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10.1093/ndt/gfw060 http://scihub22266oqcxt.onion/10.1093/ndt/gfw060 C5837351!5837351 !27190355     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27190355 &cmd=llinks): Failed to open stream: HTTP request failed! 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Tolvaptan suppresses monocyte chemotactic protein-1 excretion in autosomal-dominant polycystic kidney disease |pdf=|usr=}}{{27190355 }} gab.com Text Tolvaptan suppresses monocyte chemotactic protein-1 excretion in autosomal-dominant polycystic kidney disease JO: Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=27190355 #FOAvip BACKGROUND: Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by multitudes of expanding renal cysts associated with mononuclear interstitial infiltrates. Monocyte chemotactic protein-1 is produced in the kidneys and excreted in the urine (uMCP1) of these patients in increased amounts. In the TEMPO 3:4 trial, tolvaptan slowed the rate of increase in total kidney volume (TKV) and the rate of decline in estimated glomerular filtration rate (eGFR). In a sub-analysis, we determined whether tolvaptan administration for up to 3 years changed the urinary excretion of MCP-1 referenced to creatinine in 869 treated subjects compared with 438 placebo subjects. METHODS: Treatment group differences of uMCP1 at 0.75, 12, 24 and 36 months were evaluated by ANCOVA with factor of treatment and covariate baseline. RESULTS: At baseline, mean uMCP1 was 429 ± 224 pg/mg in the tolvaptan and 434 ± 233 pg/mg in the placebo groups, ?4-fold greater than normal. Log uMCP1 associated positively with log TKV ( r = 0.2645, P < 0.0001) and negatively with eGFR ( r = -0.1555 P < 0.0001) and fasting urine osmolality ( r = -0.1933, P < 0.0001). Tolvaptan reduced uMCP1 13.8 ± 4.4% (P < 0.0001) below placebo-treated subjects at 24 months and 14.4 ± 3.7% (P < 0.0001) at 36 months, and to the same extent in females and males. The effect of tolvaptan on uMCP1 excretion at 36 months extended across CKD Stage 1 (11.1 ± 6.4%, P = 0.0595), CKD 2 (13.9 ± 5.4%, P = 0.0050) and CKD 3 (21.4 ± 8.0%, P = 0.0020). CONCLUSION: Tolvaptan, administered for 3 years to patients with ADPKD, caused a sustained reduction in the urinary excretion of MCP-1 relative to placebo. Twit Text FOAVip Tolvaptan suppresses monocyte chemotactic protein-1 excretion in autosomal-dominant polycystic kidney disease ????Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=27190355 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27190355 #FOAvip English Wikipedia <ref>{{Cite pmid|27190355 }}</ref> Tolvaptan suppresses monocyte chemotactic protein-1 excretion in autosomal-dominant polycystic kidney disease #MMPMID27190355 Grantham JJ ; Chapman AB ; Blais J ; Czerwiec FS ; Devuyst O ; Gansevoort RT ; Higashihara E ; Krasa H ; Zhou W ; Ouyang J ; Perrone RD ; Torres VE Nephrol Dial Transplant 2017[Jun]; 32 (6 ): 969-975 PMID27190355 show ga BACKGROUND: Autosomal-dominant polycystic kidney disease (ADPKD) is characterized by multitudes of expanding renal cysts associated with mononuclear interstitial infiltrates. Monocyte chemotactic protein-1 is produced in the kidneys and excreted in the urine (uMCP1) of these patients in increased amounts. In the TEMPO 3:4 trial, tolvaptan slowed the rate of increase in total kidney volume (TKV) and the rate of decline in estimated glomerular filtration rate (eGFR). In a sub-analysis, we determined whether tolvaptan administration for up to 3 years changed the urinary excretion of MCP-1 referenced to creatinine in 869 treated subjects compared with 438 placebo subjects. METHODS: Treatment group differences of uMCP1 at 0.75, 12, 24 and 36 months were evaluated by ANCOVA with factor of treatment and covariate baseline. RESULTS: At baseline, mean uMCP1 was 429 ± 224 pg/mg in the tolvaptan and 434 ± 233 pg/mg in the placebo groups, ?4-fold greater than normal. Log uMCP1 associated positively with log TKV ( r = 0.2645, P < 0.0001) and negatively with eGFR ( r = -0.1555 P < 0.0001) and fasting urine osmolality ( r = -0.1933, P < 0.0001). Tolvaptan reduced uMCP1 13.8 ± 4.4% (P < 0.0001) below placebo-treated subjects at 24 months and 14.4 ± 3.7% (P < 0.0001) at 36 months, and to the same extent in females and males. The effect of tolvaptan on uMCP1 excretion at 36 months extended across CKD Stage 1 (11.1 ± 6.4%, P = 0.0595), CKD 2 (13.9 ± 5.4%, P = 0.0050) and CKD 3 (21.4 ± 8.0%, P = 0.0020). CONCLUSION: Tolvaptan, administered for 3 years to patients with ADPKD, caused a sustained reduction in the urinary excretion of MCP-1 relative to placebo. |Adult [MESH] |Antidiuretic Hormone Receptor Antagonists/*pharmacology/therapeutic use [MESH] |Benzazepines/*pharmacology/therapeutic use [MESH] |Biomarkers/urine [MESH] |Chemokine CCL2/*urine [MESH] |Creatinine/urine [MESH] |Female [MESH] |Humans [MESH] |Kidney/drug effects [MESH] |Male [MESH] |Middle Aged [MESH] |Polycystic Kidney, Autosomal Dominant/*drug therapy/urine [MESH]Tolvaptan suppresses monocyte chemotactic protein-1 excretion in aut(epmc).pdf DeepDyve Pubget Overpricing