Loading…
Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort
Background Hepcidin, a key iron regulatory protein, is elevated in patients with chronic kidney disease (CKD). Its role in the development and progression of the anemia of CKD in children remains poorly defined. Methods Cross-sectional and longitudinal study in children aged 1–16 years with stage 2–...
Saved in:
| Published in: | Pediatric nephrology (Berlin, West) West), 2015-04, Vol.30 (4), p.635-643 |
|---|---|
| Main Authors: | , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that this one cites Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3 |
|---|---|
| cites | cdi_FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3 |
| container_end_page | 643 |
| container_issue | 4 |
| container_start_page | 635 |
| container_title | Pediatric nephrology (Berlin, West) |
| container_volume | 30 |
| creator | Atkinson, Meredith A. Kim, Ji Young Roy, Cindy N. Warady, Bradley A. White, Colin T. Furth, Susan L. |
| description | Background
Hepcidin, a key iron regulatory protein, is elevated in patients with chronic kidney disease (CKD). Its role in the development and progression of the anemia of CKD in children remains poorly defined.
Methods
Cross-sectional and longitudinal study in children aged 1–16 years with stage 2–4 CKD in the Chronic Kidney Disease in Children (CKiD) cohort (
n
= 133) with hepcidin measured at baseline and hemoglobin (HGB) measured annually at follow-up. Anemia was defined as HGB |
| doi_str_mv | 10.1007/s00467-014-2991-4 |
| format | article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4336204</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A407669222</galeid><sourcerecordid>A407669222</sourcerecordid><originalsourceid>FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3</originalsourceid><addsrcrecordid>eNp1ks1u1DAUhSMEokPhAdigSEiIjcv1T-yEBVI1BYqoxAak7iyP4yQuHntqJ0h9e5yZUmbQoCwcXX_n2D73FsVLDGcYQLxLAIwLBJgh0jQYsUfFAjNKEG7q68fFAhqKETB8fVI8S-kGAOqq5k-LE1LRGkRdL4rVpdlo21pfKt-W0aafZejyv1lbVebq8uvF-1KVOoaUUDJ6tMErt4Vd8L0dp6zdFpS7SzbNmnEwWWcvSh2GEMfnxZNOuWRe3K-nxY9PH78vL9HVt89fludXSHPBR9RxU7eUEoYZiJXRgLEgCkSlaCs6qBqCKdQMkxVru65lhDJmRNuA4VThRtHT4sPOdzOt1qbVxo9RObmJdq3inQzKysMdbwfZh1-SUcoJsGzw9t4ghtvJpFGubdLGuRxHmJLEvBIU15zzjL7-B70JU8wZbKmq4SJf_y_VK2ek9V3I5-rZVJ7nR3LeEEIyhY5QvfEmXzJ409lcPuDPjvD5a3PT9FHBmz3BYJQbhxTcNPcyHYJ4B27bHU33EB4GOU-c3E2czBMn54mTc2iv9lN_UPwZsQyQHZDylu9N3Ivqv66_Aeho3SI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1655967011</pqid></control><display><type>article</type><title>Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort</title><source>Springer Link</source><creator>Atkinson, Meredith A. ; Kim, Ji Young ; Roy, Cindy N. ; Warady, Bradley A. ; White, Colin T. ; Furth, Susan L.</creator><creatorcontrib>Atkinson, Meredith A. ; Kim, Ji Young ; Roy, Cindy N. ; Warady, Bradley A. ; White, Colin T. ; Furth, Susan L.</creatorcontrib><description>Background
Hepcidin, a key iron regulatory protein, is elevated in patients with chronic kidney disease (CKD). Its role in the development and progression of the anemia of CKD in children remains poorly defined.
Methods
Cross-sectional and longitudinal study in children aged 1–16 years with stage 2–4 CKD in the Chronic Kidney Disease in Children (CKiD) cohort (
n
= 133) with hepcidin measured at baseline and hemoglobin (HGB) measured annually at follow-up. Anemia was defined as HGB <5th percentile for age/sex OR treatment with an erythropoiesis-stimulating agent (ESA).
Results
Hepcidin levels correlated negatively with glomerular filtration rate (GFR;
r
= −0.22,
p
= 0.01) and positively with ferritin (
r
= 0.67,
p
< 0.001). At the lower end of the GFR spectrum at baseline (10th percentile, 27.5 mL/min/1.73 m
2
), higher hepcidin was associated with a 0.87 g/dL decrease in HGB during follow-up (95 % CI −1.69, −0.05 g/dL,
p
= 0.038). At higher GFR percentiles there was no significant association between baseline hepcidin and HGB during follow-up. Among 90 non-anemic subjects at baseline, 23.3 % developed incident anemia. In subjects with GFR ≤ the median, a higher hepcidin level was associated with an increased risk of incident anemia (at the 10th percentile GFR, HR 3.471, 95 % CI 1.228, 9.810,
p
= 0.019; at the 25th percentile GFR, HR 2.641, 95 % CI 1.213, 5.750,
p
= 0.014; at the 50th percentile GFR, HR 1.953, 95 % CI 1.011, 3.772,
p
= 0.046). Among subjects with GFR at the 75th percentile or above, incrementally higher baseline hepcidin was not associated with increased anemia risk.
Conclusions
Higher hepcidin levels are associated with a decreased HGB and an increased risk of incident anemia, and this association is most significant among subjects with lower GFR.</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s00467-014-2991-4</identifier><identifier>PMID: 25380788</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Adolescent ; Anemia ; Anemia - blood ; Child ; Child, Preschool ; Chronic kidney failure ; Cohort analysis ; Complications and side effects ; Cross-Sectional Studies ; Enzyme-Linked Immunosorbent Assay ; Female ; Glomerular Filtration Rate ; Hemoglobin ; Hemoglobins - metabolism ; Hepcidins - blood ; Humans ; Infant ; Iron ; Kidney diseases ; Longitudinal Studies ; Male ; Medicine ; Medicine & Public Health ; Metalloproteins ; Nephrology ; Original Article ; Pediatrics ; Physiological aspects ; Prognosis ; Proteins ; Renal Insufficiency, Chronic - blood ; Risk Factors ; Urology</subject><ispartof>Pediatric nephrology (Berlin, West), 2015-04, Vol.30 (4), p.635-643</ispartof><rights>IPNA 2014</rights><rights>COPYRIGHT 2015 Springer</rights><rights>IPNA 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3</citedby><cites>FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25380788$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Atkinson, Meredith A.</creatorcontrib><creatorcontrib>Kim, Ji Young</creatorcontrib><creatorcontrib>Roy, Cindy N.</creatorcontrib><creatorcontrib>Warady, Bradley A.</creatorcontrib><creatorcontrib>White, Colin T.</creatorcontrib><creatorcontrib>Furth, Susan L.</creatorcontrib><title>Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><addtitle>Pediatr Nephrol</addtitle><description>Background
Hepcidin, a key iron regulatory protein, is elevated in patients with chronic kidney disease (CKD). Its role in the development and progression of the anemia of CKD in children remains poorly defined.
Methods
Cross-sectional and longitudinal study in children aged 1–16 years with stage 2–4 CKD in the Chronic Kidney Disease in Children (CKiD) cohort (
n
= 133) with hepcidin measured at baseline and hemoglobin (HGB) measured annually at follow-up. Anemia was defined as HGB <5th percentile for age/sex OR treatment with an erythropoiesis-stimulating agent (ESA).
Results
Hepcidin levels correlated negatively with glomerular filtration rate (GFR;
r
= −0.22,
p
= 0.01) and positively with ferritin (
r
= 0.67,
p
< 0.001). At the lower end of the GFR spectrum at baseline (10th percentile, 27.5 mL/min/1.73 m
2
), higher hepcidin was associated with a 0.87 g/dL decrease in HGB during follow-up (95 % CI −1.69, −0.05 g/dL,
p
= 0.038). At higher GFR percentiles there was no significant association between baseline hepcidin and HGB during follow-up. Among 90 non-anemic subjects at baseline, 23.3 % developed incident anemia. In subjects with GFR ≤ the median, a higher hepcidin level was associated with an increased risk of incident anemia (at the 10th percentile GFR, HR 3.471, 95 % CI 1.228, 9.810,
p
= 0.019; at the 25th percentile GFR, HR 2.641, 95 % CI 1.213, 5.750,
p
= 0.014; at the 50th percentile GFR, HR 1.953, 95 % CI 1.011, 3.772,
p
= 0.046). Among subjects with GFR at the 75th percentile or above, incrementally higher baseline hepcidin was not associated with increased anemia risk.
Conclusions
Higher hepcidin levels are associated with a decreased HGB and an increased risk of incident anemia, and this association is most significant among subjects with lower GFR.</description><subject>Adolescent</subject><subject>Anemia</subject><subject>Anemia - blood</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Chronic kidney failure</subject><subject>Cohort analysis</subject><subject>Complications and side effects</subject><subject>Cross-Sectional Studies</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Female</subject><subject>Glomerular Filtration Rate</subject><subject>Hemoglobin</subject><subject>Hemoglobins - metabolism</subject><subject>Hepcidins - blood</subject><subject>Humans</subject><subject>Infant</subject><subject>Iron</subject><subject>Kidney diseases</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metalloproteins</subject><subject>Nephrology</subject><subject>Original Article</subject><subject>Pediatrics</subject><subject>Physiological aspects</subject><subject>Prognosis</subject><subject>Proteins</subject><subject>Renal Insufficiency, Chronic - blood</subject><subject>Risk Factors</subject><subject>Urology</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNp1ks1u1DAUhSMEokPhAdigSEiIjcv1T-yEBVI1BYqoxAak7iyP4yQuHntqJ0h9e5yZUmbQoCwcXX_n2D73FsVLDGcYQLxLAIwLBJgh0jQYsUfFAjNKEG7q68fFAhqKETB8fVI8S-kGAOqq5k-LE1LRGkRdL4rVpdlo21pfKt-W0aafZejyv1lbVebq8uvF-1KVOoaUUDJ6tMErt4Vd8L0dp6zdFpS7SzbNmnEwWWcvSh2GEMfnxZNOuWRe3K-nxY9PH78vL9HVt89fludXSHPBR9RxU7eUEoYZiJXRgLEgCkSlaCs6qBqCKdQMkxVru65lhDJmRNuA4VThRtHT4sPOdzOt1qbVxo9RObmJdq3inQzKysMdbwfZh1-SUcoJsGzw9t4ghtvJpFGubdLGuRxHmJLEvBIU15zzjL7-B70JU8wZbKmq4SJf_y_VK2ek9V3I5-rZVJ7nR3LeEEIyhY5QvfEmXzJ409lcPuDPjvD5a3PT9FHBmz3BYJQbhxTcNPcyHYJ4B27bHU33EB4GOU-c3E2czBMn54mTc2iv9lN_UPwZsQyQHZDylu9N3Ivqv66_Aeho3SI</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>Atkinson, Meredith A.</creator><creator>Kim, Ji Young</creator><creator>Roy, Cindy N.</creator><creator>Warady, Bradley A.</creator><creator>White, Colin T.</creator><creator>Furth, Susan L.</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150401</creationdate><title>Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort</title><author>Atkinson, Meredith A. ; Kim, Ji Young ; Roy, Cindy N. ; Warady, Bradley A. ; White, Colin T. ; Furth, Susan L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adolescent</topic><topic>Anemia</topic><topic>Anemia - blood</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Chronic kidney failure</topic><topic>Cohort analysis</topic><topic>Complications and side effects</topic><topic>Cross-Sectional Studies</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Female</topic><topic>Glomerular Filtration Rate</topic><topic>Hemoglobin</topic><topic>Hemoglobins - metabolism</topic><topic>Hepcidins - blood</topic><topic>Humans</topic><topic>Infant</topic><topic>Iron</topic><topic>Kidney diseases</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metalloproteins</topic><topic>Nephrology</topic><topic>Original Article</topic><topic>Pediatrics</topic><topic>Physiological aspects</topic><topic>Prognosis</topic><topic>Proteins</topic><topic>Renal Insufficiency, Chronic - blood</topic><topic>Risk Factors</topic><topic>Urology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Atkinson, Meredith A.</creatorcontrib><creatorcontrib>Kim, Ji Young</creatorcontrib><creatorcontrib>Roy, Cindy N.</creatorcontrib><creatorcontrib>Warady, Bradley A.</creatorcontrib><creatorcontrib>White, Colin T.</creatorcontrib><creatorcontrib>Furth, Susan L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pediatric nephrology (Berlin, West)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Atkinson, Meredith A.</au><au>Kim, Ji Young</au><au>Roy, Cindy N.</au><au>Warady, Bradley A.</au><au>White, Colin T.</au><au>Furth, Susan L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><stitle>Pediatr Nephrol</stitle><addtitle>Pediatr Nephrol</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>30</volume><issue>4</issue><spage>635</spage><epage>643</epage><pages>635-643</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><abstract>Background
Hepcidin, a key iron regulatory protein, is elevated in patients with chronic kidney disease (CKD). Its role in the development and progression of the anemia of CKD in children remains poorly defined.
Methods
Cross-sectional and longitudinal study in children aged 1–16 years with stage 2–4 CKD in the Chronic Kidney Disease in Children (CKiD) cohort (
n
= 133) with hepcidin measured at baseline and hemoglobin (HGB) measured annually at follow-up. Anemia was defined as HGB <5th percentile for age/sex OR treatment with an erythropoiesis-stimulating agent (ESA).
Results
Hepcidin levels correlated negatively with glomerular filtration rate (GFR;
r
= −0.22,
p
= 0.01) and positively with ferritin (
r
= 0.67,
p
< 0.001). At the lower end of the GFR spectrum at baseline (10th percentile, 27.5 mL/min/1.73 m
2
), higher hepcidin was associated with a 0.87 g/dL decrease in HGB during follow-up (95 % CI −1.69, −0.05 g/dL,
p
= 0.038). At higher GFR percentiles there was no significant association between baseline hepcidin and HGB during follow-up. Among 90 non-anemic subjects at baseline, 23.3 % developed incident anemia. In subjects with GFR ≤ the median, a higher hepcidin level was associated with an increased risk of incident anemia (at the 10th percentile GFR, HR 3.471, 95 % CI 1.228, 9.810,
p
= 0.019; at the 25th percentile GFR, HR 2.641, 95 % CI 1.213, 5.750,
p
= 0.014; at the 50th percentile GFR, HR 1.953, 95 % CI 1.011, 3.772,
p
= 0.046). Among subjects with GFR at the 75th percentile or above, incrementally higher baseline hepcidin was not associated with increased anemia risk.
Conclusions
Higher hepcidin levels are associated with a decreased HGB and an increased risk of incident anemia, and this association is most significant among subjects with lower GFR.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>25380788</pmid><doi>10.1007/s00467-014-2991-4</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0931-041X |
| ispartof | Pediatric nephrology (Berlin, West), 2015-04, Vol.30 (4), p.635-643 |
| issn | 0931-041X 1432-198X |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4336204 |
| source | Springer Link |
| subjects | Adolescent Anemia Anemia - blood Child Child, Preschool Chronic kidney failure Cohort analysis Complications and side effects Cross-Sectional Studies Enzyme-Linked Immunosorbent Assay Female Glomerular Filtration Rate Hemoglobin Hemoglobins - metabolism Hepcidins - blood Humans Infant Iron Kidney diseases Longitudinal Studies Male Medicine Medicine & Public Health Metalloproteins Nephrology Original Article Pediatrics Physiological aspects Prognosis Proteins Renal Insufficiency, Chronic - blood Risk Factors Urology |
| title | Hepcidin and risk of anemia in CKD: a cross-sectional and longitudinal analysis in the CKiD cohort |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-03T09%3A22%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hepcidin%20and%20risk%20of%20anemia%20in%20CKD:%20a%20cross-sectional%20and%20longitudinal%20analysis%20in%20the%20CKiD%20cohort&rft.jtitle=Pediatric%20nephrology%20(Berlin,%20West)&rft.au=Atkinson,%20Meredith%20A.&rft.date=2015-04-01&rft.volume=30&rft.issue=4&rft.spage=635&rft.epage=643&rft.pages=635-643&rft.issn=0931-041X&rft.eissn=1432-198X&rft_id=info:doi/10.1007/s00467-014-2991-4&rft_dat=%3Cgale_pubme%3EA407669222%3C/gale_pubme%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c676t-f6e8d33241407bec01172a075a3d7f05921308412b4dffd42344e7d90e63a19a3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1655967011&rft_id=info:pmid/25380788&rft_galeid=A407669222&rfr_iscdi=true |