hypokalemia | definition

abnormally decreased blood levels of potassium


Source:

Betts, J. G., Young, K. A., Wise, J. A., Johnson, E., Poe, B., Kruse, D. H., … DeSaix, P. (n.d.). Anatomy and Physiology. Houston, Texas: OpenStax. Access for free at: https://openstax.org/details/books/anatomy-and-physiology


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Keywords: definition, define, what is, meaning, thesaurus, synonyms, dictionary, encyclopedia, research, research article, research study, scientific literature, science topic

Impact of plasma potassium normalization on short-term mortality in patients with hypertension and hypokalemia or low normal potassium

Background: Hypokalemia is common in patients treated with antihypertensive drugs, but the impact of correcting hypokalemia is insufficiently studied. We examined the consequences of hypokalemia and borderline hypokalemia correction in patients with hypertension.

Methods: We identified 8976 patients with hypertension and plasma potassium concentrations ≤3.7 mmol/L within 100 days from combination antihypertensive therapy initiation. The first measurement between 6 and 100 days after the episode with potassium ≤3.7 mmol/L was retained. We investigated all-cause and cardiovascular mortality within 60-days from the second potassium measurement using Cox regression. Mortality was examined for seven predefined potassium intervals derived from the second measurement: 1.5-2.9 mmol/L (n = 271), 3.0-3.4 mmol/L (n = 1341), 3.5-3.7 (n = 1982) mmol/L, 3.8-4.0 mmol/L (n = 2398, reference), 4.1-4.6 mmol/L (n = 2498), 4.7-5.0 mmol/L (n = 352) and 5.1-7.1 mmol/L (n = 134).

Results: Multivariable analysis showed that potassium concentrations 1.5-2.9 mmol/L, 3.0-3.4 mmol/L, 4.7-5.0 mmol/L and 5.1-7.1 mmol/L were associated with increased all-cause mortality (HR 2.39, 95% CI 1.66-3.43; HR 1.36, 95% CI 1.04-1.78; HR 2.36, 95% CI 1.68-3.30 and HR 2.62, 95% CI 1.73-3.98, respectively). Potassium levels <3.0 and > 4.6 mmol/L were associated with increased cardiovascular mortality. The adjusted standardized 60-day mortality risks in the seven strata were: 11.7% (95% CI 8.3-15.0%), 7.1% (95% CI 5.8-8.5%), 6.4% (95% CI 5.3-7.5%), 5.4% (4.5-6.3%), 6.3% (5.4-7.2%), 11.6% (95% CI 8.7-14.6%) and 12.6% (95% CI 8.2-16.9%), respectively.

Conclusions: Persistent hypokalemia was frequent and associated with increased all-cause and cardiovascular mortality. Increase in potassium to levels > 4.6 mmol/L in patients with initial hypokalemia or low normal potassium was associated with increased all-cause and cardiovascular mortality.

https://pubmed.ncbi.nlm.nih.gov/32838735/

Apparent mineralocorticoid excess caused by novel compound heterozygous mutations in HSD11B2 and characterized by early-onset hypertension and hypokalemia

Purpose: Apparent mineralocorticoid excess (AME) is an ultrarare autosomal recessive disorder resulting from deficiency of 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) caused by mutations in HSD11B2. The purpose of this study was to identify novel compound heterozygous HSD11B2 mutations in a Chinese pedigree with AME and conduct a systematic review evaluating the AME clinical features associated with HSD11B2 mutations.

Methods: Next-generation sequencing was performed in the proband, and Sanger sequencing was used to identify candidate variants in family members, 100 hypertensives, and 100 healthy controls. A predicted structure of 11βHSD2 was constructed by in silico modeling. A systematic review was used to identify cases of HSD11B2-related AME. Data for genotyping and clinical characterizations and complications were extracted.

Results: Next-generation sequencing showed novel compound heterozygous mutations (c.343_348del and c.1099_1101del) in the proband with early-onset hypertension and hypokalemia. Sanger sequencing verified the monoallelic form of the same mutations in five other relatives but not in 100 hypertensives or 100 healthy subjects. In silico structural modeling showed that compound mutations may simultaneously perturb the substrate and coenzyme binding pocket. A systematic review of 101 AME patients with 54 HSD11B2 mutations revealed early-onset hypertension, hypokalemia and homozygous mutations as common features. The homozygous HSD11B2 mutations correlated with low birth weight (r = 0.285, P = 0.02).

Conclusions: We report novel compound heterozygous HSD11B2 mutations in a Chinese teenager with early-onset hypertension, and enriched genotypic and phenotypic spectrums in AME. Genetic testing helps early diagnosis and treatment for AME patients, which may avoid target organ damage.

https://pubmed.ncbi.nlm.nih.gov/32816205/

Severe asymptomatic hypokalemia associated with prolonged licorice ingestion: A case report

Rationale: Excessive ingestion of licorice can cause pseudohyperaldosteronism. A few case reports in the available literature have described significant hypokalemia secondary to licorice consumption with clinical manifestations of muscle weakness, paralysis, or severe hypertension. To our knowledge, no report has discussed severe asymptomatic hypokalemia associated with licorice consumption.

Patient concerns: A 79-year-old man presented to the urology clinic with a several-month history of urinary frequency and a weak stream. Routine laboratory investigations revealed serum potassium (K) level of 1.8 mmol/L, and he was immediately admitted to the nephrology department.

Diagnoses: He was in a good state of health, and systemic and neurological examinations were unremarkable. However, laboratory investigations revealed severe hypokalemia and metabolic alkalosis accompanied with renal K wasting and hypertension, suggesting a state of mineralocorticoid excess. Hormonal studies revealed low serum renin and aldosterone but normal serum cortisol levels. Detailed history taking revealed that he had used licorice tea daily during the preceding 18 months.

Interventions and outcome: The patient’s serum K returned to normal levels after vigorous K replacement and discontinuation of licorice intake. He was also diagnosed with benign prostatic hyperplasia during hospitalization and was treated.

Lessons: Chronic licorice ingestion can precipitate severe hypokalemia, although patients may remain asymptomatic. This case report indicates that the severity of a patient’s clinical presentation depends on individual susceptibility, as well as the dose and duration of licorice intake.

https://pubmed.ncbi.nlm.nih.gov/32791684/

Hypokalemia is frequent and has prognostic implications in stable patients attending the emergency department

Background: Potassium disturbances are associated with adverse prognosis in patients with chronic conditions. Its prognostic implications in stable patients attending the emergency department (ED) is poorly described.

Aims: This study aimed to assess the prevalence of dyskalemia, describe its predisposing factors and prognostic associations in a population presenting the ED without unstable medical illness.

Methods: Post-hoc analysis of a prospective, cross-sectional, multicenter study in the ED of 11 French academic hospitals over a period of 8 weeks. All adults presenting to the ED during this period were included, except instances of self-drug poisoning, inability to complete self-medication questionnaire, presence of an unstable medical illness and decline to participate in the study. All-cause hospitalization or deaths were assessed.

Results: A total of 1242 patients were included. The mean age was 57.2±22.3 years, 51% were female. The distribution according to potassium concentrations was: hypokalemia<4mmol/L(n = 620, 49.9%), normokalemia 4-5mmol/L(n = 549, 44.2%) and hyperkalemia >5mmol/L(n = 73, 0,6%). The proportion of patients with a kalemia<3.5mmol/L was 8% (n = 101). Renal insufficiency (OR [95% CI] = 3.56[1.94-6.52], p-value <0.001) and hemoglobin <12g/dl (OR [95% CI] = 2.62[1.50-4.60], p-value = 0.001) were associated with hyperkalemia. Female sex (OR [95% CI] = 1.31[1.03-1.66], p-value = 0.029), age <45years (OR [95% CI] = 1.69 [1.20-2.37], p-value = 0.002) and the use of thiazide diuretics (OR [95% CI] = 2.04 [1.28-3.32], p-value = 0.003), were associated with hypokalemia<4mmol/l. Two patients died in the ED and 629 (52.7%) were hospitalized. Hypokalemia <3.5mmol/L was independently associated with increased odds of hospitalization or death (OR [95% CI] = 1.47 [1.00-2.15], p-value = 0.048).

Conclusions: Hypokalemia is frequently found in the ED and was associated with worse outcomes in a low-risk ED population.

https://pubmed.ncbi.nlm.nih.gov/32750075/

In the presence of hypokalemia and hypomagnesemia; remember Gitelman syndrome

Background: Hypokalemia and hypomagnesemia caused due to renal losses with chloride-resistant metabolic alkalosis in normotensive patients should remind clinicians of the rare inherited tubulopathy, Gitelman syndrome. Its diagnosis is further strengthened by the presence of consanguinity and the absence of kaliuretic medications. A definitive diagnosis should be based on genetic testing.

Case report: We present the cases of three asymptomatic adult patients who were genetically (mutation in the SCL12A3 gene) diagnosed with Gitelman syndrome of different severity and response to therapy in terms of hypokalemia, hypomagnesemia, and metabolic alkalosis.

Conclusion: This lifelong disease could cause life-threatening conditions due to the cardiac complications of hypokalemia in some of the affected patients. Therefore, it is necessary to be aware of the appropriate diagnosis and treatment for patients admitted to the clinic with hypokalemia, hypomagnesemia, hypocalciuria, and hyperreninemia. HIPPOKRATIA 2019, 23(4): 175-178.

https://pubmed.ncbi.nlm.nih.gov/32742169/

Type 2 diabetes mellitus caused by Gitelman syndrome-related hypokalemia: A case report

Introduction: Gitelman syndrome (GS) is an autosomal-recessive disease caused by SLC12A3 gene mutations. It is characterized by hypokalemic metabolic alkalosis in combination with hypomagnesemia and hypocalciuria. Recently, patients with GS are found at an increased risk for developing type 2 diabetes mellitus (T2DM). However, diagnosis of hyperglycemia in GS patients has not been thoroughly investigated, and family studies on SLC12A3 mutations and glucose metabolism are rare. Whether treatment including potassium and magnesium supplements, and spironolactone can ameliorate impaired glucose tolerance in GS patients, also needs to be investigated.

Patient concerns: We examined a 55-year-old Chinese male with intermittent fatigue and persistent hypokalemia for 17 years.

Diagnoses: Based on the results of the clinical data, including electrolytes, oral glucose tolerance test (OGTT), and genetic analysis of the SLC12A3 gene, GS and T2DM were newly diagnosed in the patient. Two mutations of the SLC12A3 gene were found in the patient, one was a missense mutation p.N359K in exon 8, and the other was a novel insert mutation p.I262delinsIIGVVSV in exon 6. SLC12A3 genetic analysis and OGTT of 9 other family members within 3 generations were also performed. Older brother, youngest sister, and son of the patient carried the p.N359K mutation in exon 8. The older brother and the youngest sister were diagnosed with T2DM and impaired glucose tolerance by OGTT, respectively.

Interventions: The patient was prescribed potassium and magnesium (potassium magnesium aspartate, potassium chloride) oral supplements and spironolactone. The patient was also suggested to maintain a high potassium diet. Acarbose was used to maintain the blood glucose levels.

Outcomes: The electrolyte imbalance including hypokalemia and hypomagnesemia, and hyperglycemia were improved with a remission of the clinical manifestations.

Conclusion: GS is one of the causes for manifestation of hypokalemia. SLC12A3 genetic analysis plays an important role in diagnosis of GS. Chinese male GS patients characterized with heterozygous SLC12A3 mutation should be careful toward occurrence of T2DM. Moreover, the patients with only 1 SLC12A3 mutant allele should pay regular attention to blood potassium and glucose levels. GS treatment with potassium and magnesium supplements, and spironolactone can improve impaired glucose metabolism.

https://pubmed.ncbi.nlm.nih.gov/32702863/


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