Thiazide-induced hyponatremia is one of the main causes of decreased sodium levels in elderly individuals. This review presents the current evidence regarding the thiazide-associated hyponatremia. Thiazide-associated ...Thiazide-induced hyponatremia is one of the main causes of decreased sodium levels in elderly individuals. This review presents the current evidence regarding the thiazide-associated hyponatremia. Thiazide-associated hyponatremia is observed mainly in patients with certain risk factors such as those receiving large doses of thiazides, having much comorbidity, such as heart failure, liver disease or malignancy, and taking several medications, such as non-steroidal anti-inflammatory drugs, selective serotonin re-uptake inhibitors or tricyclic antide- pressants. Sodium concentration should be monitored in patients with risk factors for developing thiazide-associated hyponatremia and clini- cians should measure promptly serum sodium levels in patients with neurologic signs indicating reduced sodium levels. The clinical and biochemical profile of patients with thiazide-associated hyponatremia may be that of extracellular volume depletion or the syndrome of inap- propriate antidiuretic hormone secretion （SIADH）. The investigation of possible thiazide-associated hyponatremia includes the exclusion of other causes of decreased sodium levels and the identification of the characteristics of hyponatremia due to thiazides （extracellular volume depletion-related or SIADH-like）. Treatment should be carefully monitored to avoid serious neurologic complications due to overcorrection. Clinicians should discourage prescribing thiazides in patients with a history of diuretic-associated hyponatremia and should prefer low doses of thiazides in patients with risk factors for developing thiazide-associated hyponatremia.展开更多
AIM： To quantify changes in urinary excretion of aquaporin2 water channels （u-AQP2）, the sodium-potassium-chloride co-transporter （u-NKCC2） and the epithelial sodium channels （u-ENaC） during treatment with bend...AIM： To quantify changes in urinary excretion of aquaporin2 water channels （u-AQP2）, the sodium-potassium-chloride co-transporter （u-NKCC2） and the epithelial sodium channels （u-ENaC） during treatment with bendrofumethiazide （BFTZ）, amiloride and placebo.METHODS： In a randomized, double-blinded, placebo-controlled, 3-way crossover study we examined 23 healthy subjects on a standardized diet and fuid intake. The subjects were treated with amiloride 5 mg, BFTZ 1.25 mg or placebo twice a day for 4.5 d before each examination day. On the examination day, glomerular filtration rate was measured by the constant infusion clearance technique with 51Cr-EDTA as reference substance. To estimate the changes in water transport via AQP2 and sodium transport via NKCC2 and ENaC, u-NKCC2, the gamma fraction of ENaC （u-ENaCγ）, and u-AQP2 were measured at baseline and after infusion with 3% hypertonic saline. U-NKCC2, u-ENaCγ, u-AQP2 and plasma concentrations of vasopressin （p-AVP）, renin （PRC）, angiotensin Ⅱ （p-ANG Ⅱ） and aldosterone （p-Aldo） were measured, by radioimmunoassay. Central blood pressure was estimated by applanation tonometry and body fuid volumes were estimated by bio-impedance spectroscopy. General linear model with repeated measures or related samples Friedman’s two-way analysis was used to compare differences. Post hoc Bonferroni correction was used for multiple comparisons of post infusion periods to baseline within each treatment group.RESULTS： At baseline there were no differences in u-NKCC2, u-ENaCγ and u-AQP2. PRC, p-Ang Ⅱ and p-Aldo were increased during active treatments （P 〈 0.001）. After hypertonic saline, u-NKCC2 increased during amiloride （6% ± 34%; P = 0.081） and increased significantly during placebo （17% ± 24%; P = 0.010）. U-AQP2 increased signifcantly during amiloride （31% ± 22%; P 〈 0.001） and placebo （34% ± 27%; P 〈 0.001）, while u-NKCC2 and u-AQP2 did not change signifcantly during BFTZ （-7% ± 28%; P = 0.257 and 5% ± 16%; P = 0.261）. U- ENaCγ increased in all three groups （ P 〈 0.050）. PRC, AngⅡ and p-Aldo decreased to the same extent, while AVP increased, but to a smaller degree during BFTZ （ P = 0.048）. cDBP decreased significantly during BFTZ （P 〈 0.001）, but not during amiloride or placebo. There were no significant differences in body fuid volumes.CONCLUSION： After hypertonic saline, u-NKCC2 and u-AQP2 increased during amiloride, but not during BFTZ. Lower p-AVP during BFTZ potentially caused less stimulation of NKCC2 and AQP2 and subsequent lower reabsorption of water and sodium.展开更多
Hypokalemia, defined as serum potassium below 3.5 mEq/L, can lead to severe complications such as arrhythmias and muscle paralysis, potentially resulting in rhabdomyolysis. The etiology of hypokalemia is often multifa...Hypokalemia, defined as serum potassium below 3.5 mEq/L, can lead to severe complications such as arrhythmias and muscle paralysis, potentially resulting in rhabdomyolysis. The etiology of hypokalemia is often multifactorial, involving but not limited to gastrointestinal losses, renal losses, medication effects, and inadequate dietary intake. Chronic heavy alcohol use, obstructive sleep apnea (OSA), and the use of diuretics such as hydrochlorothiazide (HCTZ) are also significant contributing factors. Effective management requires thorough evaluation and investigation to effectively treat a patient. This case report aims to illustrate the diagnostic challenges and comprehensive treatment approach required in a patient with multiple comorbidities and severe hypokalemia, emphasizing the need for a multidisciplinary and comprehensive approach to address all underlying causes.展开更多
目的探讨老年高血压患者利尿剂的使用及其对血钾和尿酸的影响。方法选择年龄≥70岁的高血压患者713例,根据入选时患者服用降压药物的情况,分为3组:利尿剂组332例、非利尿剂组270例和未用药组111例,测定血钾、尿酸和其他生化指标,并进行...目的探讨老年高血压患者利尿剂的使用及其对血钾和尿酸的影响。方法选择年龄≥70岁的高血压患者713例,根据入选时患者服用降压药物的情况,分为3组:利尿剂组332例、非利尿剂组270例和未用药组111例,测定血钾、尿酸和其他生化指标,并进行比较。结果利尿剂组和非利尿剂组患者血压显著低于未用药组(P<0.05)。与未用药组和非利尿剂组比较,利尿剂组患者尿酸、TG明显升高,血钾明显降低,差异有统计学意义(P<0.05,P<0.01)。利尿剂组低钾血症发生率明显高于非利尿剂组和未用药组(18.1% vs 10.4% vs 9.9%,P<0.05,P<0.01)。结论老年高血压患者中,使用利尿剂控制血压与使用非利尿降压药效果相似,但血钾水平低、低钾血症发生率高,血清尿酸升高;长期使用需注意血钾降低的防治。展开更多
文摘Thiazide-induced hyponatremia is one of the main causes of decreased sodium levels in elderly individuals. This review presents the current evidence regarding the thiazide-associated hyponatremia. Thiazide-associated hyponatremia is observed mainly in patients with certain risk factors such as those receiving large doses of thiazides, having much comorbidity, such as heart failure, liver disease or malignancy, and taking several medications, such as non-steroidal anti-inflammatory drugs, selective serotonin re-uptake inhibitors or tricyclic antide- pressants. Sodium concentration should be monitored in patients with risk factors for developing thiazide-associated hyponatremia and clini- cians should measure promptly serum sodium levels in patients with neurologic signs indicating reduced sodium levels. The clinical and biochemical profile of patients with thiazide-associated hyponatremia may be that of extracellular volume depletion or the syndrome of inap- propriate antidiuretic hormone secretion （SIADH）. The investigation of possible thiazide-associated hyponatremia includes the exclusion of other causes of decreased sodium levels and the identification of the characteristics of hyponatremia due to thiazides （extracellular volume depletion-related or SIADH-like）. Treatment should be carefully monitored to avoid serious neurologic complications due to overcorrection. Clinicians should discourage prescribing thiazides in patients with a history of diuretic-associated hyponatremia and should prefer low doses of thiazides in patients with risk factors for developing thiazide-associated hyponatremia.
基金Supported by Grants from The Lundbeck FoundationAase and Ejnar Danielsens Foundation+1 种基金Helen and Ejnar Bjoernows FoundationRegion Midjutlands Research Fund
文摘AIM： To quantify changes in urinary excretion of aquaporin2 water channels （u-AQP2）, the sodium-potassium-chloride co-transporter （u-NKCC2） and the epithelial sodium channels （u-ENaC） during treatment with bendrofumethiazide （BFTZ）, amiloride and placebo.METHODS： In a randomized, double-blinded, placebo-controlled, 3-way crossover study we examined 23 healthy subjects on a standardized diet and fuid intake. The subjects were treated with amiloride 5 mg, BFTZ 1.25 mg or placebo twice a day for 4.5 d before each examination day. On the examination day, glomerular filtration rate was measured by the constant infusion clearance technique with 51Cr-EDTA as reference substance. To estimate the changes in water transport via AQP2 and sodium transport via NKCC2 and ENaC, u-NKCC2, the gamma fraction of ENaC （u-ENaCγ）, and u-AQP2 were measured at baseline and after infusion with 3% hypertonic saline. U-NKCC2, u-ENaCγ, u-AQP2 and plasma concentrations of vasopressin （p-AVP）, renin （PRC）, angiotensin Ⅱ （p-ANG Ⅱ） and aldosterone （p-Aldo） were measured, by radioimmunoassay. Central blood pressure was estimated by applanation tonometry and body fuid volumes were estimated by bio-impedance spectroscopy. General linear model with repeated measures or related samples Friedman’s two-way analysis was used to compare differences. Post hoc Bonferroni correction was used for multiple comparisons of post infusion periods to baseline within each treatment group.RESULTS： At baseline there were no differences in u-NKCC2, u-ENaCγ and u-AQP2. PRC, p-Ang Ⅱ and p-Aldo were increased during active treatments （P 〈 0.001）. After hypertonic saline, u-NKCC2 increased during amiloride （6% ± 34%; P = 0.081） and increased significantly during placebo （17% ± 24%; P = 0.010）. U-AQP2 increased signifcantly during amiloride （31% ± 22%; P 〈 0.001） and placebo （34% ± 27%; P 〈 0.001）, while u-NKCC2 and u-AQP2 did not change signifcantly during BFTZ （-7% ± 28%; P = 0.257 and 5% ± 16%; P = 0.261）. U- ENaCγ increased in all three groups （ P 〈 0.050）. PRC, AngⅡ and p-Aldo decreased to the same extent, while AVP increased, but to a smaller degree during BFTZ （ P = 0.048）. cDBP decreased significantly during BFTZ （P 〈 0.001）, but not during amiloride or placebo. There were no significant differences in body fuid volumes.CONCLUSION： After hypertonic saline, u-NKCC2 and u-AQP2 increased during amiloride, but not during BFTZ. Lower p-AVP during BFTZ potentially caused less stimulation of NKCC2 and AQP2 and subsequent lower reabsorption of water and sodium.
文摘Hypokalemia, defined as serum potassium below 3.5 mEq/L, can lead to severe complications such as arrhythmias and muscle paralysis, potentially resulting in rhabdomyolysis. The etiology of hypokalemia is often multifactorial, involving but not limited to gastrointestinal losses, renal losses, medication effects, and inadequate dietary intake. Chronic heavy alcohol use, obstructive sleep apnea (OSA), and the use of diuretics such as hydrochlorothiazide (HCTZ) are also significant contributing factors. Effective management requires thorough evaluation and investigation to effectively treat a patient. This case report aims to illustrate the diagnostic challenges and comprehensive treatment approach required in a patient with multiple comorbidities and severe hypokalemia, emphasizing the need for a multidisciplinary and comprehensive approach to address all underlying causes.
文摘目的探讨老年高血压患者利尿剂的使用及其对血钾和尿酸的影响。方法选择年龄≥70岁的高血压患者713例,根据入选时患者服用降压药物的情况,分为3组:利尿剂组332例、非利尿剂组270例和未用药组111例,测定血钾、尿酸和其他生化指标,并进行比较。结果利尿剂组和非利尿剂组患者血压显著低于未用药组(P<0.05)。与未用药组和非利尿剂组比较,利尿剂组患者尿酸、TG明显升高,血钾明显降低,差异有统计学意义(P<0.05,P<0.01)。利尿剂组低钾血症发生率明显高于非利尿剂组和未用药组(18.1% vs 10.4% vs 9.9%,P<0.05,P<0.01)。结论老年高血压患者中,使用利尿剂控制血压与使用非利尿降压药效果相似,但血钾水平低、低钾血症发生率高,血清尿酸升高;长期使用需注意血钾降低的防治。
