Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report

Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in ob...
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Gespeichert in:

Autor*in:	Tanaka, Kenichi [verfasserIn] Mori, Hiroko Sakamoto, Rieko Matsumoto, Shirou Mitsubuchi, Hiroshi Nakamura, Kimitoshi Iwai, Masanori

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Neonatal nonoliguric hyperkalemia Progressive early-onset hyperkalemia Maternal hypermagnesemia Na /K -ATPase Renal outer medullary potassium channel

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: BMC pediatrics - London : BioMed Central, 2001, 18(2018), 1 vom: 13. Feb.
Übergeordnetes Werk:	volume:18 ; year:2018 ; number:1 ; day:13 ; month:02

Links:	Volltext

DOI / URN:	10.1186/s12887-018-1048-4

Katalog-ID:	SPR027766519

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520			\|a Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery.
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allfields	10.1186/s12887-018-1048-4 doi (DE-627)SPR027766519 (SPR)s12887-018-1048-4-e DE-627 ger DE-627 rakwb eng Tanaka, Kenichi verfasserin aut Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213 Mori, Hiroko aut Sakamoto, Rieko aut Matsumoto, Shirou aut Mitsubuchi, Hiroshi aut Nakamura, Kimitoshi aut Iwai, Masanori (orcid)0000-0002-9173-0652 aut Enthalten in BMC pediatrics London : BioMed Central, 2001 18(2018), 1 vom: 13. Feb. (DE-627)326643621 (DE-600)2041342-7 1471-2431 nnns volume:18 year:2018 number:1 day:13 month:02 https://dx.doi.org/10.1186/s12887-018-1048-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 13 02
spelling	10.1186/s12887-018-1048-4 doi (DE-627)SPR027766519 (SPR)s12887-018-1048-4-e DE-627 ger DE-627 rakwb eng Tanaka, Kenichi verfasserin aut Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213 Mori, Hiroko aut Sakamoto, Rieko aut Matsumoto, Shirou aut Mitsubuchi, Hiroshi aut Nakamura, Kimitoshi aut Iwai, Masanori (orcid)0000-0002-9173-0652 aut Enthalten in BMC pediatrics London : BioMed Central, 2001 18(2018), 1 vom: 13. Feb. (DE-627)326643621 (DE-600)2041342-7 1471-2431 nnns volume:18 year:2018 number:1 day:13 month:02 https://dx.doi.org/10.1186/s12887-018-1048-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 13 02
allfields_unstemmed	10.1186/s12887-018-1048-4 doi (DE-627)SPR027766519 (SPR)s12887-018-1048-4-e DE-627 ger DE-627 rakwb eng Tanaka, Kenichi verfasserin aut Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213 Mori, Hiroko aut Sakamoto, Rieko aut Matsumoto, Shirou aut Mitsubuchi, Hiroshi aut Nakamura, Kimitoshi aut Iwai, Masanori (orcid)0000-0002-9173-0652 aut Enthalten in BMC pediatrics London : BioMed Central, 2001 18(2018), 1 vom: 13. Feb. (DE-627)326643621 (DE-600)2041342-7 1471-2431 nnns volume:18 year:2018 number:1 day:13 month:02 https://dx.doi.org/10.1186/s12887-018-1048-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 13 02
allfieldsGer	10.1186/s12887-018-1048-4 doi (DE-627)SPR027766519 (SPR)s12887-018-1048-4-e DE-627 ger DE-627 rakwb eng Tanaka, Kenichi verfasserin aut Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213 Mori, Hiroko aut Sakamoto, Rieko aut Matsumoto, Shirou aut Mitsubuchi, Hiroshi aut Nakamura, Kimitoshi aut Iwai, Masanori (orcid)0000-0002-9173-0652 aut Enthalten in BMC pediatrics London : BioMed Central, 2001 18(2018), 1 vom: 13. Feb. (DE-627)326643621 (DE-600)2041342-7 1471-2431 nnns volume:18 year:2018 number:1 day:13 month:02 https://dx.doi.org/10.1186/s12887-018-1048-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 13 02
allfieldsSound	10.1186/s12887-018-1048-4 doi (DE-627)SPR027766519 (SPR)s12887-018-1048-4-e DE-627 ger DE-627 rakwb eng Tanaka, Kenichi verfasserin aut Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213 Mori, Hiroko aut Sakamoto, Rieko aut Matsumoto, Shirou aut Mitsubuchi, Hiroshi aut Nakamura, Kimitoshi aut Iwai, Masanori (orcid)0000-0002-9173-0652 aut Enthalten in BMC pediatrics London : BioMed Central, 2001 18(2018), 1 vom: 13. Feb. (DE-627)326643621 (DE-600)2041342-7 1471-2431 nnns volume:18 year:2018 number:1 day:13 month:02 https://dx.doi.org/10.1186/s12887-018-1048-4 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 18 2018 1 13 02
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Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. 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author	Tanaka, Kenichi
spellingShingle	Tanaka, Kenichi misc Neonatal nonoliguric hyperkalemia misc Progressive early-onset hyperkalemia misc Maternal hypermagnesemia misc Na misc /K misc -ATPase misc Renal outer medullary potassium channel Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
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topic_title	Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report Neonatal nonoliguric hyperkalemia (dpeaa)DE-He213 Progressive early-onset hyperkalemia (dpeaa)DE-He213 Maternal hypermagnesemia (dpeaa)DE-He213 Na (dpeaa)DE-He213 /K (dpeaa)DE-He213 -ATPase (dpeaa)DE-He213 Renal outer medullary potassium channel (dpeaa)DE-He213
topic	misc Neonatal nonoliguric hyperkalemia misc Progressive early-onset hyperkalemia misc Maternal hypermagnesemia misc Na misc /K misc -ATPase misc Renal outer medullary potassium channel
topic_unstemmed	misc Neonatal nonoliguric hyperkalemia misc Progressive early-onset hyperkalemia misc Maternal hypermagnesemia misc Na misc /K misc -ATPase misc Renal outer medullary potassium channel
topic_browse	misc Neonatal nonoliguric hyperkalemia misc Progressive early-onset hyperkalemia misc Maternal hypermagnesemia misc Na misc /K misc -ATPase misc Renal outer medullary potassium channel
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title	Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
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title_full	Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
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title_sort	early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
title_auth	Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
abstract	Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. © The Author(s). 2018
abstractGer	Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. © The Author(s). 2018
abstract_unstemmed	Background Neonatal nonoliguric hyperkalemia (NOHK) is a metabolic abnormality that occurs in extremely premature neonates at approximately 24 h after birth and is mainly due to the immature functioning of the sodium ($ Na^{+} $)/potassium ($ K^{+} $) pump. Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery. © The Author(s). 2018
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title_short	Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report
url	https://dx.doi.org/10.1186/s12887-018-1048-4
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author2	Mori, Hiroko Sakamoto, Rieko Matsumoto, Shirou Mitsubuchi, Hiroshi Nakamura, Kimitoshi Iwai, Masanori
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up_date	2024-07-03T15:01:46.648Z
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Magnesium sulfate is frequently used in obstetrical practice to prevent preterm labor and to treat preeclampsia; this medication can also cause hypermagnesemia and hyperkalemia by a mechanism that is different from that of NOHK. Herein, we report the first case of very early-onset neonatal hyperkalemia induced by maternal hypermagnesemia. Case presentation A neonate born at 32 weeks of gestation developed hyperkalemia ($ K^{+} $ 6.4 mmol/L) 2 h after birth. The neonate’s blood potassium concentration reached 7.0 mmol/L 4 h after birth, despite good urine output. The neonate and his mother had severe hypermagnesemia caused by intravenous infusion of magnesium sulfate given for tocolysis due to pre-term labor. Conclusion The early-onset hyperkalemia may have been caused by the accumulation of potassium ions transported through the placenta, the shift of potassium ions from the intracellular to the extracellular space in the infant due to the malfunctioning of the $ Na^{+} $/$ K^{+} $ pump and the inhibition of renal distal tube potassium ion secretion, there is a possibility that these mechanisms were induced by maternal and fetal hypermagnesemia after maternal magnesium sulfate administration. Because neonatal hyperkalemia poses a significant risk for the development of life-threatening cardiac arrhythmia, this case highlights the necessity of maternal blood magnesium monitoring during magnesium sulfate administration and neonatal blood potassium monitoring when there is severe maternal hypermagnesemia at delivery.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Neonatal nonoliguric hyperkalemia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Progressive early-onset hyperkalemia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Maternal hypermagnesemia</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Na</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">/K</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">-ATPase</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Renal outer medullary potassium channel</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mori, Hiroko</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sakamoto, Rieko</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Matsumoto, Shirou</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Mitsubuchi, Hiroshi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Nakamura, Kimitoshi</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Iwai, Masanori</subfield><subfield code="0">(orcid)0000-0002-9173-0652</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">BMC pediatrics</subfield><subfield code="d">London : BioMed Central, 2001</subfield><subfield code="g">18(2018), 1 vom: 13. 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Early-onset neonatal hyperkalemia associated with maternal hypermagnesemia: a case report

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