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10.1007/s00240-014-0664-1 http://scihub22266oqcxt.onion/10.1007/s00240-014-0664-1 C5602548!5602548!24817661     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 269.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Urolithiasis 2014 ; 42 (4): 301-7 Nephropedia Template TP {{tp|p=24817661|t=2014. Determination of urinary lithogenic parameters in murine models orthologous to Autosomal Dominant Polycystic Kidney Disease |pdf=|usr=}}{{24817661}} gab.com Text Determination of urinary lithogenic parameters in murine models orthologous to Autosomal Dominant Polycystic Kidney Disease JO: Urolithiasis http://www.kidney.de/pget.php?&tw=1&pmid=24817661 #FOAvip Autosomal Dominant Polycystic Kidney Disease (ADPKD), a genetic disease caused by mutations in PKD1 gene, is associated with a high prevalence of nephrolithiasis. The underlying mechanisms may encompass structural abnormalities resulting from cyst growth, urinary metabolic abnormalities or both. An increased frequency of hypocitraturia has been described in ADPKD even in the absence of nephrolithiasis, suggesting that metabolic alterations may be associated with ADPKD per se. We aimed to investigate whether non-cystic Pkd1-haploinsufficient (Pkd1+/?) and/or nestin-Cre Pkd1-targeted cystic (Pkd1cond/cond:Nestincre) mouse models develop urinary metabolic abnormalities potentially related to nephrolithiasis in ADPKD. Twenty-four hour urine samples were collected during 3 non-consecutive days from 10?12 and 18?20 week-old animals. At 10?12 weeks of age, urinary oxalate, calcium, magnesium, citrate and uric acid did not differ between test and their respective control groups. At 18?20 weeks, Pkd1+/? showed slightly but significantly higher urinary uric acid vs controls while cystic animals did not. Conclusion: The absence of hypocitraturia, hyperoxaluria and hyperuricosuria in the cystic model at both ages and the finding of hyperuricosuria in the 18?20 week-old animals suggest that anatomic cystic distortions per se do not generate the metabolic disturbances described in human ADPKD-related nephrolithiasis, while Pkd1 haploinsufficiency may contribute to this phenotype in this animal model. Twit Text FOAVip Determination of urinary lithogenic parameters in murine models orthologous to Autosomal Dominant Polycystic Kidney Disease ????Urolithiasis http://www.kidney.de/pget.php?&tw=1&pmid=24817661 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24817661 #FOAvip English Wikipedia <ref>{{Cite pmid|24817661}}</ref> Determination of urinary lithogenic parameters in murine models orthologous to Autosomal Dominant Polycystic Kidney Disease #MMPMID24817661 Ferraz RRN; Fonseca JM; Germino GG; Onuchic LF; Heilberg IP Urolithiasis 2014[Aug]; 42 (4): 301-7 PMID24817661show ga Autosomal Dominant Polycystic Kidney Disease (ADPKD), a genetic disease caused by mutations in PKD1 gene, is associated with a high prevalence of nephrolithiasis. The underlying mechanisms may encompass structural abnormalities resulting from cyst growth, urinary metabolic abnormalities or both. An increased frequency of hypocitraturia has been described in ADPKD even in the absence of nephrolithiasis, suggesting that metabolic alterations may be associated with ADPKD per se. We aimed to investigate whether non-cystic Pkd1-haploinsufficient (Pkd1+/?) and/or nestin-Cre Pkd1-targeted cystic (Pkd1cond/cond:Nestincre) mouse models develop urinary metabolic abnormalities potentially related to nephrolithiasis in ADPKD. Twenty-four hour urine samples were collected during 3 non-consecutive days from 10?12 and 18?20 week-old animals. At 10?12 weeks of age, urinary oxalate, calcium, magnesium, citrate and uric acid did not differ between test and their respective control groups. At 18?20 weeks, Pkd1+/? showed slightly but significantly higher urinary uric acid vs controls while cystic animals did not. Conclusion: The absence of hypocitraturia, hyperoxaluria and hyperuricosuria in the cystic model at both ages and the finding of hyperuricosuria in the 18?20 week-old animals suggest that anatomic cystic distortions per se do not generate the metabolic disturbances described in human ADPKD-related nephrolithiasis, while Pkd1 haploinsufficiency may contribute to this phenotype in this animal model. äDetermination of urinary lithogenic parameters in murine models orthol(epmc).pdf DeepDyve Pubget Overpricing