Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan; Department of Medicine, Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan.
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan.
Am J Med. 2017 Jul;130(7):846-855. doi: 10.1016/j.amjmed.2017.01.023. Epub 2017 Feb 14.
Uncovering the correct diagnosis of chronic hypokalemia with potassium (K) wasting from the kidneys or gut can be fraught with challenges. We identified clinical and laboratory parameters helpful for differentiating the causes of chronic hypokalemia.
Normotensive patients referred to our tertiary academic medical center for the evaluation of chronic hypokalemia were prospectively enrolled over 5 years. Clinical features, laboratory examinations-including blood and spot urine electrolytes, acid-base status, biochemistries, and hormones-as well as genetic analysis, were determined.
Ninety-nine patients with chronic normotensive hypokalemia (serum K 2.8 ± 0.4 mmol/L, duration 4.1 ± 0.9 years) were enrolled. Neuromuscular symptoms were the most common complaints. Although Gitelman syndrome (n = 33), Bartter syndrome (n = 10), and distal renal tubular acidosis (n = 12) were the predominant renal tubular disorders, 44 patients (44%) were diagnosed with anorexia/bulimia nervosa (n = 21), surreptitious use of laxatives (n = 11), or diuretics (n = 12). Patients with gastrointestinal causes and surreptitious diuretics use exhibited a female predominance, lower body mass index, and less K supplementation. High urine K excretion (transtubular potassium gradient >3, urine K/Cr >2 mmol/mmol) was universally present in patients with renal tubular disorders, but also found in >50% patients with gastrointestinal causes. Of interest, while urine sodium (Na) and chloride (Cl) excretions were high and coupled (urine Na/Cl ratio ∼1) in renal tubular disorders and "on" diuretics use, skewed or uncoupled urine Na and Cl excretions were found in anorexia/bulimia nervosa and laxatives abuse (urine Na/Cl ratio: 5.0 ± 2.2, 0.4 ± 0.2, respectively) and low urine Na and Cl excretions with fixed Na/Cl ratios (0.9 ± 0.2) when "off" diuretics.
Besides body mass index, sex, and blood acid-base status, integrated interpretation of the urine Na:Cl excretion and their ratio is important to make an accurate diagnosis and treatment plan for patients with chronic normotensive hypokalemia.
从肾脏或肠道中发现导致慢性低钾血症伴钾（K）丢失的正确诊断可能充满挑战。我们确定了有助于区分慢性低钾血症病因的临床和实验室参数。
5 年来，我们前瞻性地招募了因慢性低钾血症就诊于我们三级学术医学中心的血压正常患者。确定了临床特征、实验室检查（包括血液和随机尿液电解质、酸碱状态、生化和激素）以及基因分析。
共纳入 99 例慢性血压正常性低钾血症患者（血清 K 2.8±0.4mmol/L，病程 4.1±0.9 年）。神经肌肉症状是最常见的主诉。尽管 Gitelman 综合征（n=33）、Bartter 综合征（n=10）和远端肾小管酸中毒（n=12）是主要的肾小管疾病，但 44 例（44%）患者被诊断为神经性厌食/贪食症（n=21）、秘密使用泻药（n=11）或利尿剂（n=12）。胃肠道疾病和秘密使用利尿剂的患者以女性为主，体重指数较低，K 补充较少。肾小管疾病患者普遍存在高尿 K 排泄（跨肾小管钾梯度>3，尿 K/Cr>2mmol/mmol），但>50%胃肠道疾病患者也存在这种情况。有趣的是，虽然肾小管疾病和“服用”利尿剂时尿钠（Na）和氯（Cl）排泄量高且耦合（尿 Na/Cl 比值约为 1），但神经性厌食/贪食症和滥用泻药时则存在偏斜或不耦合的尿 Na 和 Cl 排泄（尿 Na/Cl 比值：5.0±2.2、0.4±0.2），“停用”利尿剂时则表现为低尿 Na 和 Cl 排泄及固定的 Na/Cl 比值（0.9±0.2）。
除了体重指数、性别和血液酸碱状态外，综合解读尿 Na:Cl 排泄及其比值对于对慢性血压正常性低钾血症患者做出准确的诊断和治疗计划非常重要。
