Starek Renato V M, Gomes Samirah A, Helou Claudia M B
Ambulatório de Nefrolitíase, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Laboratório de Pesquisa Básica da Unidade de Doenças Renais (LIM 12), Nefrologia, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.
Kidney Blood Press Res. 2024;49(1):987-1002. doi: 10.1159/000540953. Epub 2024 Oct 24.
The literature lacks whether metabolic alkalemia occurs in outpatients with hypercalciuric nephrolithiasis. Thus, we aim to investigate it because these patients are often treated with thiazides to reduce urinary calcium excretion. However, thiazides induce chloride losses due to the inhibition of Na-Cl cotransporter expressed in the renal distal tubule cells. Besides thiazide prescription, many of these patients are also supplemented with potassium citrate, which is an addition of alkali source in their bodies.
We collected clinical, demographic characteristics, and laboratory data from electronic medical charts of outpatients with calcium kidney stones followed in our institution from January 2013 to July 2021. We diagnosed those cases as metabolic alkalemia, in which the venous blood gas tests showed pH ≥7.46 and bicarbonate concentration >26 mEq/L. Then, we applied statistical analysis to compare distinct categories between patients with and without metabolic alkalemia.
We diagnosed metabolic alkalemia in 4.3% of hypercalciuric nephrolithiasis outpatients, and we verified that thiazides had been used in all of them except in one case. Furthermore, we observed that the amount of thiazide taken daily was higher in patients with metabolic alkalemia than in those without this imbalance. Additionally, hypokalemia was present in 37% of patients who developed metabolic alkalemia. We also found lower chloride, magnesium and ionic calcium serum concentrations in patients with metabolic alkalemia than in those without an acid-base disequilibrium.
Despite the low prevalence of metabolic alkalemia in hypercalciuric kidney stone formers, it is important to monitor these patients due to the high incidence of hypokalemia and the potential presence of other electrolyte disorders.
关于高钙尿性肾结石门诊患者是否会发生代谢性碱血症,目前尚无相关文献报道。因此,我们旨在对此进行研究,因为这些患者常使用噻嗪类药物来减少尿钙排泄。然而,噻嗪类药物会抑制肾远曲小管细胞中表达的钠 - 氯共转运体,从而导致氯化物丢失。除了使用噻嗪类药物外,这些患者中的许多人还补充了柠檬酸钾,这会增加体内的碱源。
我们收集了2013年1月至2021年7月在我院就诊的肾结石门诊患者的电子病历中的临床、人口统计学特征和实验室数据。我们将静脉血气检查显示pH≥7.46且碳酸氢盐浓度>26 mEq/L的病例诊断为代谢性碱血症。然后,我们进行统计分析,比较有和没有代谢性碱血症患者之间的不同类别。
我们在4.3%的高钙尿性肾结石门诊患者中诊断出代谢性碱血症,并且我们证实除了1例患者外,其余所有患者都使用过噻嗪类药物。此外,我们观察到发生代谢性碱血症的患者每日服用噻嗪类药物的量高于未发生这种失衡的患者。此外,发生代谢性碱血症的患者中有37%存在低钾血症。我们还发现,与没有酸碱失衡的患者相比,发生代谢性碱血症的患者血清氯化物、镁和离子钙浓度较低。
尽管高钙尿性肾结石患者中代谢性碱血症的患病率较低,但由于低钾血症的高发生率以及其他电解质紊乱的潜在存在,对这些患者进行监测很重要。