Resolution of hypertension during pregnancy in familial hyperkalemia and hypertension with the WNK4 Q565E mutation
Secondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. The purpose of...
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Published in | American journal of obstetrics and gynecology Vol. 192; no. 2; pp. 598 - 603 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
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Philadelphia, PA
Mosby, Inc
01.02.2005
Elsevier |
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Abstract | Secondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. The purpose of the study was to examine the course of pregnancy in hypertensive women with familial hyperkalemia and hypertension.
We prospectively studied 2 pregnancies of a woman with familial hyperkalemia and hypertension and the Q565E WNK4 mutation (pregnancies 1 and 2) and retrospectively studied the course of 2 pregnancies in another woman who was an affected member of this largest family described in the literature.
Both women had hypertension (170-190/105-110 mm Hg), hyperkalemia (5.3-6.0 mmol/L), and hypercalciuria, all of which were well controlled by thiazides. During pregnancies, thiazides were discontinued; throughout the pregnancy, the blood pressure remained normal at 120 to 130/75 to 85 mm Hg; however, hyperkalemia and hypercalciuria, which were documented in pregnancies 1 and 2, persisted. Renin and aldosterone levels (which were measured in pregnancies 1 and 2) rose towards their end. Four normal infants were born. A woman with familial hyperkalemia and hypertension of unknown molecular defect who had 2 pregnancies with hypertension exacerbation and premature deliveries was described previously.
In familial hyperkalemia and hypertension with the WNK4 mutation, pregnancy ameliorates hypertension; however, hyperkalemia and hypercalciuria persist. This dissociation may shed light on the pathogenesis of familial hyperkalemia and hypertension, on pregnancy-related hypertension, and on the mechanism of action of WNK4 kinase, a major regulator of cellular ion transport. |
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AbstractList | Secondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. The purpose of the study was to examine the course of pregnancy in hypertensive women with familial hyperkalemia and hypertension.
We prospectively studied 2 pregnancies of a woman with familial hyperkalemia and hypertension and the Q565E WNK4 mutation (pregnancies 1 and 2) and retrospectively studied the course of 2 pregnancies in another woman who was an affected member of this largest family described in the literature.
Both women had hypertension (170-190/105-110 mm Hg), hyperkalemia (5.3-6.0 mmol/L), and hypercalciuria, all of which were well controlled by thiazides. During pregnancies, thiazides were discontinued; throughout the pregnancy, the blood pressure remained normal at 120 to 130/75 to 85 mm Hg; however, hyperkalemia and hypercalciuria, which were documented in pregnancies 1 and 2, persisted. Renin and aldosterone levels (which were measured in pregnancies 1 and 2) rose towards their end. Four normal infants were born. A woman with familial hyperkalemia and hypertension of unknown molecular defect who had 2 pregnancies with hypertension exacerbation and premature deliveries was described previously.
In familial hyperkalemia and hypertension with the WNK4 mutation, pregnancy ameliorates hypertension; however, hyperkalemia and hypercalciuria persist. This dissociation may shed light on the pathogenesis of familial hyperkalemia and hypertension, on pregnancy-related hypertension, and on the mechanism of action of WNK4 kinase, a major regulator of cellular ion transport. OBJECTIVESecondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is familial hyperkalemia and hypertension, which is caused by mutations in the kinases WNK1 or WNK4 and other unknown molecular defects. The purpose of the study was to examine the course of pregnancy in hypertensive women with familial hyperkalemia and hypertension.STUDY DESIGNWe prospectively studied 2 pregnancies of a woman with familial hyperkalemia and hypertension and the Q565E WNK4 mutation (pregnancies 1 and 2) and retrospectively studied the course of 2 pregnancies in another woman who was an affected member of this largest family described in the literature.RESULTSBoth women had hypertension (170-190/105-110 mm Hg), hyperkalemia (5.3-6.0 mmol/L), and hypercalciuria, all of which were well controlled by thiazides. During pregnancies, thiazides were discontinued; throughout the pregnancy, the blood pressure remained normal at 120 to 130/75 to 85 mm Hg; however, hyperkalemia and hypercalciuria, which were documented in pregnancies 1 and 2, persisted. Renin and aldosterone levels (which were measured in pregnancies 1 and 2) rose towards their end. Four normal infants were born. A woman with familial hyperkalemia and hypertension of unknown molecular defect who had 2 pregnancies with hypertension exacerbation and premature deliveries was described previously.CONCLUSIONIn familial hyperkalemia and hypertension with the WNK4 mutation, pregnancy ameliorates hypertension; however, hyperkalemia and hypercalciuria persist. This dissociation may shed light on the pathogenesis of familial hyperkalemia and hypertension, on pregnancy-related hypertension, and on the mechanism of action of WNK4 kinase, a major regulator of cellular ion transport. |
Author | Mouallem, Meir Farfel, Zvi Shaharabany, Miriam Mayan, Haim Pauzner, Rachel |
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CitedBy_id | crossref_primary_10_1016_j_ecl_2011_01_007 crossref_primary_10_1177_1753495X221146331 crossref_primary_10_1111_j_1742_4658_2008_06318_x crossref_primary_10_1210_jc_2008_2572 crossref_primary_10_1016_j_jcf_2020_11_014 crossref_primary_10_1111_j_1365_2362_2005_01504_x crossref_primary_10_3390_genes14101878 |
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Keywords | Hypertension during pregnancy Hyperkalemia Pseudohypoaldosteronism type II Familial hyperkalemia and hypertension WNK kinase Hypertension Hydroelectrolytic balance disorder Enzyme Transferases Gynecology Cardiovascular disease Inorganic element Obstetrics Hypertension during pregnancy Familial hyperkalemia and hypertension Pseudohypoaldo- steronism type II Hyperkalemia WNK kinase Pregnancy Hyperkaliemia Metabolic disorder Kinase Female Genetics Mutation Potassium |
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Snippet | Secondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension is... OBJECTIVESecondary hypertension during pregnancy usually carries high maternal and fetal morbidity and mortality rates. A rare form of monogenic hypertension... |
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SubjectTerms | Adult Biological and medical sciences Familial hyperkalemia and hypertension Female Gynecology. Andrology. Obstetrics Humans Hyperkalemia Hyperkalemia - genetics Hyperkalemia - physiopathology Hypertension - genetics Hypertension - physiopathology Hypertension during pregnancy Medical sciences Middle Aged Mutation Pregnancy Pregnancy Complications, Cardiovascular - physiopathology Protein-Serine-Threonine Kinases - genetics Pseudohypoaldosteronism type II WNK kinase |
Title | Resolution of hypertension during pregnancy in familial hyperkalemia and hypertension with the WNK4 Q565E mutation |
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