Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease
Abstract Background Hypomagnesemia (Hypo-Mg) predicts mortality and chronic kidney disease (CKD) progression. However, in CKD, its prevalence, kidney-intrinsic risk factors, and the effectiveness of oral magnesium (Mg) therapy on serum Mg levels is uncertain. Methods In a cross-sectional study enrol...
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| Veröffentlicht in: | Nephrology, dialysis, transplantation dialysis, transplantation, 2019-07, Vol.34 (7), p.1154-1162 |
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| creator | Oka, Tatsufumi Hamano, Takayuki Sakaguchi, Yusuke Yamaguchi, Satoshi Kubota, Keiichi Senda, Masamitsu Yonemoto, Sayoko Shimada, Karin Matsumoto, Ayumi Hashimoto, Nobuhiro Mori, Daisuke Monden, Chikako Takahashi, Atsushi Obi, Yoshitsugu Yamamoto, Ryohei Takabatake, Yoshitsugu Kaimori, Jun-Ya Moriyama, Toshiki Horio, Masaru Matsui, Isao Isaka, Yoshitaka |
| description | Abstract
Background
Hypomagnesemia (Hypo-Mg) predicts mortality and chronic kidney disease (CKD) progression. However, in CKD, its prevalence, kidney-intrinsic risk factors, and the effectiveness of oral magnesium (Mg) therapy on serum Mg levels is uncertain.
Methods
In a cross-sectional study enrolling pre-dialysis outpatients with CKD, the prevalence of electrolyte abnormalities (Mg, sodium, potassium, calcium and phosphorus) was compared. In an open-label randomized controlled trial (RCT), we randomly assigned CKD patients to either the magnesium oxide (MgO) or control arm. The outcome was serum Mg levels at 1 year.
Results
In 5126 patients, Hypo-Mg was the most common electrolyte abnormality (14.7%) with similar prevalence across stages of CKD. Positive proteinuria was a risk factor of Hypo-Mg (odds ratio 2.2; 95% confidence interval 1.2–4.0). However, stratifying the analyses by diabetes mellitus (DM), it was not significant in DM (Pinteraction = 0.04). We enrolled 114 patients in the RCT. Baseline analyses showed that higher proteinuria was associated with higher fractional excretion of Mg. This relationship between proteinuria and renal Mg wasting was mediated by urinary tubular markers in mediation analyses. In the MgO arm, higher proteinuria or tubular markers predicted a significantly lower 1-year increase in serum Mg. In patients with a urinary protein-to-creatinine ratio (uPCR) |
| doi_str_mv | 10.1093/ndt/gfy119 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2045273704</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/ndt/gfy119</oup_id><sourcerecordid>2045273704</sourcerecordid><originalsourceid>FETCH-LOGICAL-c467t-6ecd1371bab28615e2614526e4186e58ebde7241ab449d5cb5bc5ffa124edc0f3</originalsourceid><addsrcrecordid>eNp9kM1q3DAYRUVo6Ex-NnmAok0hBJxIsiyPuyshfxBIFs3afJY-z6i1pKkkU7ztk8fFaZZZ3cU9nMUh5IyzS86a8sqbfLXtJ86bA7LmUrFClJvqE1nPJy9YxZoVOUrpJ2OsEXX9maxEUzdKMb4mf59jyGj9GC0UkFLQFjIaGtHDQB1sPSY7OvoHUrZ-SwcEk2gOdDftw3Kjs_CNAtXBueApDqhzDMOUkULnQ3Qw2DxR66nexeCtpr-s8ThRYxNCwhNy2MOQ8PRtj8nL7c2P6_vi8enu4fr7Y6GlqnOhUBte1ryDTmwUr1AoLiuhUPKNwmqDncFaSA6dlI2pdFd1uup74EKi0awvj8n54t3H8HvElFtnk8ZhAI9hTK1gs64uayZn9GJBdQwpRezbfbQO4tRy1v5r3s7N26X5DH95846dQ_OO_o88A18XIIz7j0Sv1k2OVA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2045273704</pqid></control><display><type>article</type><title>Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Oka, Tatsufumi ; Hamano, Takayuki ; Sakaguchi, Yusuke ; Yamaguchi, Satoshi ; Kubota, Keiichi ; Senda, Masamitsu ; Yonemoto, Sayoko ; Shimada, Karin ; Matsumoto, Ayumi ; Hashimoto, Nobuhiro ; Mori, Daisuke ; Monden, Chikako ; Takahashi, Atsushi ; Obi, Yoshitsugu ; Yamamoto, Ryohei ; Takabatake, Yoshitsugu ; Kaimori, Jun-Ya ; Moriyama, Toshiki ; Horio, Masaru ; Matsui, Isao ; Isaka, Yoshitaka</creator><creatorcontrib>Oka, Tatsufumi ; Hamano, Takayuki ; Sakaguchi, Yusuke ; Yamaguchi, Satoshi ; Kubota, Keiichi ; Senda, Masamitsu ; Yonemoto, Sayoko ; Shimada, Karin ; Matsumoto, Ayumi ; Hashimoto, Nobuhiro ; Mori, Daisuke ; Monden, Chikako ; Takahashi, Atsushi ; Obi, Yoshitsugu ; Yamamoto, Ryohei ; Takabatake, Yoshitsugu ; Kaimori, Jun-Ya ; Moriyama, Toshiki ; Horio, Masaru ; Matsui, Isao ; Isaka, Yoshitaka</creatorcontrib><description>Abstract
Background
Hypomagnesemia (Hypo-Mg) predicts mortality and chronic kidney disease (CKD) progression. However, in CKD, its prevalence, kidney-intrinsic risk factors, and the effectiveness of oral magnesium (Mg) therapy on serum Mg levels is uncertain.
Methods
In a cross-sectional study enrolling pre-dialysis outpatients with CKD, the prevalence of electrolyte abnormalities (Mg, sodium, potassium, calcium and phosphorus) was compared. In an open-label randomized controlled trial (RCT), we randomly assigned CKD patients to either the magnesium oxide (MgO) or control arm. The outcome was serum Mg levels at 1 year.
Results
In 5126 patients, Hypo-Mg was the most common electrolyte abnormality (14.7%) with similar prevalence across stages of CKD. Positive proteinuria was a risk factor of Hypo-Mg (odds ratio 2.2; 95% confidence interval 1.2–4.0). However, stratifying the analyses by diabetes mellitus (DM), it was not significant in DM (Pinteraction = 0.04). We enrolled 114 patients in the RCT. Baseline analyses showed that higher proteinuria was associated with higher fractional excretion of Mg. This relationship between proteinuria and renal Mg wasting was mediated by urinary tubular markers in mediation analyses. In the MgO arm, higher proteinuria or tubular markers predicted a significantly lower 1-year increase in serum Mg. In patients with a urinary protein-to-creatinine ratio (uPCR) <0.3 g/gCre, serum Mg at 1 year was 2.4 and 2.0 mg/dL in the MgO and control arms, respectively (P < 0.001), with no significant between-group difference in patients whose uPCR was ≥0.3 g/gCre (Pinteraction=0.001).
Conclusions
Proteinuria leads to renal Mg wasting through tubular injuries, which explains the high prevalence of Hypo-Mg in CKD.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfy119</identifier><identifier>PMID: 29796601</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Adult ; Biomarkers - blood ; Biomarkers - urine ; Cross-Sectional Studies ; Disease Progression ; Electrolytes - metabolism ; Female ; Follow-Up Studies ; Humans ; Japan - epidemiology ; Kidney Function Tests ; Magnesium - metabolism ; Magnesium Oxide - therapeutic use ; Male ; Middle Aged ; Outpatients ; Prevalence ; Proteinuria - complications ; Proteinuria - drug therapy ; Proteinuria - metabolism ; Renal Insufficiency, Chronic - complications ; Renal Insufficiency, Chronic - drug therapy ; Renal Insufficiency, Chronic - metabolism ; Renal Tubular Transport, Inborn Errors - epidemiology ; Renal Tubular Transport, Inborn Errors - etiology ; Renal Tubular Transport, Inborn Errors - prevention & control ; Retrospective Studies</subject><ispartof>Nephrology, dialysis, transplantation, 2019-07, Vol.34 (7), p.1154-1162</ispartof><rights>The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. 2018</rights><rights>The Author(s) 2018. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c467t-6ecd1371bab28615e2614526e4186e58ebde7241ab449d5cb5bc5ffa124edc0f3</citedby><cites>FETCH-LOGICAL-c467t-6ecd1371bab28615e2614526e4186e58ebde7241ab449d5cb5bc5ffa124edc0f3</cites><orcidid>0000-0001-7032-4383</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1578,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29796601$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Oka, Tatsufumi</creatorcontrib><creatorcontrib>Hamano, Takayuki</creatorcontrib><creatorcontrib>Sakaguchi, Yusuke</creatorcontrib><creatorcontrib>Yamaguchi, Satoshi</creatorcontrib><creatorcontrib>Kubota, Keiichi</creatorcontrib><creatorcontrib>Senda, Masamitsu</creatorcontrib><creatorcontrib>Yonemoto, Sayoko</creatorcontrib><creatorcontrib>Shimada, Karin</creatorcontrib><creatorcontrib>Matsumoto, Ayumi</creatorcontrib><creatorcontrib>Hashimoto, Nobuhiro</creatorcontrib><creatorcontrib>Mori, Daisuke</creatorcontrib><creatorcontrib>Monden, Chikako</creatorcontrib><creatorcontrib>Takahashi, Atsushi</creatorcontrib><creatorcontrib>Obi, Yoshitsugu</creatorcontrib><creatorcontrib>Yamamoto, Ryohei</creatorcontrib><creatorcontrib>Takabatake, Yoshitsugu</creatorcontrib><creatorcontrib>Kaimori, Jun-Ya</creatorcontrib><creatorcontrib>Moriyama, Toshiki</creatorcontrib><creatorcontrib>Horio, Masaru</creatorcontrib><creatorcontrib>Matsui, Isao</creatorcontrib><creatorcontrib>Isaka, Yoshitaka</creatorcontrib><title>Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol Dial Transplant</addtitle><description>Abstract
Background
Hypomagnesemia (Hypo-Mg) predicts mortality and chronic kidney disease (CKD) progression. However, in CKD, its prevalence, kidney-intrinsic risk factors, and the effectiveness of oral magnesium (Mg) therapy on serum Mg levels is uncertain.
Methods
In a cross-sectional study enrolling pre-dialysis outpatients with CKD, the prevalence of electrolyte abnormalities (Mg, sodium, potassium, calcium and phosphorus) was compared. In an open-label randomized controlled trial (RCT), we randomly assigned CKD patients to either the magnesium oxide (MgO) or control arm. The outcome was serum Mg levels at 1 year.
Results
In 5126 patients, Hypo-Mg was the most common electrolyte abnormality (14.7%) with similar prevalence across stages of CKD. Positive proteinuria was a risk factor of Hypo-Mg (odds ratio 2.2; 95% confidence interval 1.2–4.0). However, stratifying the analyses by diabetes mellitus (DM), it was not significant in DM (Pinteraction = 0.04). We enrolled 114 patients in the RCT. Baseline analyses showed that higher proteinuria was associated with higher fractional excretion of Mg. This relationship between proteinuria and renal Mg wasting was mediated by urinary tubular markers in mediation analyses. In the MgO arm, higher proteinuria or tubular markers predicted a significantly lower 1-year increase in serum Mg. In patients with a urinary protein-to-creatinine ratio (uPCR) <0.3 g/gCre, serum Mg at 1 year was 2.4 and 2.0 mg/dL in the MgO and control arms, respectively (P < 0.001), with no significant between-group difference in patients whose uPCR was ≥0.3 g/gCre (Pinteraction=0.001).
Conclusions
Proteinuria leads to renal Mg wasting through tubular injuries, which explains the high prevalence of Hypo-Mg in CKD.</description><subject>Adult</subject><subject>Biomarkers - blood</subject><subject>Biomarkers - urine</subject><subject>Cross-Sectional Studies</subject><subject>Disease Progression</subject><subject>Electrolytes - metabolism</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Japan - epidemiology</subject><subject>Kidney Function Tests</subject><subject>Magnesium - metabolism</subject><subject>Magnesium Oxide - therapeutic use</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Outpatients</subject><subject>Prevalence</subject><subject>Proteinuria - complications</subject><subject>Proteinuria - drug therapy</subject><subject>Proteinuria - metabolism</subject><subject>Renal Insufficiency, Chronic - complications</subject><subject>Renal Insufficiency, Chronic - drug therapy</subject><subject>Renal Insufficiency, Chronic - metabolism</subject><subject>Renal Tubular Transport, Inborn Errors - epidemiology</subject><subject>Renal Tubular Transport, Inborn Errors - etiology</subject><subject>Renal Tubular Transport, Inborn Errors - prevention & control</subject><subject>Retrospective Studies</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1q3DAYRUVo6Ex-NnmAok0hBJxIsiyPuyshfxBIFs3afJY-z6i1pKkkU7ztk8fFaZZZ3cU9nMUh5IyzS86a8sqbfLXtJ86bA7LmUrFClJvqE1nPJy9YxZoVOUrpJ2OsEXX9maxEUzdKMb4mf59jyGj9GC0UkFLQFjIaGtHDQB1sPSY7OvoHUrZ-SwcEk2gOdDftw3Kjs_CNAtXBueApDqhzDMOUkULnQ3Qw2DxR66nexeCtpr-s8ThRYxNCwhNy2MOQ8PRtj8nL7c2P6_vi8enu4fr7Y6GlqnOhUBte1ryDTmwUr1AoLiuhUPKNwmqDncFaSA6dlI2pdFd1uup74EKi0awvj8n54t3H8HvElFtnk8ZhAI9hTK1gs64uayZn9GJBdQwpRezbfbQO4tRy1v5r3s7N26X5DH95846dQ_OO_o88A18XIIz7j0Sv1k2OVA</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Oka, Tatsufumi</creator><creator>Hamano, Takayuki</creator><creator>Sakaguchi, Yusuke</creator><creator>Yamaguchi, Satoshi</creator><creator>Kubota, Keiichi</creator><creator>Senda, Masamitsu</creator><creator>Yonemoto, Sayoko</creator><creator>Shimada, Karin</creator><creator>Matsumoto, Ayumi</creator><creator>Hashimoto, Nobuhiro</creator><creator>Mori, Daisuke</creator><creator>Monden, Chikako</creator><creator>Takahashi, Atsushi</creator><creator>Obi, Yoshitsugu</creator><creator>Yamamoto, Ryohei</creator><creator>Takabatake, Yoshitsugu</creator><creator>Kaimori, Jun-Ya</creator><creator>Moriyama, Toshiki</creator><creator>Horio, Masaru</creator><creator>Matsui, Isao</creator><creator>Isaka, Yoshitaka</creator><general>Oxford University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7032-4383</orcidid></search><sort><creationdate>20190701</creationdate><title>Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease</title><author>Oka, Tatsufumi ; Hamano, Takayuki ; Sakaguchi, Yusuke ; Yamaguchi, Satoshi ; Kubota, Keiichi ; Senda, Masamitsu ; Yonemoto, Sayoko ; Shimada, Karin ; Matsumoto, Ayumi ; Hashimoto, Nobuhiro ; Mori, Daisuke ; Monden, Chikako ; Takahashi, Atsushi ; Obi, Yoshitsugu ; Yamamoto, Ryohei ; Takabatake, Yoshitsugu ; Kaimori, Jun-Ya ; Moriyama, Toshiki ; Horio, Masaru ; Matsui, Isao ; Isaka, Yoshitaka</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c467t-6ecd1371bab28615e2614526e4186e58ebde7241ab449d5cb5bc5ffa124edc0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Biomarkers - blood</topic><topic>Biomarkers - urine</topic><topic>Cross-Sectional Studies</topic><topic>Disease Progression</topic><topic>Electrolytes - metabolism</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Humans</topic><topic>Japan - epidemiology</topic><topic>Kidney Function Tests</topic><topic>Magnesium - metabolism</topic><topic>Magnesium Oxide - therapeutic use</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Outpatients</topic><topic>Prevalence</topic><topic>Proteinuria - complications</topic><topic>Proteinuria - drug therapy</topic><topic>Proteinuria - metabolism</topic><topic>Renal Insufficiency, Chronic - complications</topic><topic>Renal Insufficiency, Chronic - drug therapy</topic><topic>Renal Insufficiency, Chronic - metabolism</topic><topic>Renal Tubular Transport, Inborn Errors - epidemiology</topic><topic>Renal Tubular Transport, Inborn Errors - etiology</topic><topic>Renal Tubular Transport, Inborn Errors - prevention & control</topic><topic>Retrospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Oka, Tatsufumi</creatorcontrib><creatorcontrib>Hamano, Takayuki</creatorcontrib><creatorcontrib>Sakaguchi, Yusuke</creatorcontrib><creatorcontrib>Yamaguchi, Satoshi</creatorcontrib><creatorcontrib>Kubota, Keiichi</creatorcontrib><creatorcontrib>Senda, Masamitsu</creatorcontrib><creatorcontrib>Yonemoto, Sayoko</creatorcontrib><creatorcontrib>Shimada, Karin</creatorcontrib><creatorcontrib>Matsumoto, Ayumi</creatorcontrib><creatorcontrib>Hashimoto, Nobuhiro</creatorcontrib><creatorcontrib>Mori, Daisuke</creatorcontrib><creatorcontrib>Monden, Chikako</creatorcontrib><creatorcontrib>Takahashi, Atsushi</creatorcontrib><creatorcontrib>Obi, Yoshitsugu</creatorcontrib><creatorcontrib>Yamamoto, Ryohei</creatorcontrib><creatorcontrib>Takabatake, Yoshitsugu</creatorcontrib><creatorcontrib>Kaimori, Jun-Ya</creatorcontrib><creatorcontrib>Moriyama, Toshiki</creatorcontrib><creatorcontrib>Horio, Masaru</creatorcontrib><creatorcontrib>Matsui, Isao</creatorcontrib><creatorcontrib>Isaka, Yoshitaka</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Oka, Tatsufumi</au><au>Hamano, Takayuki</au><au>Sakaguchi, Yusuke</au><au>Yamaguchi, Satoshi</au><au>Kubota, Keiichi</au><au>Senda, Masamitsu</au><au>Yonemoto, Sayoko</au><au>Shimada, Karin</au><au>Matsumoto, Ayumi</au><au>Hashimoto, Nobuhiro</au><au>Mori, Daisuke</au><au>Monden, Chikako</au><au>Takahashi, Atsushi</au><au>Obi, Yoshitsugu</au><au>Yamamoto, Ryohei</au><au>Takabatake, Yoshitsugu</au><au>Kaimori, Jun-Ya</au><au>Moriyama, Toshiki</au><au>Horio, Masaru</au><au>Matsui, Isao</au><au>Isaka, Yoshitaka</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><addtitle>Nephrol Dial Transplant</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>34</volume><issue>7</issue><spage>1154</spage><epage>1162</epage><pages>1154-1162</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><abstract>Abstract
Background
Hypomagnesemia (Hypo-Mg) predicts mortality and chronic kidney disease (CKD) progression. However, in CKD, its prevalence, kidney-intrinsic risk factors, and the effectiveness of oral magnesium (Mg) therapy on serum Mg levels is uncertain.
Methods
In a cross-sectional study enrolling pre-dialysis outpatients with CKD, the prevalence of electrolyte abnormalities (Mg, sodium, potassium, calcium and phosphorus) was compared. In an open-label randomized controlled trial (RCT), we randomly assigned CKD patients to either the magnesium oxide (MgO) or control arm. The outcome was serum Mg levels at 1 year.
Results
In 5126 patients, Hypo-Mg was the most common electrolyte abnormality (14.7%) with similar prevalence across stages of CKD. Positive proteinuria was a risk factor of Hypo-Mg (odds ratio 2.2; 95% confidence interval 1.2–4.0). However, stratifying the analyses by diabetes mellitus (DM), it was not significant in DM (Pinteraction = 0.04). We enrolled 114 patients in the RCT. Baseline analyses showed that higher proteinuria was associated with higher fractional excretion of Mg. This relationship between proteinuria and renal Mg wasting was mediated by urinary tubular markers in mediation analyses. In the MgO arm, higher proteinuria or tubular markers predicted a significantly lower 1-year increase in serum Mg. In patients with a urinary protein-to-creatinine ratio (uPCR) <0.3 g/gCre, serum Mg at 1 year was 2.4 and 2.0 mg/dL in the MgO and control arms, respectively (P < 0.001), with no significant between-group difference in patients whose uPCR was ≥0.3 g/gCre (Pinteraction=0.001).
Conclusions
Proteinuria leads to renal Mg wasting through tubular injuries, which explains the high prevalence of Hypo-Mg in CKD.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>29796601</pmid><doi>10.1093/ndt/gfy119</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-7032-4383</orcidid></addata></record> |
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| identifier | ISSN: 0931-0509 |
| ispartof | Nephrology, dialysis, transplantation, 2019-07, Vol.34 (7), p.1154-1162 |
| issn | 0931-0509 1460-2385 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2045273704 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Biomarkers - blood Biomarkers - urine Cross-Sectional Studies Disease Progression Electrolytes - metabolism Female Follow-Up Studies Humans Japan - epidemiology Kidney Function Tests Magnesium - metabolism Magnesium Oxide - therapeutic use Male Middle Aged Outpatients Prevalence Proteinuria - complications Proteinuria - drug therapy Proteinuria - metabolism Renal Insufficiency, Chronic - complications Renal Insufficiency, Chronic - drug therapy Renal Insufficiency, Chronic - metabolism Renal Tubular Transport, Inborn Errors - epidemiology Renal Tubular Transport, Inborn Errors - etiology Renal Tubular Transport, Inborn Errors - prevention & control Retrospective Studies |
| title | Proteinuria-associated renal magnesium wasting leads to hypomagnesemia: a common electrolyte abnormality in chronic kidney disease |
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