title: Renal Function and Hematology in Rats with Congenital Renal Hypoplasia.
abstract: Renal hypoplasia due to a congenitally reduced number of nephrons progresses to chronic kidney disease and may cause renal anemia, given that the kidneys are a major source of erythropoietin in adults. Hypoplastic kidney (HPK) rats have only about 20% of the normal number of nephrons and develop CKD. This study assessed the renal function and hematologic changes in HPK rats from 70 to 210 d of age. HPK rats demonstrated deterioration of renal excretory function, slightly macrocytic erythropenia at all days examined, age-related increases in splenic hemosiderosis accompanied by a tendency toward increased hemolysis, normal plasma erythropoietin levels associated with increased hepatic and decreased renal erythropoietin production, and maintenance of the response for erythropoietin production to hypoxic conditions, with increased interstitial fibrosis at 140 d of age. These results indicate that increases in splenic hemosiderosis and the membrane fragility of RBC might be associated with erythropenia and that hepatic production of erythropoietin might contribute to maintaining the blood Hgb concentration in HPK rats.
authors.affiliation: Laboratory of Veterinary Physiology, Unit of Functional Morphology, Department of Basic Veterinary Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan.
authors.forename: Hidenori
authors.initials: H
authors.lastname: Yasuda
authors.affiliation: Laboratory of Veterinary Physiology, Unit of Functional Morphology, Department of Basic Veterinary Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan.
authors.forename: Kohei
authors.initials: K
authors.lastname: Amakasu
authors.affiliation: Laboratory of Veterinary Physiology, Unit of Functional Morphology, Department of Basic Veterinary Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Tochigi
authors.affiliation: Laboratory of Veterinary Physiology, Unit of Functional Morphology, Department of Basic Veterinary Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan.
authors.forename: Kentaro
authors.initials: K
authors.lastname: Katayama
authors.affiliation: Laboratory of Veterinary Physiology, Unit of Functional Morphology, Department of Basic Veterinary Medicine, School of Veterinary Medicine, Faculty of Veterinary Science, Nippon Veterinary and Life Science University, Tokyo, Japan. hiroetsu@nvlu.ac.jp.
authors.forename: Hiroetsu
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000367:Age Factors; D000740:Anemia / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D000818:Animals; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000235:genetics; D004195:Disease Models, Animal; D018450:Disease Progression; D004912:Erythrocytes / Q000378:metabolism / Q000473:pathology; D004921:Erythropoietin / Q000097:blood; D005355:Fibrosis; D020022:Genetic Predisposition to Disease; D006461:Hemolysis; D006486:Hemosiderosis / Q000097:blood / Q000209:etiology / Q000503:physiopathology; D007501:Iron / Q000097:blood; D007668:Kidney / Q000002:abnormalities / Q000378:metabolism / Q000503:physiopathology*; D007674:Kidney Diseases / Q000097:blood / Q000151:congenital / Q000503:physiopathology*; D008297:Male; D009154:Mutation; D009996:Osmotic Fragility; D010641:Phenotype; D051381:Rats; D011919:Rats, Inbred Strains; D051436:Renal Insufficiency, Chronic / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D013154:Spleen / Q000378:metabolism / Q000473:pathology
chemical_list: D015415:Biomarkers; D002352:Carrier Proteins; C436025:Spag5 protein, rat; C000599851:erythropoietin, rat; D004921:Erythropoietin; D007501:Iron