Benign primary hematuria
Identifieur interne : 001130 ( Istex/Corpus ); précédent : 001129; suivant : 001131Benign primary hematuria
Auteurs : Victoriano Pardo ; M. Gregg Berian ; Donald F. Levi ; Jose StraussSource :
- The American Journal of Medicine [ 0002-9343 ] ; 1979.
Abstract
Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix® in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.
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DOI: 10.1016/0002-9343(79)90741-1
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Benign primary hematuria</title><author><name sortKey="Pardo, Victoriano" sort="Pardo, Victoriano" uniqKey="Pardo V" first="Victoriano" last="Pardo">Victoriano Pardo</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author><author><name sortKey="Berian, M Gregg" sort="Berian, M Gregg" uniqKey="Berian M" first="M. Gregg" last="Berian">M. Gregg Berian</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author><author><name sortKey="Levi, Donald F" sort="Levi, Donald F" uniqKey="Levi D" first="Donald F." last="Levi">Donald F. Levi</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author><author><name sortKey="Strauss, Jose" sort="Strauss, Jose" uniqKey="Strauss J" first="Jose" last="Strauss">Jose Strauss</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F05E2156E7EBB65330C5E883C5900048D8297C01</idno><date when="1979" year="1979">1979</date><idno type="doi">10.1016/0002-9343(79)90741-1</idno><idno type="url">https://api.istex.fr/document/F05E2156E7EBB65330C5E883C5900048D8297C01/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001130</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Benign primary hematuria</title><author><name sortKey="Pardo, Victoriano" sort="Pardo, Victoriano" uniqKey="Pardo V" first="Victoriano" last="Pardo">Victoriano Pardo</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author><author><name sortKey="Berian, M Gregg" sort="Berian, M Gregg" uniqKey="Berian M" first="M. 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Levi</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author><author><name sortKey="Strauss, Jose" sort="Strauss, Jose" uniqKey="Strauss J" first="Jose" last="Strauss">Jose Strauss</name><affiliation><mods:affiliation>Miami, Florida USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="ISSN">0002-9343</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1979">1979</date><biblScope unit="volume">67</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="817">817</biblScope><biblScope unit="page" to="822">822</biblScope></imprint><idno type="ISSN">0002-9343</idno></series><idno type="istex">F05E2156E7EBB65330C5E883C5900048D8297C01</idno><idno type="DOI">10.1016/0002-9343(79)90741-1</idno><idno type="PII">0002-9343(79)90741-1</idno><idno type="ArticleID">79907411</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0002-9343</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix® in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Victoriano Pardo M.D.</name><affiliations><json:string>Miami, Florida USA</json:string></affiliations></json:item><json:item><name>M.Gregg Berian M.D.</name><affiliations><json:string>Miami, Florida USA</json:string></affiliations></json:item><json:item><name>Donald F. Levi M.D.</name><affiliations><json:string>Miami, Florida USA</json:string></affiliations></json:item><json:item><name>Jose Strauss M.D.</name><affiliations><json:string>Miami, Florida USA</json:string></affiliations></json:item></author><articleId><json:string>79907411</json:string></articleId><language><json:string>eng</json:string></language><abstract>Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix® in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.</abstract><qualityIndicators><score>5.902</score><pdfVersion>1.4</pdfVersion><pdfPageSize>576 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>0</keywordCount><abstractCharCount>1997</abstractCharCount><pdfWordCount>2402</pdfWordCount><pdfCharCount>16899</pdfCharCount><pdfPageCount>6</pdfPageCount><abstractWordCount>301</abstractWordCount></qualityIndicators><title>Benign primary 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Administration Hospital, 1201 N.W. 16th Street, Miami, Florida 33125.</note><note type="biography">From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</note><affiliation>Requests for reprints should be addressed to Dr. Victoriano Pardo, Laboratory Service, Veterans Administration Hospital, 1201 N.W. 16th Street, Miami, Florida 33125.</affiliation><affiliation>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</affiliation><affiliation>Miami, Florida USA</affiliation></author><author><persName><forename type="first">M.Gregg</forename><surname>Berian</surname></persName><roleName type="degree">M.D.</roleName><note type="biography">From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</note><affiliation>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</affiliation><affiliation>Miami, Florida USA</affiliation></author><author><persName><forename type="first">Donald F.</forename><surname>Levi</surname></persName><roleName type="degree">M.D.</roleName><note type="biography">From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</note><affiliation>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</affiliation><affiliation>Miami, Florida USA</affiliation></author><author><persName><forename type="first">Jose</forename><surname>Strauss</surname></persName><roleName type="degree">M.D.</roleName><note type="biography">From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</note><affiliation>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</affiliation><affiliation>Miami, Florida USA</affiliation></author></analytic><monogr><title level="j">The American Journal of Medicine</title><title level="j" type="abbrev">AJM</title><idno type="pISSN">0002-9343</idno><idno type="PII">S0002-9343(00)X0527-X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1979"></date><biblScope unit="volume">67</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="817">817</biblScope><biblScope unit="page" to="822">822</biblScope></imprint></monogr><idno type="istex">F05E2156E7EBB65330C5E883C5900048D8297C01</idno><idno type="DOI">10.1016/0002-9343(79)90741-1</idno><idno type="PII">0002-9343(79)90741-1</idno><idno type="ArticleID">79907411</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1979</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix® in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.</p></abstract></profileDesc><revisionDesc><change when="1979-06-29">Registration</change><change when="1979">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>AJM</jid><aid>79907411</aid><ce:pii>0002-9343(79)90741-1</ce:pii><ce:doi>10.1016/0002-9343(79)90741-1</ce:doi><ce:copyright type="unknown" year="1979"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Clinical study</ce:textfn></ce:dochead><ce:title>Benign primary hematuria</ce:title><ce:subtitle>Clinicopathologic study of 65 patients</ce:subtitle><ce:author-group><ce:author><ce:given-name>Victoriano</ce:given-name><ce:surname>Pardo</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="COR1"><ce:sup loc="post">∗</ce:sup></ce:cross-ref><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>M.Gregg</ce:given-name><ce:surname>Berian</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Donald F.</ce:given-name><ce:surname>Levi</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Jose</ce:given-name><ce:surname>Strauss</ce:surname><ce:degrees>M.D.</ce:degrees><ce:cross-ref refid="FN1"><ce:sup loc="post">1</ce:sup></ce:cross-ref></ce:author><ce:affiliation><ce:textfn>Miami, Florida USA</ce:textfn></ce:affiliation><ce:correspondence id="COR1"><ce:label>∗</ce:label><ce:text>Requests for reprints should be addressed to Dr. Victoriano Pardo, Laboratory Service, Veterans Administration Hospital, 1201 N.W. 16th Street, Miami, Florida 33125.</ce:text></ce:correspondence><ce:footnote id="FN1"><ce:label>1</ce:label><ce:note-para>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</ce:note-para></ce:footnote></ce:author-group><ce:date-accepted day="29" month="6" year="1979"></ce:date-accepted><ce:abstract class="author"><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para view="all" id="simple-para.0010">Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix<ce:sup loc="post">®</ce:sup> in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Benign primary hematuria</title><subTitle>Clinicopathologic study of 65 patients</subTitle></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Benign primary hematuria</title><subTitle>Clinicopathologic study of 65 patients</subTitle></titleInfo><name type="personal"><namePart type="given">Victoriano</namePart><namePart type="family">Pardo</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Miami, Florida USA</affiliation><description>Requests for reprints should be addressed to Dr. Victoriano Pardo, Laboratory Service, Veterans Administration Hospital, 1201 N.W. 16th Street, Miami, Florida 33125.</description><description>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.Gregg</namePart><namePart type="family">Berian</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Miami, Florida USA</affiliation><description>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Donald F.</namePart><namePart type="family">Levi</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Miami, Florida USA</affiliation><description>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jose</namePart><namePart type="family">Strauss</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Miami, Florida USA</affiliation><description>From the Departments of Pathology and Pediatrics, University of Miami, School of Medicine, and Laboratory Service, Veterans Administration Hospital, Miami, Florida.</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1979</dateIssued><dateValid encoding="w3cdtf">1979-06-29</dateValid><copyrightDate encoding="w3cdtf">1979</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Renal biopsy specimens were examined in a group of 65 patients with primary hematuria who met the following criteria: urine protein excretion under 1 g in 24 hours or a negative Albustix® in a concentrated specimen, absence of hypertension and normal renal function. The median age at discovery of the disease was 13 years, and the median duration of the hematuria at biopsy was two years. Recurrent gross hematuria was present in 38 instances. Thirty of the 65 renal biopsy specimens showed mesangial proliferative glomerulonephritis and in 44 there were red blood cells in the tubules. Mesangial deposits of a variety of immunoglobulins and/or third component of complement (C3) were identified in 30 of the 44 biopsy specimens examined. Immunoglobulin M (IgM) was the predominant immunoglobulin. Electron dense mesangial deposits were identified only in 12 cases; however, ultrastructural study of the biopsy specimens led to the detection of one patient who was probably suffering from Alport's syndrome. There was a poor correlation between histologic lesions and immunohistochemical findings. Thirty-nine patients were followed for a median period of four years without evidence of any deterioration of renal or any other manifestation of renal or systemic disease, although half of these patients still showed bleeding in the last urinalysis. Thus, the name benign primary hematuria appears appropriate to designate this clinical syndrome. The use of pathologic terms such as focal glomerulonephritis or immunoglobulin A (IgA) nephropathy (Berger's disease) has been a cause of ambiguity since there is not a consistent correlation between these lesions and clinical manifestations. Because the discrete mesangial changes may be predicted virtually from the clinical presentation, kidney biopsy may not seem to be indicated in the majority of these patients unless there is an increase in urinary protein excretion or other manifestations of renal, genitourinary or systemic disease appear.</abstract><note type="content">Section title: Clinical study</note><relatedItem type="host"><titleInfo><title>The American Journal of Medicine</title></titleInfo><titleInfo type="abbreviated"><title>AJM</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">197911</dateIssued></originInfo><identifier type="ISSN">0002-9343</identifier><identifier type="PII">S0002-9343(00)X0527-X</identifier><part><date>197911</date><detail type="volume"><number>67</number><caption>vol.</caption></detail><detail type="issue"><number>5</number><caption>no.</caption></detail><extent unit="issue pages"><start>A1</start><end>A32</end></extent><extent unit="issue pages"><start>A36</start></extent><extent unit="issue pages"><start>A37</start></extent><extent unit="issue pages"><start>A40</start><end>A41</end></extent><extent unit="issue pages"><start>A48</start></extent><extent unit="issue pages"><start>A53</start><end>A59</end></extent><extent unit="issue pages"><start>A62</start><end>A68</end></extent><extent unit="issue pages"><start>729</start><end>912</end></extent><extent unit="pages"><start>817</start><end>822</end></extent></part></relatedItem><identifier type="istex">F05E2156E7EBB65330C5E883C5900048D8297C01</identifier><identifier type="DOI">10.1016/0002-9343(79)90741-1</identifier><identifier type="PII">0002-9343(79)90741-1</identifier><identifier type="ArticleID">79907411</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:refBibTEI uri="https://api.istex.fr/document/F05E2156E7EBB65330C5E883C5900048D8297C01/enrichments/refBib"><teiHeader></teiHeader><text><front></front><body></body><back><listBibl><biblStruct><analytic><title level="a" type="main">The Kidney 9: 1, 1976 Recurrent hematuria in childhood Symptomlass he-maturia in childhood</title><author><persName><forename type="first">Jp</forename><surname>Hayslett</surname></persName></author><author><persName><surname>Primary</surname></persName></author><author><persName><forename type="middle">M</forename><surname>Bodian</surname></persName></author><author><persName><forename type="middle">Ja</forename><surname>Black</surname></persName></author><author><persName><forename type="middle">N</forename><surname>Kobayashi</surname></persName></author></analytic><monogr><title level="j">Q J Med Br Med J</title><imprint><biblScope unit="volume">34</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="359" to="687"></biblScope><date type="published" when="1965"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Clinical, light and electron microscopv findings in idiopathic hematuria Idiopathic recurrent hematuria and mesangia! IgA-IgG deposits in children (Berger's disease)</title><author><persName><forename type="first">Alexander</forename><forename type="middle">F R</forename><surname>Lannigan</surname></persName></author><author><persName><forename type="first">Bull</forename><forename type="middle">M</forename></persName></author><author><persName><forename type="first">Beufils</forename><forename type="middle">H</forename><surname>Gubler</surname></persName></author><author><persName><surname>Mc</surname></persName></author></analytic><monogr><title level="j">J Clin Path01 Clin Nephrol</title><imprint><biblScope unit="volume">26</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="750" to="63"></biblScope><date type="published" when="1973"></date></imprint></monogr><note>Sinniah. HS. Pwee HS. Lim CH: Glomerular lesions in 16. 17. 18</note></biblStruct><biblStruct><analytic><title level="a" type="main">Immunoglobulin A ne-phropathy</title><author><persName><surname>Zimmermann</surname></persName></author><author><persName><surname>Sw</surname></persName></author><author><persName><surname>Burkholder</surname></persName></author><author><persName><forename type="first">Travis</forename><forename type="middle">M Lb H</forename><surname>Berger</surname></persName></author></analytic><monogr><title level="j">Arch Jntern Med IgA nephropathy in children. Texas Rep Biol Med</title><imprint><biblScope unit="volume">135</biblScope><biblScope unit="issue">239</biblScope><biblScope unit="page">1217</biblScope><date type="published" when="1975"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">asymptomatic microsdopjc hematuria discovered on rou-tine medical examination</title></analytic><monogr><title level="j">Clin</title><imprint><biblScope unit="volume">15</biblScope><biblScope unit="page">216</biblScope><date type="published" when="1976"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Ross JH: Recurrent focal nephritis Idiopathic focal proliferative nephritis associated with persistent hematuria and normal renal function Ann Intern Med 73: 921,197o Benign hematuria with focal glomerulonephritis in adults Recurrent microscopic hematuria, focal nephritis and deposition of immuno-globulin and complement Vernier RL, Resnick JS, hjayer SN: Recurrent hematuria and focal glomerulonephritis Immunoglobulin A associated glomerulonephritis Isolated glomerulonephritis with mesangial IgA deposits</title><author><persName><forename type="first">Michael</forename><forename type="middle">J</forename></persName></author><author><persName><forename type="first">Jones</forename><forename type="middle">Nf</forename></persName></author><author><persName><forename type="first">Dr</forename><forename type="middle">A Da</forename><surname>Davidson</surname></persName></author><author><persName><surname>Deveber</surname></persName></author><author><persName><surname>Ga</surname></persName></author></analytic><monogr><title level="j">Br Med J Q J Med Arch Intern Med J Pediatr Kidney Int Kidney Int Am J Path01 Br Med J</title><imprint><biblScope unit="volume">1</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="686" to="391"></biblScope><date type="published" when="1960"></date></imprint></monogr><note>Recurrent. hematuria</note></biblStruct><biblStruct><analytic><title level="a" type="main">IgA and rlomerular disease</title><author><persName><forename type="middle">Ja</forename><surname>Whitworth</surname></persName></author><author><persName><forename type="middle">S</forename><surname>Leibowitz</surname></persName></author><author><persName><surname>Kennedy</surname></persName></author><author><persName><surname>Mc</surname></persName></author></analytic><monogr><title level="j">Clin Nephrol</title><imprint><biblScope unit="volume">5</biblScope><biblScope unit="page" from="33" to="17"></biblScope></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">JgA ne-phropathy. A syndrome of uniform morphology, diverse clinical features and uncertain prognosis Clin Nephro18: 459,1977 IgA-IGG nephropathy</title><author><persName><surname>Cl&kson</surname></persName></author><author><persName><surname>Ar</surname></persName></author><author><persName><forename type="middle">Ae</forename><surname>Seymour</surname></persName></author><author><persName><surname>Thompson</surname></persName></author><author><persName><surname>Aj</surname></persName></author></analytic><monogr><title level="j">Am J Clin Path01</title><imprint><biblScope unit="volume">67</biblScope><biblScope unit="issue">289</biblScope><date type="published" when="1977"></date></imprint></monogr></biblStruct><biblStruct><analytic><title level="a" type="main">Clinicopathologic correlations of primary hematuria Recurrent or persistent hematuria Berger J: IgA glomerular deposits in renal disease Recurrence of mesangial deposition of IgA after renal transplantation Hereditary nephritis with a characteristic renal lesion Progression of mesangial and focal to diffuse lupus nephritis</title><author><persName><forename type="middle">Ed</forename><surname>Hendler</surname></persName></author><author><persName><forename type="first">M</forename><surname>Kashgarian</surname></persName></author><author><persName><surname>Hayslett Jp Germuth Fg</surname></persName></author><author><persName><surname>Rodriguez</surname></persName></author><author><persName><forename type="middle">J</forename><surname>Berger</surname></persName></author><author><persName><forename type="middle">H</forename><surname>Yaneva</surname></persName></author><author><persName><forename type="middle">B</forename><surname>Nabarra</surname></persName></author></analytic><monogr><title level="m">Immunopathology of the Renal Glomerulus, Boston, Little & Brown Heptinstall RH: Pathology of the Kidney</title><meeting><address>Boston, Little ; Singer DB, Hill LL, Rosenberg HS, et</address></meeting><imprint><publisher>Brown & Co</publisher><date type="published" when="1968"></date><biblScope unit="page" from="458" to="1165"></biblScope></imprint></monogr><note>Recurrent. hematuria in childhood</note></biblStruct></listBibl></back></text></istex:refBibTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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