BACKGROUND AND AIMS: The aim of the study was to investigate the role of the D18S880 microsatellite polymorphism of carnosinase 1 gene (CNDP1), which encodes serum carnosinase, in the development and progression of chronic kidney disease (CKD) of nondiabetic etiology. METHODS: We applied two different approaches. First, a family-based study was carried out comprising 109 patients with CKD caused by chronic glomerulonephritis (GN) or tubulointerstitial nephritis (IN) and their 218 healthy parents using the transmission/disequilibrium test. CNDP1 polymorphism and serum carnosinase activity were determined in all subjects. Serum carnosinase activity was also measured in 20 healthy controls. Second, we performed a case-control study to determine whether polymorphism in CNDP1 gene and other factors influence the progression of renal impairment. RESULTS: Preferential transmission of the 5 allele of CNDP1 polymorphism from heterozygous parents to their offspring with CKD caused by GN was found. There was no association between that polymorphism and the loss of glomerular filtration rate. Serum carnosinase activity was significantly higher in CKD patients than in controls. CONCLUSION: This study found no association between the CNDP1 polymorphism and increased risk for development of CKD caused by IN. However, the polymorphism can influence CKD caused by GN. The progression rate of CKD does not depend on this polymorphism. The increased serum carnosinase activity in the CKD patients may suggest its role in the pathomechanism of the disease.
BACKGROUND AND AIMS: The aim of the study was to investigate the role of the D18S880 microsatellite polymorphism of carnosinase 1 gene (CNDP1), which encodes serum carnosinase, in the development and progression of chronic kidney disease (CKD) of nondiabetic etiology. METHODS: We applied two different approaches. First, a family-based study was carried out comprising 109 patients with CKD caused by chronic glomerulonephritis (GN) or tubulointerstitial nephritis (IN) and their 218 healthy parents using the transmission/disequilibrium test. CNDP1 polymorphism and serum carnosinase activity were determined in all subjects. Serum carnosinase activity was also measured in 20 healthy controls. Second, we performed a case-control study to determine whether polymorphism in CNDP1 gene and other factors influence the progression of renal impairment. RESULTS: Preferential transmission of the 5 allele of CNDP1 polymorphism from heterozygous parents to their offspring with CKD caused by GN was found. There was no association between that polymorphism and the loss of glomerular filtration rate. Serum carnosinase activity was significantly higher in CKDpatients than in controls. CONCLUSION: This study found no association between the CNDP1 polymorphism and increased risk for development of CKD caused by IN. However, the polymorphism can influence CKD caused by GN. The progression rate of CKD does not depend on this polymorphism. The increased serum carnosinase activity in the CKDpatients may suggest its role in the pathomechanism of the disease.
Authors: Thomas Albrecht; Shiqi Zhang; Jana D Braun; Li Xia; Angelica Rodriquez; Jiedong Qiu; Verena Peters; Claus P Schmitt; Jacob van den Born; Stephan J L Bakker; Alexander Lammert; Hannes Köppel; Peter Schnuelle; Bernhard K Krämer; Benito A Yard; Sibylle J Hauske Journal: J Diabetes Res Date: 2017-05-03 Impact factor: 4.011
Authors: Shiqi Zhang; Holger A Lindner; Sarah Kabtni; Jaap van den Born; Stephan Bakker; Gerjan Navis; Bernard Krämer; Benito Yard; Sibylle Hauske Journal: PLoS One Date: 2016-01-22 Impact factor: 3.240
Authors: Angelica Rodriguez-Niño; Sibylle J Hauske; Anna Herold; Jiedong Qiu; Jacob van den Born; Stephan J L Bakker; Bernhard K Krämer; Benito A Yard Journal: J Diabetes Res Date: 2019-12-24 Impact factor: 4.011