Absorptive Hyperoxaluria Leads to an Increased Risk for Urolithiasis or Nephrocalcinosis in Cystic Fibrosis

Background: Hyperoxaluria has been incriminated to account for the increased incidence of urolithiasis or nephrocalcinosis in patients with cystic fibrosis (CF). Hyperoxaluria presumably is caused by fat malabsorption and the absence of such intestinal oxalate-degrading bacteria as Oxalobacter formi...

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Veröffentlicht in:American journal of kidney diseases 2005-09, Vol.46 (3), p.440-445
Hauptverfasser: Hoppe, Bernd, von Unruh, Gerd E., Blank, Gesa, Rietschel, Ernst, Sidhu, Harmeet, Laube, Norbert, Hesse, Albrecht
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container_end_page 445
container_issue 3
container_start_page 440
container_title American journal of kidney diseases
container_volume 46
creator Hoppe, Bernd
von Unruh, Gerd E.
Blank, Gesa
Rietschel, Ernst
Sidhu, Harmeet
Laube, Norbert
Hesse, Albrecht
description Background: Hyperoxaluria has been incriminated to account for the increased incidence of urolithiasis or nephrocalcinosis in patients with cystic fibrosis (CF). Hyperoxaluria presumably is caused by fat malabsorption and the absence of such intestinal oxalate-degrading bacteria as Oxalobacter formigenes. To better elucidate its pathophysiological characteristics, we prospectively studied patients with CF by determining these parameters and performing renal ultrasonography twice yearly. Methods: In addition to routine tests in urine (lithogenic and stone-inhibitory substances), the presence of O formigenes was tested in stool, plasma oxalate was measured, and a [ 13 C 2 ]oxalate absorption test was performed in 37 patients with CF aged 5 to 37 years (15 females, 22 males) who were constantly hyperoxaluric before the study. Results: Hyperoxaluria (oxalate, 46 to 141 mg/1.73 m 2 /24 h [0.51 to 1.57 mmol/1.73 m 2 /24 h]; normal, 3.3 mg/1.73 m 2 /24 h [>1.9 mmol/1.73 m 2 /24 h]). Urine calcium oxalate saturation was elevated in 17 patients (5.62 to 28.9 relative units; normal female,
doi_str_mv 10.1053/j.ajkd.2005.06.003
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Hyperoxaluria presumably is caused by fat malabsorption and the absence of such intestinal oxalate-degrading bacteria as Oxalobacter formigenes. To better elucidate its pathophysiological characteristics, we prospectively studied patients with CF by determining these parameters and performing renal ultrasonography twice yearly. Methods: In addition to routine tests in urine (lithogenic and stone-inhibitory substances), the presence of O formigenes was tested in stool, plasma oxalate was measured, and a [ 13 C 2 ]oxalate absorption test was performed in 37 patients with CF aged 5 to 37 years (15 females, 22 males) who were constantly hyperoxaluric before the study. Results: Hyperoxaluria (oxalate, 46 to 141 mg/1.73 m 2 /24 h [0.51 to 1.57 mmol/1.73 m 2 /24 h]; normal, &lt;45 mg/1.73 m 2 /24 h [&lt;0.5 mmol/1.73 m 2 /24 h]) was now found in 24 patients (64.8%). Plasma oxalate levels were elevated in 6 patients (7.92 to 19.5 μmol/L; normal, 6.3 ± 1.1 μmol/L). Oxalobacter species were detected in only 1 patient. Intestinal oxalate absorption was elevated (11.4% to 28.5%; normal, &lt;10%) in 23 patients. Hypocitraturia was present in 17 patients (citrate, 0.35 to 2.8 g/1.73 m 2 /24 h [0.2 to 1.1 mmol/1.73 m 2 /24 h]; normal female, &gt;2.8 mg/1.73 m 2 /24 h [&gt;1.6 mmol/1.73 m 2 /24 h]; male, &gt;3.3 mg/1.73 m 2 /24 h [&gt;1.9 mmol/1.73 m 2 /24 h]). Urine calcium oxalate saturation was elevated in 17 patients (5.62 to 28.9 relative units; normal female, &lt;5.5 relative units; male, &lt;6.3 relative units). In 16% of patients, urolithiasis (n = 2) or nephrocalcinosis (n = 4) was diagnosed ultrasonographically. Conclusion: Absorptive hyperoxaluria and hypocitraturia are the main culprits for the increased incidence of urolithiasis and nephrocalcinosis in patients with CF. We advocate high fluid intake, low-oxalate/high-calcium diet, and alkali citrate medication, if necessary. Additional studies are necessary to determine the influence of Oxalobacter species or other oxalate-degrading bacteria on oxalate handling in patients with CF.</description><identifier>ISSN: 0272-6386</identifier><identifier>EISSN: 1523-6838</identifier><identifier>DOI: 10.1053/j.ajkd.2005.06.003</identifier><identifier>PMID: 16129205</identifier><language>eng</language><publisher>Orlando, FL: Elsevier Inc</publisher><subject>[ 13C 2]oxalate absorption test ; absorptive hyperoxaluria ; Adolescent ; Adult ; Biological and medical sciences ; Calcium, Dietary - administration &amp; dosage ; Carbon Isotopes - pharmacokinetics ; Child ; Child, Preschool ; Citrates - therapeutic use ; Citrates - urine ; cystic fibrosis ; Cystic Fibrosis - complications ; Cystic Fibrosis - urine ; Dietary Fats - pharmacokinetics ; Errors of metabolism ; Feces - microbiology ; Female ; Fluid Therapy ; Humans ; Hyperoxaluria - etiology ; Intestinal Absorption ; Intestines - microbiology ; Malabsorption Syndromes - etiology ; Malabsorption Syndromes - metabolism ; Male ; Medical sciences ; Metabolic diseases ; Miscellaneous hereditary metabolic disorders ; nephrocalcinosis ; Nephrocalcinosis - epidemiology ; Nephrocalcinosis - etiology ; Nephrology. Urinary tract diseases ; Oxalates - blood ; Oxalates - pharmacokinetics ; Oxalobacter formigenes ; Oxalobacter formigenes - isolation &amp; purification ; Risk ; Urinary Calculi - epidemiology ; Urinary Calculi - etiology ; Urinary lithiasis ; urolithiasis</subject><ispartof>American journal of kidney diseases, 2005-09, Vol.46 (3), p.440-445</ispartof><rights>2005 National Kidney Foundation, Inc.</rights><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c384t-e35fc9e3a8e3d0a500267a95c8795ba84b91121f6d2def5eaf50415e778817373</citedby><cites>FETCH-LOGICAL-c384t-e35fc9e3a8e3d0a500267a95c8795ba84b91121f6d2def5eaf50415e778817373</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1053/j.ajkd.2005.06.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=17226579$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16129205$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hoppe, Bernd</creatorcontrib><creatorcontrib>von Unruh, Gerd E.</creatorcontrib><creatorcontrib>Blank, Gesa</creatorcontrib><creatorcontrib>Rietschel, Ernst</creatorcontrib><creatorcontrib>Sidhu, Harmeet</creatorcontrib><creatorcontrib>Laube, Norbert</creatorcontrib><creatorcontrib>Hesse, Albrecht</creatorcontrib><title>Absorptive Hyperoxaluria Leads to an Increased Risk for Urolithiasis or Nephrocalcinosis in Cystic Fibrosis</title><title>American journal of kidney diseases</title><addtitle>Am J Kidney Dis</addtitle><description>Background: Hyperoxaluria has been incriminated to account for the increased incidence of urolithiasis or nephrocalcinosis in patients with cystic fibrosis (CF). Hyperoxaluria presumably is caused by fat malabsorption and the absence of such intestinal oxalate-degrading bacteria as Oxalobacter formigenes. To better elucidate its pathophysiological characteristics, we prospectively studied patients with CF by determining these parameters and performing renal ultrasonography twice yearly. Methods: In addition to routine tests in urine (lithogenic and stone-inhibitory substances), the presence of O formigenes was tested in stool, plasma oxalate was measured, and a [ 13 C 2 ]oxalate absorption test was performed in 37 patients with CF aged 5 to 37 years (15 females, 22 males) who were constantly hyperoxaluric before the study. Results: Hyperoxaluria (oxalate, 46 to 141 mg/1.73 m 2 /24 h [0.51 to 1.57 mmol/1.73 m 2 /24 h]; normal, &lt;45 mg/1.73 m 2 /24 h [&lt;0.5 mmol/1.73 m 2 /24 h]) was now found in 24 patients (64.8%). Plasma oxalate levels were elevated in 6 patients (7.92 to 19.5 μmol/L; normal, 6.3 ± 1.1 μmol/L). Oxalobacter species were detected in only 1 patient. Intestinal oxalate absorption was elevated (11.4% to 28.5%; normal, &lt;10%) in 23 patients. Hypocitraturia was present in 17 patients (citrate, 0.35 to 2.8 g/1.73 m 2 /24 h [0.2 to 1.1 mmol/1.73 m 2 /24 h]; normal female, &gt;2.8 mg/1.73 m 2 /24 h [&gt;1.6 mmol/1.73 m 2 /24 h]; male, &gt;3.3 mg/1.73 m 2 /24 h [&gt;1.9 mmol/1.73 m 2 /24 h]). Urine calcium oxalate saturation was elevated in 17 patients (5.62 to 28.9 relative units; normal female, &lt;5.5 relative units; male, &lt;6.3 relative units). In 16% of patients, urolithiasis (n = 2) or nephrocalcinosis (n = 4) was diagnosed ultrasonographically. Conclusion: Absorptive hyperoxaluria and hypocitraturia are the main culprits for the increased incidence of urolithiasis and nephrocalcinosis in patients with CF. We advocate high fluid intake, low-oxalate/high-calcium diet, and alkali citrate medication, if necessary. Additional studies are necessary to determine the influence of Oxalobacter species or other oxalate-degrading bacteria on oxalate handling in patients with CF.</description><subject>[ 13C 2]oxalate absorption test</subject><subject>absorptive hyperoxaluria</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Calcium, Dietary - administration &amp; dosage</subject><subject>Carbon Isotopes - pharmacokinetics</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Citrates - therapeutic use</subject><subject>Citrates - urine</subject><subject>cystic fibrosis</subject><subject>Cystic Fibrosis - complications</subject><subject>Cystic Fibrosis - urine</subject><subject>Dietary Fats - pharmacokinetics</subject><subject>Errors of metabolism</subject><subject>Feces - microbiology</subject><subject>Female</subject><subject>Fluid Therapy</subject><subject>Humans</subject><subject>Hyperoxaluria - etiology</subject><subject>Intestinal Absorption</subject><subject>Intestines - microbiology</subject><subject>Malabsorption Syndromes - etiology</subject><subject>Malabsorption Syndromes - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Miscellaneous hereditary metabolic disorders</subject><subject>nephrocalcinosis</subject><subject>Nephrocalcinosis - epidemiology</subject><subject>Nephrocalcinosis - etiology</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oxalates - blood</subject><subject>Oxalates - pharmacokinetics</subject><subject>Oxalobacter formigenes</subject><subject>Oxalobacter formigenes - isolation &amp; purification</subject><subject>Risk</subject><subject>Urinary Calculi - epidemiology</subject><subject>Urinary Calculi - etiology</subject><subject>Urinary lithiasis</subject><subject>urolithiasis</subject><issn>0272-6386</issn><issn>1523-6838</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1r3DAQhkVpabZp_0APRZf2Zlcfqw9DL2FJmsDSQmnOYiyPiXa9lit5Q_ffV2YXcutpmJdnhpeHkI-c1Zwp-XVXw27f1YIxVTNdMyZfkRVXQlbaSvuarJgwotLS6ivyLucdY6yRWr8lV1xz0QimVmR_0-aYpjk8I70_TZjiXxiOKQDdInSZzpHCSB9GnxAydvRXyHvax0QfUxzC_BQgh0zL_gOnpxQ9DD6MccnCSDenPAdP70Kblug9edPDkPHDZV6Tx7vb35v7avvz-8PmZlt5addzhVL1vkEJFmXHQDEmtIFGeWsa1YJdtw3ngve6Ex32CqFXbM0VGmMtN9LIa_Ll_HdK8c8R8-wOIXscBhgxHrPTVolGy3UBxRn0pV9O2LsphQOkk-PMLYrdzi2K3aLYMe2K4nL06fL92B6wezm5OC3A5wsAufjoE4w-5BfOCKGVaQr37cxhcfEcMLnsA44eu5DQz66L4X89_gGnEJrT</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Hoppe, Bernd</creator><creator>von Unruh, Gerd E.</creator><creator>Blank, Gesa</creator><creator>Rietschel, Ernst</creator><creator>Sidhu, Harmeet</creator><creator>Laube, Norbert</creator><creator>Hesse, Albrecht</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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></search><sort><creationdate>20050901</creationdate><title>Absorptive Hyperoxaluria Leads to an Increased Risk for Urolithiasis or Nephrocalcinosis in Cystic Fibrosis</title><author>Hoppe, Bernd ; von Unruh, Gerd E. ; Blank, Gesa ; Rietschel, Ernst ; Sidhu, Harmeet ; Laube, Norbert ; Hesse, Albrecht</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c384t-e35fc9e3a8e3d0a500267a95c8795ba84b91121f6d2def5eaf50415e778817373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>[ 13C 2]oxalate absorption test</topic><topic>absorptive hyperoxaluria</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Calcium, Dietary - administration &amp; dosage</topic><topic>Carbon Isotopes - pharmacokinetics</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Citrates - therapeutic use</topic><topic>Citrates - urine</topic><topic>cystic fibrosis</topic><topic>Cystic Fibrosis - complications</topic><topic>Cystic Fibrosis - urine</topic><topic>Dietary Fats - pharmacokinetics</topic><topic>Errors of metabolism</topic><topic>Feces - microbiology</topic><topic>Female</topic><topic>Fluid Therapy</topic><topic>Humans</topic><topic>Hyperoxaluria - etiology</topic><topic>Intestinal Absorption</topic><topic>Intestines - microbiology</topic><topic>Malabsorption Syndromes - etiology</topic><topic>Malabsorption Syndromes - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Miscellaneous hereditary metabolic disorders</topic><topic>nephrocalcinosis</topic><topic>Nephrocalcinosis - epidemiology</topic><topic>Nephrocalcinosis - etiology</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Oxalates - blood</topic><topic>Oxalates - pharmacokinetics</topic><topic>Oxalobacter formigenes</topic><topic>Oxalobacter formigenes - isolation &amp; purification</topic><topic>Risk</topic><topic>Urinary Calculi - epidemiology</topic><topic>Urinary Calculi - etiology</topic><topic>Urinary lithiasis</topic><topic>urolithiasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hoppe, Bernd</creatorcontrib><creatorcontrib>von Unruh, Gerd E.</creatorcontrib><creatorcontrib>Blank, Gesa</creatorcontrib><creatorcontrib>Rietschel, Ernst</creatorcontrib><creatorcontrib>Sidhu, Harmeet</creatorcontrib><creatorcontrib>Laube, Norbert</creatorcontrib><creatorcontrib>Hesse, Albrecht</creatorcontrib><collection>Pascal-Francis</collection><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>American journal of kidney diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hoppe, Bernd</au><au>von Unruh, Gerd E.</au><au>Blank, Gesa</au><au>Rietschel, Ernst</au><au>Sidhu, Harmeet</au><au>Laube, Norbert</au><au>Hesse, Albrecht</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Absorptive Hyperoxaluria Leads to an Increased Risk for Urolithiasis or Nephrocalcinosis in Cystic Fibrosis</atitle><jtitle>American journal of kidney diseases</jtitle><addtitle>Am J Kidney Dis</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>46</volume><issue>3</issue><spage>440</spage><epage>445</epage><pages>440-445</pages><issn>0272-6386</issn><eissn>1523-6838</eissn><abstract>Background: Hyperoxaluria has been incriminated to account for the increased incidence of urolithiasis or nephrocalcinosis in patients with cystic fibrosis (CF). Hyperoxaluria presumably is caused by fat malabsorption and the absence of such intestinal oxalate-degrading bacteria as Oxalobacter formigenes. To better elucidate its pathophysiological characteristics, we prospectively studied patients with CF by determining these parameters and performing renal ultrasonography twice yearly. Methods: In addition to routine tests in urine (lithogenic and stone-inhibitory substances), the presence of O formigenes was tested in stool, plasma oxalate was measured, and a [ 13 C 2 ]oxalate absorption test was performed in 37 patients with CF aged 5 to 37 years (15 females, 22 males) who were constantly hyperoxaluric before the study. Results: Hyperoxaluria (oxalate, 46 to 141 mg/1.73 m 2 /24 h [0.51 to 1.57 mmol/1.73 m 2 /24 h]; normal, &lt;45 mg/1.73 m 2 /24 h [&lt;0.5 mmol/1.73 m 2 /24 h]) was now found in 24 patients (64.8%). Plasma oxalate levels were elevated in 6 patients (7.92 to 19.5 μmol/L; normal, 6.3 ± 1.1 μmol/L). Oxalobacter species were detected in only 1 patient. Intestinal oxalate absorption was elevated (11.4% to 28.5%; normal, &lt;10%) in 23 patients. Hypocitraturia was present in 17 patients (citrate, 0.35 to 2.8 g/1.73 m 2 /24 h [0.2 to 1.1 mmol/1.73 m 2 /24 h]; normal female, &gt;2.8 mg/1.73 m 2 /24 h [&gt;1.6 mmol/1.73 m 2 /24 h]; male, &gt;3.3 mg/1.73 m 2 /24 h [&gt;1.9 mmol/1.73 m 2 /24 h]). Urine calcium oxalate saturation was elevated in 17 patients (5.62 to 28.9 relative units; normal female, &lt;5.5 relative units; male, &lt;6.3 relative units). In 16% of patients, urolithiasis (n = 2) or nephrocalcinosis (n = 4) was diagnosed ultrasonographically. Conclusion: Absorptive hyperoxaluria and hypocitraturia are the main culprits for the increased incidence of urolithiasis and nephrocalcinosis in patients with CF. We advocate high fluid intake, low-oxalate/high-calcium diet, and alkali citrate medication, if necessary. Additional studies are necessary to determine the influence of Oxalobacter species or other oxalate-degrading bacteria on oxalate handling in patients with CF.</abstract><cop>Orlando, FL</cop><pub>Elsevier Inc</pub><pmid>16129205</pmid><doi>10.1053/j.ajkd.2005.06.003</doi><tpages>6</tpages></addata></record>
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subjects [ 13C 2]oxalate absorption test
absorptive hyperoxaluria
Adolescent
Adult
Biological and medical sciences
Calcium, Dietary - administration & dosage
Carbon Isotopes - pharmacokinetics
Child
Child, Preschool
Citrates - therapeutic use
Citrates - urine
cystic fibrosis
Cystic Fibrosis - complications
Cystic Fibrosis - urine
Dietary Fats - pharmacokinetics
Errors of metabolism
Feces - microbiology
Female
Fluid Therapy
Humans
Hyperoxaluria - etiology
Intestinal Absorption
Intestines - microbiology
Malabsorption Syndromes - etiology
Malabsorption Syndromes - metabolism
Male
Medical sciences
Metabolic diseases
Miscellaneous hereditary metabolic disorders
nephrocalcinosis
Nephrocalcinosis - epidemiology
Nephrocalcinosis - etiology
Nephrology. Urinary tract diseases
Oxalates - blood
Oxalates - pharmacokinetics
Oxalobacter formigenes
Oxalobacter formigenes - isolation & purification
Risk
Urinary Calculi - epidemiology
Urinary Calculi - etiology
Urinary lithiasis
urolithiasis
title Absorptive Hyperoxaluria Leads to an Increased Risk for Urolithiasis or Nephrocalcinosis in Cystic Fibrosis
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