Mc Greevy C, Horan J, Jones D, Biswas K, O'Meara Y M, Mulkerrin E C
Department of Medicine in the Elderly, University College Hospital, Galway, Ireland.
J Nutr Health Aging. 2008 Feb;12(2):152-5. doi: 10.1007/BF02982569.
Sustained hyperkalaemia usually indicates a defect in renal potassium (K+) excretion and can be due to severe impairment of glomerular filtration rate (GFR). The major determinants of renal K+ secretion were studied in hyperkalaemic and normokalaemic elderly subjects to probe the major determinants of hyperkalaemia in this setting.
The transtubular potassium gradient (TTKG) provides an index of tubular K+ secretion and normally rises in patients with significant hyperkalaemia. Both GFR(glomerular filtration rate) and TTKG were assessed at baseline and repeated after 3 hours following ingestion of 0.1mg of fludrocortisone in three groups.
An acute general hospital in the West of Ireland.
23 subjects in total; 8 older patients with unexplained hyperkalaemia (OHK), 8 older patients with normokalaemia (ONK) and 9 young normokalaemic controls (YNK).
The GFR was either measured by 24 hour creatinine clearance estimation or calculated using the Cockroft and Gault formula.TTKG was calculated using a specific formula.
Mean baseline TTKG was similar in all three groups and consequently inappropriately low in hyperkalaemic subjects. Three hours post fludrocortisone, the TTKG had risen significantly from baseline levels in the young subjects only (from 7.5+/-0.09 to 11.6+/-1.1, p<0.05). No significant increase was noted in either older group at this timepoint.
The inappropriately low baseline TTKG in the OHK group as well as the absence of a response to fludrocortisone indicate tubular insensitivity to aldosterone. GFR values in both OHK (40.06+/-2.31) and ONK (55.58+/-6.1) groups were significantly lower than those in the YNK group (101.66+/-6.9). In aggregate, these findings indicate that older hyperkalaemic patients typically have both impairment of glomerular filtration and renal tubular K+ secretion and highlights the requirement for vigilance in elderly patients when using medications which interfere with tubular function.
持续性高钾血症通常提示肾脏排钾功能缺陷,可能是由于肾小球滤过率(GFR)严重受损所致。本研究在高钾血症和正常血钾的老年受试者中,对肾脏钾分泌的主要决定因素进行了研究,以探究该情况下高钾血症的主要决定因素。
跨肾小管钾梯度(TTKG)可反映肾小管钾分泌情况,在显著高钾血症患者中通常会升高。在三组受试者中,分别于基线时及口服0.1mg氟氢可的松3小时后评估肾小球滤过率(GFR)和TTKG。
爱尔兰西部的一家急性综合医院。
共23名受试者;8例不明原因高钾血症老年患者(OHK),8例正常血钾老年患者(ONK),9例正常血钾年轻对照者(YNK)。
GFR通过24小时肌酐清除率估算或使用Cockcroft和Gault公式计算。TTKG使用特定公式计算。
三组受试者的平均基线TTKG相似,因此高钾血症受试者的TTKG基线水平异常低。口服氟氢可的松3小时后,仅年轻受试者的TTKG较基线水平显著升高(从7.5±0.09升至11.6±1.1,p<0.05)。此时,两组老年受试者的TTKG均未显著升高。
OHK组TTKG基线水平异常低以及对氟氢可的松无反应,提示肾小管对醛固酮不敏感。OHK组(40.06±2.31)和ONK组(55.58±6.1)的GFR值均显著低于YNK组(101.66±6.9)。总体而言,这些发现表明老年高钾血症患者通常存在肾小球滤过功能和肾小管钾分泌功能受损,这凸显了在老年患者使用干扰肾小管功能的药物时需保持警惕。