾小球和肾小管增生的细胞核抗原(PCNA)阳性细胞、 平滑肌动蛋白和肌纤维蛋白染色。
结果：与非治疗组相比，第1周，治疗组肾小球和小管间质细胞增殖明显减轻(P< 0.05)，第10周，肾小球细胞转分化显著减低，血浆碳酸氢盐浓度显著升高(P< 0.05)，第20周，肾小球和小管间质组织学损害得分减少(P< 0.05)。治疗组菊粉清除率明显高于非治疗组(P< 0.05)，尿蛋白排泄明显低于非治疗组(P< 0.05)，而NFX-CIT组动脉血压没有显著不同。
结论：枸橼酸钙减慢5/6肾切除模型慢性肾损伤的进程，改善代谢行酸中毒，减少细胞增殖和转分化，不影响收缩压。
Kidney International.2004;65(4):1224.
CELL BIOLOGY - IMMUNOLOGY - PATHOLOGY
Calcium citrate ameliorates the progression of chronic renal injury
LILIANA GADOLA, OSCAR NOBOA, MARÍA NATALIA MÁRQUEZ, MARÍA JOSÉ RODRIGUEZ, NICOLÁS NIN, JOSÉ BOGGIA, ALEJANDRO FERREIRO, SILVIA GARCÍA, VIRGINIA ORTEGA, MARÍA LUISA MUSTO, PAOLO PONTE, PABLO SESSER, CARLOS PIZARROSA, SILVANA RAVAGLIO, and ANA VALLEGA
Background. Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation.
Methods. Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks.
Results. The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P< 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P< 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P< 0.05). Inulin clearances were higher (P< 0.05), and urine protein excretion rates were lower (P< 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group.
Conclusion. Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.
背景：慢性肾衰竭的结果之一就是代谢性酸中毒，它可引起骨质去矿化、肌蛋白水解，促进慢性肾衰竭进展。本研究旨在利用肾大部分切除实验模型评价枸橼酸钙纠正代谢性酸中毒的效果。
方法：将Wistar大鼠进行5/6肾大部分切除术，然后随机分成非治疗组（NFX）、枸橼酸钙治疗组(NFX-CIT)、卡托普利治疗组(NFX-CAP)与枸橼酸钙和卡托普利联合治疗组(NFX-CAP-CIT)。每100g饲料含枸橼酸钙1.45g，每1升水含卡托普利500mg。于第1、10和20周时，测定体重、收缩压、蛋白尿、动脉血碳酸氢盐浓度、尿枸橼酸排泄、血浆钙水平和菊粉清除率，并计算肾小球和肾小管间质损害得分。在第1周和第10周采用免疫组织化学方法观察肾小球和肾小管增生的细胞核抗原(PCNA)阳性细胞、 平滑肌动蛋白和肌纤维蛋白染色。
结果：与非治疗组相比，第1周，治疗组肾小球和小管间质细胞增殖明显减轻(P< 0.05)，第10周，肾小球细胞转分化显著减低，血浆碳酸氢盐浓度显著升高(P< 0.05)，第20周，肾小球和小管间质组织学损害得分减少(P< 0.05)。治疗组菊粉清除率明显高于非治疗组(P< 0.05)，尿蛋白排泄明显低于非治疗组(P< 0.05)，而NFX-CIT组动脉血压没有显著不同。
结论：枸橼酸钙减慢5/6肾切除模型慢性肾损伤的进程，改善代谢行酸中毒，减少细胞增殖和转分化，不影响收缩压。
Kidney International.2004;65(4):1224.
CELL BIOLOGY - IMMUNOLOGY - PATHOLOGY
Calcium citrate ameliorates the progression of chronic renal injury
LILIANA GADOLA, OSCAR NOBOA, MARÍA NATALIA MÁRQUEZ, MARÍA JOSÉ RODRIGUEZ, NICOLÁS NIN, JOSÉ BOGGIA, ALEJANDRO FERREIRO, SILVIA GARCÍA, VIRGINIA ORTEGA, MARÍA LUISA MUSTO, PAOLO PONTE, PABLO SESSER, CARLOS PIZARROSA, SILVANA RAVAGLIO, and ANA VALLEGA
Background. Metabolic acidosis is a consequence of chronic renal failure and it may produce bone demineralization, muscle proteolysis, and progression of chronic renal failure. The aim of this study was to evaluate the effects of correction of metabolic acidosis with calcium citrate in an experimental model of renal mass ablation.
Methods. Wistar rats were subjected to 5/6 nephrectomy and were randomly assigned to one of 4 groups: nontreated (NFX); treated with calcium citrate (1.45 g/100 g feed) (NFX-CIT); treated with captopril (500 mg/L water) (NFX-CAP); or treated with both (NFX-CAP-CIT) during 1, 10, or 20 weeks. Body weight, systolic blood pressure, proteinuria, arterial bicarbonate concentration, urine citrate excretion, plasma calcium, and inulin clearance were measured. Histologic glomerular and tubulointerstitial damage scores were measured at 1, 10, and 20 weeks, and glomerular and tubular proliferating cell nuclear antigen (PCNA)-positive cells, smooth muscle actin, and desmin staining were studied by immunohistochemistry at 1 and 10 weeks.
Results. The treated groups showed significantly less glomerular and tubulointerstitial cellular proliferation in the first week (P< 0.05), less glomerular cell transdifferentiation and higher plasma bicarbonate at 10 weeks (P< 0.05), as well as diminished histologic glomerular and tubulointerstitial damage scores at 20 weeks (P< 0.05). Inulin clearances were higher (P< 0.05), and urine protein excretion rates were lower (P< 0.05) than in the NFX non-treated group, but arterial blood pressure was not significantly different in the NFX-CIT group.
Conclusion. Calcium citrate slows the progression of chronic renal injury in the 5/6 NFX model. It improves metabolic acidosis and diminishes cell proliferation and transdifferentiation without changes in systolic blood pressure.
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