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Hereditary Nephritis (hereditary + nephritis)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Haplotype sharing excludes orthologous COL4A3, COL4A4 or MYH9 loci in hereditary nephritis in bull terriers

ANIMAL GENETICS, Issue 2 2009
C. A. O'Leary
No abstract is available for this article. [source]

Renal pathology of polycystic kidney disease and concurrent hereditary nephritis in Bull Terriers

AUSTRALIAN VETERINARY JOURNAL, Issue 6 2002
CA O'LEARY
Objective To describe the renal lesions in Bull Terrier poly-cystic kidney disease (BTPKD), to confirm that the renal cysts in BTPKD arise from the nephron or collecting tubule, and to identify lesions consistent with concurrent BTPKD and Bull Terrier hereditary nephritis (BTHN). Design Renal tissue from five Bull Terriers with BTPKD and eight control dogs was examined by light and transmission electron microscopy. Clinical data were collected from all dogs, and family history of BTPKD and BTHN for all Bull Terriers. Results In BTPKD the renal cysts were lined by epithelial cells of nephron or collecting duct origin that were usually squamous or cuboidal, with few organelles. They had normal junctional complexes, and basal laminae of varying thicknesses. Glomeruli with small, atrophic tufts and dilated Bowman's capsules, tubular loss and dilation, and interstitial inflammation and fibrosis were common. Whereas the lesions seen in BTHN by light microscope were nonspecific, the presence of characteristic ultrastructural glomerular basement membrane (GMB) lesions and a family history of this disease indicated concurrent BTHN was likely in three of five cases of BTPKD. Conclusion This paper provides evidence that renal cysts in BTPKD are of nephron or collecting duct origin. In addition, GBM lesions are described that strongly suggest that BTPKD and BTHN may occur simultaneously. [source]

ABO-incompatible renal transplantation in Epstein syndrome

CLINICAL TRANSPLANTATION, Issue 2010
Masao Ogura
Ogura M, Kikuchi E, Kaito H, Kamei K, Matsuoka K, Tanaka H, Kuroda T, Sekine T, Ito S. ABO-incompatible renal transplantation in Epstein syndrome. Clin Transplant 2010: 24 (Suppl. 22): 31,34. © 2010 John Wiley & Sons A/S. Abstract:, Epstein syndrome (ES) is an autosomal dominant hereditary disease characterized by hereditary nephritis, sensory deafness, and thrombocytopenia. We herein report the case of a 20-yr-old man with ES who underwent ABO blood type-incompatible living-donor kidney transplantation from his mother. He was given platelet transfusion, and his pre-operative number of platelets were 108 × 103/,L. After transplantation, urine output and the decrease in serum creatinine (sCr) were within the acceptable ranges. On the seventh post-operative day (POD), sCr had risen and urine output decreased. Anti-type A antibody rapidly elevated from <2 times (×2) just before transplantation to 64 times (×64), and the patient required hemodialysis again. Resistance index (RI) by ultrasound increased from an average of 0.5 , 0.6 on POD 1 to an average of 0.7 , 0.8 on POD 7. However, several biopsies (POD 4, 7, and 10) showed no obvious findings of acute rejection except for intense C4d deposition. Because acute antibody-mediated rejection was not completely ruled out, he was treated with methyl-prednisolone pulse therapy, plasma exchange, cyclophosphamide, and immunoglobulin. Regardless, his titer of anti-type A antibody was still high, and he still presented oliguria. We performed an emergent splenectomy. Consequently, the levels of anti-type A antibody decreased, the RI also dropped to an average of 0.6. However, on POD 19 and 25 (platelets were 27 × 103/,L and 36 × 103/,L), he developed a massive intraperitoneal hematoma around the graft and region of the removed spleen, which pushed the graft out and caused acute tubular necrosis, resulting in anuria. The RI rose to an average of 0.8 , 1.0 after these episodes. He also experienced bleeding from a duodenal ulcer on POD 21. However, his renal function has fully recovered after acute hemodialysis for 35 d. The latest sCr was 1.5 mg/dL with a recovery in RI to 0.6. Although his platelet count was maintained at a minimum of 50 × 103/,L, he had several severe bleeding episodes, concluding that sufficient platelets are necessary after transplantation in ES. [source]