Schirpenbach Caroline, Seiler Lysann, Maser-Gluth Christiane, Rüdiger Frank, Nickel Christian, Beuschlein Felix, Reincke Martin
Medical Department II, Albert-Ludwig-University, Freiburg, Germany.
Eur J Endocrinol. 2006 Jun;154(6):865-73. doi: 10.1530/eje.1.02164.
Primary aldosteronism has recently been recognized as the most frequent cause of secondary hypertension. Since most patients are normokalaemic, differentiation to essential hypertension is challenging. As differentiation by baseline aldosterone/renin ratio may be insufficient, diagnosis should be confirmed by additional tests. However, as most confirmatory tests have been evaluated in hypokalaemic primary aldosteronism only, we reassessed the value of the saline infusion test and 24 h urinary aldosterone metabolites as confirmatory tests for both normo- and hypokalaemic primary aldosteronism under current antihypertensive medication.
25 patients with primary aldosteronism (11 hypokalaemic, 14 normokalaemic), 29 patients with essential hypertension and 47 normotensive subjects were studied. The hypertensives received their usual medication with the exception of spironolactone. All subjects underwent a standard saline infusion test (determination of plasma aldosterone before and after 2.0 liters of isotonic saline for 4 hours i.v.) and collected a 24 h urine sample for examination of urinary tetrahydroaldosterone and aldosterone-18-glucuronide.
In hypokalaemic primary aldosteronism the saline infusion test showed a reasonable sensitivity (91%) and specificity (90%). However, the test failed to differentiate sufficiently between essential hypertension and normokalaemic primary aldosteronism (sensitivity 57%, specificity 90%). Similarly, urinary tetrahydroaldosterone had higher sensitivity in hypokalaemic than in normokalaemic primary aldosteronism (sensitivity 64% vs 36%, specificity 100%), whereas for aldosterone-18-glucuronide, no differences in hypo- and normokalaemic primary aldosteronism were found (sensitivity 45% and 43%, specificity 100%).
These data show that the saline infusion test as an established test in classical hypokalaemic primary aldosteronism is not a reliable test in the normokalaemic variant of the disease. Due to its low accuracy, determination of urinary aldosterone metabolites did not prove useful in confirming either normo- or hypokalaemic patients. We conclude from our data that these tests should not be used as confirmatory testing in the normokalaemic variant of primary aldosteronism.
原发性醛固酮增多症最近被认为是继发性高血压最常见的病因。由于大多数患者血钾正常，因此与原发性高血压进行鉴别具有挑战性。鉴于仅通过基线醛固酮/肾素比值进行鉴别可能并不充分，诊断应通过额外的检查来确认。然而，由于大多数确诊试验仅在低钾血症性原发性醛固酮增多症中进行了评估，我们重新评估了生理盐水输注试验和24小时尿醛固酮代谢产物作为目前抗高血压药物治疗下正常血钾和低钾血症性原发性醛固酮增多症确诊试验的价值。
研究了25例原发性醛固酮增多症患者（11例低钾血症，14例正常血钾）、29例原发性高血压患者和47例血压正常的受试者。高血压患者除螺内酯外，继续服用其常用药物。所有受试者均接受了标准的生理盐水输注试验（静脉输注2.0升等渗盐水4小时前后测定血浆醛固酮），并收集24小时尿液样本以检测尿四氢醛固酮和醛固酮-18-葡萄糖醛酸苷。
在低钾血症性原发性醛固酮增多症中，生理盐水输注试验显示出合理的敏感性（91%）和特异性（90%）。然而，该试验在原发性高血压和正常血钾性原发性醛固酮增多症之间未能充分区分（敏感性57%，特异性90%）。同样，尿四氢醛固酮在低钾血症性原发性醛固酮增多症中的敏感性高于正常血钾性原发性醛固酮增多症（敏感性64%对36%，特异性100%），而对于醛固酮-18-葡萄糖醛酸苷，低钾血症和正常血钾性原发性醛固酮增多症之间未发现差异（敏感性45%和43%，特异性100%）。
这些数据表明，生理盐水输注试验作为经典低钾血症性原发性醛固酮增多症的既定检查方法，在该疾病的正常血钾变体中并非可靠的检查。由于其准确性较低，尿醛固酮代谢产物的测定在确诊正常血钾或低钾血症患者方面未被证明有用。我们从数据中得出结论，这些检查不应作为原发性醛固酮增多症正常血钾变体的确诊检查。
