饮食中钠摄入量对腹透患者残余肾功能的影响:33例前瞻性研究
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摘要
目的探讨腹膜透析患者摄钠量与残余肾功能之间的关系。方法对33例稳定透析、规律随访的腹膜透析患者进行12月的随访观察。以3 d饮食记录计算患者的日摄盐量,以平均日摄钠量为依据,将患者分为低盐组(摄钠量≤3.0 g/d,19例)和高盐组(摄钠量>3.0 g/d,14例)。记录患者基线资料,检测患者残余肾功能、腹膜功能等指标。按1次/3月进行规律随访。记录尿量、腹透超滤量等临床指标,检测患者生化指标,评估患者残余肾功能、腹膜功能的变化情况。结果钠排泄总量与腹透患者钠摄入量呈正相关(r=0.536,P=0.0013);腹透清除钠的总量与腹透患者钠摄入量呈正相关(r=0.901,P=0.000),而残余肾的钠排泄量与腹透患者钠摄入量无明显相关关系。回归分析发现,钠排泄总量、腹透液钠的排泄均与钠的摄入相关(β=0.416,95%CI:0.170～0.666,P<0.0018;β=0.489,95%CI:0.395～0.582,P<0.001)。腹透患者残余肾功能的下降值,低盐组为17.48±11.22 L/(w·1.73 m2),高盐组为30.20±18.30 L/(w·1.73 m2),差异有统计学意义(P=0.032)。患者残余肾功能的下降与摄钠量之间存在相关关系(r=0.409,P=0.018),多因素回归分析显示摄钠量是残余肾功能下降的独立影响因素(β=14.646,95%CI:7.426～21.866,P<0.001)。结论腹透患者腹透清除钠的总量与患者钠摄入量呈正相关;腹透患者残余肾功能的下降和摄钠量相关,高钠饮食可使残余肾功能下降更快。
Objective To explore the impact of dietary sodium-intake on residual renal function in patients undergoing peritoneal dialysis(PD). Methods Thirty-three patients on PD with stable dialysis were regularly followed up for 12 months.The daily sodium intake of the patients was calculated based on the 3-day dietary record. Based on the mean daily sodium intake, the patients enrolled were divided into low-salt group(sodium intake≤3.0 g/day, 19 patients) and high-salt group(sodium intake>3.0 g/day, 14 patients). The baseline data of the patients were recorded, and the indicators of residual renal function and peritoneal function were regularly tested. The patients were followed-up at 3-month intervals, and their urine volume, peritoneal ultrafiltration volume and other clinical indicators were recorded and the biochemical indexes were detected to evaluate the changes in the residual renal function and peritoneal function. Results There was a positive correlation between the total sodium excretion and dietary sodium intake in these patients(r=0.536, P=0.0013), and sodium excretion by dialysis was positively correlated with their sodium intake(r=0.901, P=0.000). Regression analysis suggested that the total sodium excretion was correlated with dietary sodium intake(β =0.416, 95% CI: 0.170-0.666; P<0.0018); sodium excretion by dialysis was associated with dietary sodium intake(β =0.489, 95% CI: 0.395-0.582; P<0.001). The residual renal function was reduced by 17.48 ± 11.22 L/(w·1.73 m2) in the low-salt group, as compared to 30.20 ± 18.30 L/(w·1.73 m2) in the high-salt group(P=0.032). The reduction in the residual renal function was correlated with sodium intake in the PD patients(r=0.409, P=0.018). Multivariate regression analysis showed that sodium intake was an independent factor contributing to the reduction of residual renal function(β =14.646, 95% CI 7.426-21.866, P<0.001). Conclusion Sodium excretion by PD in patients with continuous ambulatory PD is positively correlated with their dietary sodium intake, which contribute to the decrease of residual renal function. A high dietary sodium intake may accelerate the reduction of residual renal function in these patients.
Objective To explore the impact of dietary sodium-intake on residual renal function in patients undergoing peritoneal dialysis(PD). Methods Thirty-three patients on PD with stable dialysis were regularly followed up for 12 months.The daily sodium intake of the patients was calculated based on the 3-day dietary record. Based on the mean daily sodium intake, the patients enrolled were divided into low-salt group(sodium intake≤3.0 g/day, 19 patients) and high-salt group(sodium intake>3.0 g/day, 14 patients). The baseline data of the patients were recorded, and the indicators of residual renal function and peritoneal function were regularly tested. The patients were followed-up at 3-month intervals, and their urine volume, peritoneal ultrafiltration volume and other clinical indicators were recorded and the biochemical indexes were detected to evaluate the changes in the residual renal function and peritoneal function. Results There was a positive correlation between the total sodium excretion and dietary sodium intake in these patients(r=0.536, P=0.0013), and sodium excretion by dialysis was positively correlated with their sodium intake(r=0.901, P=0.000). Regression analysis suggested that the total sodium excretion was correlated with dietary sodium intake(β =0.416, 95% CI: 0.170-0.666; P<0.0018); sodium excretion by dialysis was associated with dietary sodium intake(β =0.489, 95% CI: 0.395-0.582; P<0.001). The residual renal function was reduced by 17.48 ± 11.22 L/(w·1.73 m2) in the low-salt group, as compared to 30.20 ± 18.30 L/(w·1.73 m2) in the high-salt group(P=0.032). The reduction in the residual renal function was correlated with sodium intake in the PD patients(r=0.409, P=0.018). Multivariate regression analysis showed that sodium intake was an independent factor contributing to the reduction of residual renal function(β =14.646, 95% CI 7.426-21.866, P<0.001). Conclusion Sodium excretion by PD in patients with continuous ambulatory PD is positively correlated with their dietary sodium intake, which contribute to the decrease of residual renal function. A high dietary sodium intake may accelerate the reduction of residual renal function in these patients.
引文
[1]国家肾病学医疗质量管理与控制中心. 2016年全国腹膜透析登记数据分析[C].北京:全国质控工作会议, 2016-12-23.
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[3] Szeto CC, Kwan BC, Chow K, et al. Predictors of residual renal function decline in patients undergoing continuous ambulatory peritoneal dialysis[J]. Perit Dial Int, 2015, 35(2):180-8.
[4] Nongnuch A, Assanatham M, Panorchan K, et al. Strategies for preserving residual renal function in peritoneal dialysis patients[J].Clin Kidney J, 2015, 8(2):202-11.
[5]Htay H, Cho Y, Pascoe EM, et al. Predictors of residual renal function decline in peritoneal dialysis patients:the balANZ trial[J]. Perit Dial Int, 2017, 37(3):283-9.
[6] Shen JI, Saxena AB, Vangala S, et al. Renin-angiotensin system blockers and residual kidney function loss in patients initiating peritoneal dialysis:an observational cohort study[J]. BMC Nephrol,2017, 18(1):196-207.
[7] Dworkin LD, Benstein JA, Tolbert E, et al. Salt restriction inhibits renal growth and stabilizes injury in rats with established renal disease[J]. J Am Soc Nephrol, 1996, 7(3):437-42.
[8]Kobori H, Navar LG. Urinary angiotensinogen as an novel biomarker of intrarenal renin-angiotensin system in chronic kidney disease[J].Int Rev Thromb, 2011, 6(2):108-16.
[9] Zhuo JL, Ferrao FM, Zheng Y, et al. New frontiers in the intrarenal renin-angiotensin system:a critical review of classical and new paradigms[J]. Front Endocrinol(Lausanne), 2013, 21(4):166-75.
[10]Cao W, Li A, Wang L, et al. A salt-induced reno-cerebral reflex activates renin-angiotensin systems and promotes CKD progression[J]. JAm Soc Nephrol, 2015, 26(7):1619-33.
[11]Cianciaruso B, Bellizzi V, Minutolo R, et al. Salt intake and renal outcome in patients with progressive renal disease[J]. Miner Electrolyte Metab, 1998, 24(4):296-301.
[12]Sanders PW. Effect of salt intake on progression of chronic kidney disease[J]. Curr Opin Nephrol Hypertens, 2006, 15(1):54-60.
[13]Verhave JC, Hillege HL, Burgerhof JG, et al. Sodium intake affects urinary albumin excretion especially in overweight subjects[J]. J Intern Med, 2004, 256(4):324-30.
[14]Titze J, Ritz E. Salt and its effect on blood pressure, target organ damage:new pieces in an old puzzle[J]. J nephrol, 2009, 22(2):177-89.
[15]Krikken JA, Lely AT, Bakker SJ, et al. The effect of a shift in sodium intake on renal hemodynamics is determined by body mass index in healthy young men[J]. Kidney Int, 2007, 71(3):260-5.
[16]Mancia G, De Backer G, Dominiczak A, et al. 2007 guidelines for the management of arterial hypertension:the task force for the management of arterial hypertension of the European society of hypertension(ESH)and of the European society of cardiology[J]. J Hypertens, 2007, 25(6):1105-87.
[17]Jiang JP, Chen PY, Chen JH, et al. Accumulation of tissue advanced glycation end products correlated with glucose exposure dose and associated with cardiovascular morbidity in patients on peritoneal dialysis[J]. Atherosclerosis, 2012, 224(1):187-94.
[18]《中国高血压防治指南》修订委员会.中国高血压防治指南2018年修订版[J].心脑血管病防治, 2019, 19(1):1-44.
[19]Dong J, Li Y, Yang Z, et al. Time-dependent associations between total sodium removal and mortality in patients on peritoneal dialysis[J]. Perit Dial Int, 2011, 31(4):412-21.
[20]van Olden RW, Krediet RT, Struijk DG, et al. Measurement of residual renal function in patients treated with continuous ambulatory peritoneal dialysis[J]. J Am Soc Nephrol, 1996, 7(5):745-50.
[21]Diaz-Buxo JA, White SA, Himmele R. The importance of residual renal function in peritoneal dialysis patients[J]. Adv Perit Dial, 2013,40(29):19-24.
[22]Sanghavi S, Vassalotti JA. Dietary Sodium:a therapeutic target in the treatment of hypertension and CKD[J]. J Ren Nutr, 2013, 23(3):223-7.
[23]Krikken JA, Laverman GD, Navis G. Benefits of dietary Sodium restriction in the management of chronic kidney disease[J]. Curr Opin Nephrol Hypertens, 2009, 18(6):531-8.
[24]Susic D, Frohlich ED. Salt consumption and cardiovascular, renal,and hypertensive diseases:clinical and mechanistic aspects[J]. Curr Opin Lipidol, 2012, 23(1):11-6.
[25]Wright JA, Cavanaugh KL. Dietary Sodium in chronic kidney disease:a comprehensive approach[J]. Semin Dial, 2010, 23(4):415-21.
[26]Liu X, Dai C. Advances in understanding and management of residual renal function in patients with chronic kidney disease[J]. Kidney Dis,2016, 2(4):187-96.
[27]Vilar E, Farrington K. Emerging importance of residual renal function in end-stage renal failure[J]. Semin Dial, 2011, 24(5):487-94.
[28]Nessim SJ, Bargman JM. The peritoneal-renal syndrome[J]. Nat Rev Nephrol, 2013, 9(5):302-6.
[29]Lambers Heerspink HJ, Navis G, Ritz E. Salt intake in kidney disease-a missed therapeutic opportunity[J]. Nephrol Dial Transplant, 2012, 27(9):3435-42.
[30]Dong J, Li YJ, Yang ZK, et al. Low dietary sodium intake increases the death risk in peritoneal dialysis[J]. Clin J Am Soc Nephrol, 2010,5(2):240-7.
[31]Alderman MH. Presidential address:21st scientific meeting of the international society of hypertension-dietary sodium and cardiovascular disease:the'J'-shaped relation[J]. J Hypertens, 2007, 25(5):903-7.
[32]Smyth A, Dunkler D, Gao P, et al. The relationship between estimated sodium and potassium excretion and subsequent renal outcomes[J].Kidney Int, 2014, 86(6):1205-12.
[33]Bourgoignie JJ, Kaplan M, Gavellas G, et al. The relationship between estimated sodium and potassium excretion and subsequent renal outcomes[J]. Kidney Int, 1982, 21(6):820-6.
[34]Kim SM, Lee EK, Kang SS, et al. Simple method to estimate daily sodium intake during measurement of dialysis adequacy in chronic peritoneal dialysis patients[J]. Asia Pac J Clin Nutr, 2017, 26(6):1001-6.
[35]Cheng LT, Wang T. Changes in total sodium intake do not lead to proportionate changes in total sodium removal in CAPD patients[J].Perit Dial Int, 2006, 26(2):218-23.
[36]Liu Z. Dietary Sodium and the incidence of hypertension in the Chinese population:a review of nationwide surveys[J]. Am J Hypertens, 2009, 22(9):929-33.
[37]国务院办公厅.国务院办公厅关于印发中国防治慢性病中长期规划(2017~2025年)的通知[EB/OL].[2017-02-14]. http://www.gov.cn/zhengce/content/2017-02/14/content_5167886.htm.
[38]李园,骆蓉,张普洪.减盐防控慢性病进展[J].中华预防医学杂志,2018, 52(7):757-60.
[2] Wang AY, Brimble KS, Brunier GA, et al. ISPD cardiovascular and metabolic guidelines in adult peritoneal dialysis patients part Iassessment and management of various cardiovascular risk factors[J]. Perit Dial Int, 2015, 35(4):379-87.
[3] Szeto CC, Kwan BC, Chow K, et al. Predictors of residual renal function decline in patients undergoing continuous ambulatory peritoneal dialysis[J]. Perit Dial Int, 2015, 35(2):180-8.
[4] Nongnuch A, Assanatham M, Panorchan K, et al. Strategies for preserving residual renal function in peritoneal dialysis patients[J].Clin Kidney J, 2015, 8(2):202-11.
[5]Htay H, Cho Y, Pascoe EM, et al. Predictors of residual renal function decline in peritoneal dialysis patients:the balANZ trial[J]. Perit Dial Int, 2017, 37(3):283-9.
[6] Shen JI, Saxena AB, Vangala S, et al. Renin-angiotensin system blockers and residual kidney function loss in patients initiating peritoneal dialysis:an observational cohort study[J]. BMC Nephrol,2017, 18(1):196-207.
[7] Dworkin LD, Benstein JA, Tolbert E, et al. Salt restriction inhibits renal growth and stabilizes injury in rats with established renal disease[J]. J Am Soc Nephrol, 1996, 7(3):437-42.
[8]Kobori H, Navar LG. Urinary angiotensinogen as an novel biomarker of intrarenal renin-angiotensin system in chronic kidney disease[J].Int Rev Thromb, 2011, 6(2):108-16.
[9] Zhuo JL, Ferrao FM, Zheng Y, et al. New frontiers in the intrarenal renin-angiotensin system:a critical review of classical and new paradigms[J]. Front Endocrinol(Lausanne), 2013, 21(4):166-75.
[10]Cao W, Li A, Wang L, et al. A salt-induced reno-cerebral reflex activates renin-angiotensin systems and promotes CKD progression[J]. JAm Soc Nephrol, 2015, 26(7):1619-33.
[11]Cianciaruso B, Bellizzi V, Minutolo R, et al. Salt intake and renal outcome in patients with progressive renal disease[J]. Miner Electrolyte Metab, 1998, 24(4):296-301.
[12]Sanders PW. Effect of salt intake on progression of chronic kidney disease[J]. Curr Opin Nephrol Hypertens, 2006, 15(1):54-60.
[13]Verhave JC, Hillege HL, Burgerhof JG, et al. Sodium intake affects urinary albumin excretion especially in overweight subjects[J]. J Intern Med, 2004, 256(4):324-30.
[14]Titze J, Ritz E. Salt and its effect on blood pressure, target organ damage:new pieces in an old puzzle[J]. J nephrol, 2009, 22(2):177-89.
[15]Krikken JA, Lely AT, Bakker SJ, et al. The effect of a shift in sodium intake on renal hemodynamics is determined by body mass index in healthy young men[J]. Kidney Int, 2007, 71(3):260-5.
[16]Mancia G, De Backer G, Dominiczak A, et al. 2007 guidelines for the management of arterial hypertension:the task force for the management of arterial hypertension of the European society of hypertension(ESH)and of the European society of cardiology[J]. J Hypertens, 2007, 25(6):1105-87.
[17]Jiang JP, Chen PY, Chen JH, et al. Accumulation of tissue advanced glycation end products correlated with glucose exposure dose and associated with cardiovascular morbidity in patients on peritoneal dialysis[J]. Atherosclerosis, 2012, 224(1):187-94.
[18]《中国高血压防治指南》修订委员会.中国高血压防治指南2018年修订版[J].心脑血管病防治, 2019, 19(1):1-44.
[19]Dong J, Li Y, Yang Z, et al. Time-dependent associations between total sodium removal and mortality in patients on peritoneal dialysis[J]. Perit Dial Int, 2011, 31(4):412-21.
[20]van Olden RW, Krediet RT, Struijk DG, et al. Measurement of residual renal function in patients treated with continuous ambulatory peritoneal dialysis[J]. J Am Soc Nephrol, 1996, 7(5):745-50.
[21]Diaz-Buxo JA, White SA, Himmele R. The importance of residual renal function in peritoneal dialysis patients[J]. Adv Perit Dial, 2013,40(29):19-24.
[22]Sanghavi S, Vassalotti JA. Dietary Sodium:a therapeutic target in the treatment of hypertension and CKD[J]. J Ren Nutr, 2013, 23(3):223-7.
[23]Krikken JA, Laverman GD, Navis G. Benefits of dietary Sodium restriction in the management of chronic kidney disease[J]. Curr Opin Nephrol Hypertens, 2009, 18(6):531-8.
[24]Susic D, Frohlich ED. Salt consumption and cardiovascular, renal,and hypertensive diseases:clinical and mechanistic aspects[J]. Curr Opin Lipidol, 2012, 23(1):11-6.
[25]Wright JA, Cavanaugh KL. Dietary Sodium in chronic kidney disease:a comprehensive approach[J]. Semin Dial, 2010, 23(4):415-21.
[26]Liu X, Dai C. Advances in understanding and management of residual renal function in patients with chronic kidney disease[J]. Kidney Dis,2016, 2(4):187-96.
[27]Vilar E, Farrington K. Emerging importance of residual renal function in end-stage renal failure[J]. Semin Dial, 2011, 24(5):487-94.
[28]Nessim SJ, Bargman JM. The peritoneal-renal syndrome[J]. Nat Rev Nephrol, 2013, 9(5):302-6.
[29]Lambers Heerspink HJ, Navis G, Ritz E. Salt intake in kidney disease-a missed therapeutic opportunity[J]. Nephrol Dial Transplant, 2012, 27(9):3435-42.
[30]Dong J, Li YJ, Yang ZK, et al. Low dietary sodium intake increases the death risk in peritoneal dialysis[J]. Clin J Am Soc Nephrol, 2010,5(2):240-7.
[31]Alderman MH. Presidential address:21st scientific meeting of the international society of hypertension-dietary sodium and cardiovascular disease:the'J'-shaped relation[J]. J Hypertens, 2007, 25(5):903-7.
[32]Smyth A, Dunkler D, Gao P, et al. The relationship between estimated sodium and potassium excretion and subsequent renal outcomes[J].Kidney Int, 2014, 86(6):1205-12.
[33]Bourgoignie JJ, Kaplan M, Gavellas G, et al. The relationship between estimated sodium and potassium excretion and subsequent renal outcomes[J]. Kidney Int, 1982, 21(6):820-6.
[34]Kim SM, Lee EK, Kang SS, et al. Simple method to estimate daily sodium intake during measurement of dialysis adequacy in chronic peritoneal dialysis patients[J]. Asia Pac J Clin Nutr, 2017, 26(6):1001-6.
[35]Cheng LT, Wang T. Changes in total sodium intake do not lead to proportionate changes in total sodium removal in CAPD patients[J].Perit Dial Int, 2006, 26(2):218-23.
[36]Liu Z. Dietary Sodium and the incidence of hypertension in the Chinese population:a review of nationwide surveys[J]. Am J Hypertens, 2009, 22(9):929-33.
[37]国务院办公厅.国务院办公厅关于印发中国防治慢性病中长期规划(2017~2025年)的通知[EB/OL].[2017-02-14]. http://www.gov.cn/zhengce/content/2017-02/14/content_5167886.htm.
[38]李园,骆蓉,张普洪.减盐防控慢性病进展[J].中华预防医学杂志,2018, 52(7):757-60.