Pharmacologic Treatment of Hyperlipidemia Reduces Glomerular Injury in Rat 5/6 Nephrectomy Model of Chronic Renal Failure
The role of lipid abnormalities in the pathogenesis of focal glomerulosclerosis was investigated in the rat remnant kidney model of chronic renal failure. Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the l...
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| Veröffentlicht in: | Circulation research 1988-02, Vol.62 (2), p.367-374 |
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| creator | Kasiske, Bertram L OʼDonnell, Michael P Garvis, William J Keane, William F |
| description | The role of lipid abnormalities in the pathogenesis of focal glomerulosclerosis was investigated in the rat remnant kidney model of chronic renal failure. Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the lipid-lowering agent clofibric add. Both serum cholesterol and urine albumin excretion were significantly reduced by cloflbric add. At 10 weeks, the percent of glomeruli with focal glomerulosclerosis was 5 ± 2% in clofibric acid-treated and 24 ± 5% in untreated 5/6 nephrectomy rats (p 0.05) in 5/6 nephrectomy rats. In a separate set of experiments, 5/6 nephrectomy rats were treated with the specific cholesterol synthesis inhibitor, mevinolin. Mevinolin improved serum lipid levels and reduced albnminuria in 5/6 nephrectomy rats without causing significant alterations in blood pressure. Focal glomerulosderosis was also reduced by mevinolln (11±2% versus 30±3%, p |
| doi_str_mv | 10.1161/01.res.62.2.367 |
| format | Article |
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Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the lipid-lowering agent clofibric add. Both serum cholesterol and urine albumin excretion were significantly reduced by cloflbric add. At 10 weeks, the percent of glomeruli with focal glomerulosclerosis was 5 ± 2% in clofibric acid-treated and 24 ± 5% in untreated 5/6 nephrectomy rats (p <0.01). Inulin clearance was greater in clofibric add-treated than in untreated 5/6 nephrectomy rats (0.28 ±0.02 versus 0.22 ±0.02 ml/min 100 g body wt, p <0.05). Body weight, kidney weight, and systemic blood pressure were not significantly altered by clofibric add. Micropuncture studies, performed in separate groups of clofibric add-treated and untreated 5/6 nephrectomy rats, demonstrated elevated single nephron glomerular filtration rates and glomerular capillary pressures 4 weeks after surgery. However, cloflbric add did not significantly alter single nephron glomerular filtration rates (95 ±2.1 nl/min in treated versus 97.0 ± 6.2 nl/min in untreated, p > 0.05) or glomerular capillary pressures (56.6 ± 1.5 mm Hg in treated versus 57.8 ±0.8 mm Hg in untreated, p > 0.05) in 5/6 nephrectomy rats. In a separate set of experiments, 5/6 nephrectomy rats were treated with the specific cholesterol synthesis inhibitor, mevinolin. Mevinolin improved serum lipid levels and reduced albnminuria in 5/6 nephrectomy rats without causing significant alterations in blood pressure. Focal glomerulosderosis was also reduced by mevinolln (11±2% versus 30±3%, p <0.01). These results suggest that lipid abnormalities may be important in the pathogenesis of focal glomerulosderosis in the rat 5/6 nephrectomy model of chronic renal failure.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.res.62.2.367</identifier><identifier>PMID: 3338121</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Cholesterol - blood ; Clofibrate - analogs & derivatives ; Clofibric Acid - pharmacology ; Disease Models, Animal ; Glomerulonephritis - etiology ; Glomerulosclerosis, Focal Segmental - etiology ; Glomerulosclerosis, Focal Segmental - prevention & control ; Hyperlipidemias - complications ; Hyperlipidemias - drug therapy ; Kidney - physiopathology ; Kidney Failure, Chronic - complications ; Kidney Glomerulus - pathology ; Lovastatin - pharmacology ; Male ; Medical sciences ; Nephrectomy ; Nephrons - physiopathology ; Pharmacology. Drug treatments ; Rats ; Rats, Inbred Strains ; Triglycerides - blood ; Urinary system</subject><ispartof>Circulation research, 1988-02, Vol.62 (2), p.367-374</ispartof><rights>1988 American Heart Association, Inc.</rights><rights>1988 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5559-9118ebd4f95cd846d4f71b386054d1dce15aca15efd7d4dd53f3e4a4705c8ed43</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=7651041$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/3338121$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kasiske, Bertram L</creatorcontrib><creatorcontrib>OʼDonnell, Michael P</creatorcontrib><creatorcontrib>Garvis, William J</creatorcontrib><creatorcontrib>Keane, William F</creatorcontrib><title>Pharmacologic Treatment of Hyperlipidemia Reduces Glomerular Injury in Rat 5/6 Nephrectomy Model of Chronic Renal Failure</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>The role of lipid abnormalities in the pathogenesis of focal glomerulosclerosis was investigated in the rat remnant kidney model of chronic renal failure. Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the lipid-lowering agent clofibric add. Both serum cholesterol and urine albumin excretion were significantly reduced by cloflbric add. At 10 weeks, the percent of glomeruli with focal glomerulosclerosis was 5 ± 2% in clofibric acid-treated and 24 ± 5% in untreated 5/6 nephrectomy rats (p <0.01). Inulin clearance was greater in clofibric add-treated than in untreated 5/6 nephrectomy rats (0.28 ±0.02 versus 0.22 ±0.02 ml/min 100 g body wt, p <0.05). Body weight, kidney weight, and systemic blood pressure were not significantly altered by clofibric add. Micropuncture studies, performed in separate groups of clofibric add-treated and untreated 5/6 nephrectomy rats, demonstrated elevated single nephron glomerular filtration rates and glomerular capillary pressures 4 weeks after surgery. However, cloflbric add did not significantly alter single nephron glomerular filtration rates (95 ±2.1 nl/min in treated versus 97.0 ± 6.2 nl/min in untreated, p > 0.05) or glomerular capillary pressures (56.6 ± 1.5 mm Hg in treated versus 57.8 ±0.8 mm Hg in untreated, p > 0.05) in 5/6 nephrectomy rats. In a separate set of experiments, 5/6 nephrectomy rats were treated with the specific cholesterol synthesis inhibitor, mevinolin. Mevinolin improved serum lipid levels and reduced albnminuria in 5/6 nephrectomy rats without causing significant alterations in blood pressure. Focal glomerulosderosis was also reduced by mevinolln (11±2% versus 30±3%, p <0.01). These results suggest that lipid abnormalities may be important in the pathogenesis of focal glomerulosderosis in the rat 5/6 nephrectomy model of chronic renal failure.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cholesterol - blood</subject><subject>Clofibrate - analogs & derivatives</subject><subject>Clofibric Acid - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Glomerulonephritis - etiology</subject><subject>Glomerulosclerosis, Focal Segmental - etiology</subject><subject>Glomerulosclerosis, Focal Segmental - prevention & control</subject><subject>Hyperlipidemias - complications</subject><subject>Hyperlipidemias - drug therapy</subject><subject>Kidney - physiopathology</subject><subject>Kidney Failure, Chronic - complications</subject><subject>Kidney Glomerulus - pathology</subject><subject>Lovastatin - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrectomy</subject><subject>Nephrons - physiopathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Triglycerides - blood</subject><subject>Urinary system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1988</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kctv1DAQxi1EVZbCmROSD4hbsh4_8jiiVV9SKWgpZ8trT0iKEwc7UZX_nqx21cNoZvT95jt8Q8gnYDlAAVsGecSUFzznuSjKN2QDistMqhLekg1jrM5KIdg78j6lZ8ZACl5fkkshRAUcNmT52ZrYGxt8-NNZ-hTRTD0OEw0NvVtGjL4bO4d9Z-ge3Wwx0VsfeoyzN5HeD89zXGg30L2ZqNoW9BHHNqKdQr_Q78GhPxrt2hiG1X2Pg_H0xnR-jviBXDTGJ_x47lfk98310-4ue_hxe7_79pBZpVSd1QAVHpxsamVdJYt1KuEgqoIp6cBZBGWsAYWNK510TolGoDSyZMpW6KS4Il9PvmMM_2ZMk-67ZNF7M2CYky4rVnFesBXcnkAbQ0oRGz3Grjdx0cD0MWzNQO-vf-mCa67XsNeLz2fr-dCje-XP6a76l7NukjW-iWawXXrFykIBk0dMnrCX4CeM6a-fXzDqFo2fWr3-kAkGPIO6qhhft2wtqMV_BBeYCw</recordid><startdate>198802</startdate><enddate>198802</enddate><creator>Kasiske, Bertram L</creator><creator>OʼDonnell, Michael P</creator><creator>Garvis, William J</creator><creator>Keane, William F</creator><general>American Heart Association, Inc</general><general>Lippincott</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>198802</creationdate><title>Pharmacologic Treatment of Hyperlipidemia Reduces Glomerular Injury in Rat 5/6 Nephrectomy Model of Chronic Renal Failure</title><author>Kasiske, Bertram L ; OʼDonnell, Michael P ; Garvis, William J ; Keane, William F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5559-9118ebd4f95cd846d4f71b386054d1dce15aca15efd7d4dd53f3e4a4705c8ed43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1988</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cholesterol - blood</topic><topic>Clofibrate - analogs & derivatives</topic><topic>Clofibric Acid - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Glomerulonephritis - etiology</topic><topic>Glomerulosclerosis, Focal Segmental - etiology</topic><topic>Glomerulosclerosis, Focal Segmental - prevention & control</topic><topic>Hyperlipidemias - complications</topic><topic>Hyperlipidemias - drug therapy</topic><topic>Kidney - physiopathology</topic><topic>Kidney Failure, Chronic - complications</topic><topic>Kidney Glomerulus - pathology</topic><topic>Lovastatin - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nephrectomy</topic><topic>Nephrons - physiopathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Triglycerides - blood</topic><topic>Urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kasiske, Bertram L</creatorcontrib><creatorcontrib>OʼDonnell, Michael P</creatorcontrib><creatorcontrib>Garvis, William J</creatorcontrib><creatorcontrib>Keane, William F</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kasiske, Bertram L</au><au>OʼDonnell, Michael P</au><au>Garvis, William J</au><au>Keane, William F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacologic Treatment of Hyperlipidemia Reduces Glomerular Injury in Rat 5/6 Nephrectomy Model of Chronic Renal Failure</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1988-02</date><risdate>1988</risdate><volume>62</volume><issue>2</issue><spage>367</spage><epage>374</epage><pages>367-374</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>The role of lipid abnormalities in the pathogenesis of focal glomerulosclerosis was investigated in the rat remnant kidney model of chronic renal failure. Rats subjected to right nephrectomy and two-thirds segmental infarction of the left kidney (5/6 nephrectomy) were treated for 10 weeks with the lipid-lowering agent clofibric add. Both serum cholesterol and urine albumin excretion were significantly reduced by cloflbric add. At 10 weeks, the percent of glomeruli with focal glomerulosclerosis was 5 ± 2% in clofibric acid-treated and 24 ± 5% in untreated 5/6 nephrectomy rats (p <0.01). Inulin clearance was greater in clofibric add-treated than in untreated 5/6 nephrectomy rats (0.28 ±0.02 versus 0.22 ±0.02 ml/min 100 g body wt, p <0.05). Body weight, kidney weight, and systemic blood pressure were not significantly altered by clofibric add. Micropuncture studies, performed in separate groups of clofibric add-treated and untreated 5/6 nephrectomy rats, demonstrated elevated single nephron glomerular filtration rates and glomerular capillary pressures 4 weeks after surgery. However, cloflbric add did not significantly alter single nephron glomerular filtration rates (95 ±2.1 nl/min in treated versus 97.0 ± 6.2 nl/min in untreated, p > 0.05) or glomerular capillary pressures (56.6 ± 1.5 mm Hg in treated versus 57.8 ±0.8 mm Hg in untreated, p > 0.05) in 5/6 nephrectomy rats. In a separate set of experiments, 5/6 nephrectomy rats were treated with the specific cholesterol synthesis inhibitor, mevinolin. Mevinolin improved serum lipid levels and reduced albnminuria in 5/6 nephrectomy rats without causing significant alterations in blood pressure. Focal glomerulosderosis was also reduced by mevinolln (11±2% versus 30±3%, p <0.01). These results suggest that lipid abnormalities may be important in the pathogenesis of focal glomerulosderosis in the rat 5/6 nephrectomy model of chronic renal failure.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>3338121</pmid><doi>10.1161/01.res.62.2.367</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Circulation research, 1988-02, Vol.62 (2), p.367-374 |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Biological and medical sciences Cholesterol - blood Clofibrate - analogs & derivatives Clofibric Acid - pharmacology Disease Models, Animal Glomerulonephritis - etiology Glomerulosclerosis, Focal Segmental - etiology Glomerulosclerosis, Focal Segmental - prevention & control Hyperlipidemias - complications Hyperlipidemias - drug therapy Kidney - physiopathology Kidney Failure, Chronic - complications Kidney Glomerulus - pathology Lovastatin - pharmacology Male Medical sciences Nephrectomy Nephrons - physiopathology Pharmacology. Drug treatments Rats Rats, Inbred Strains Triglycerides - blood Urinary system |
| title | Pharmacologic Treatment of Hyperlipidemia Reduces Glomerular Injury in Rat 5/6 Nephrectomy Model of Chronic Renal Failure |
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