Journal of Veterinary Clinics (한국임상수의학회지)

The Korean Society of Veterinary Clinics (한국임상수의학회)
권호 표지

Description of Clinicopathologic Changes during the Development and Clinical Resolution of Experimentally induced Canine Nephrotic Syndrome

실험적으로 유발한 개 신증후군의 진행 및 치유과정에서의 임상병리학적 변화

  • Eun-wha, Choi (Department of Veterinary Clinical Pathology, College of Veterinary Medicine, Seoul National University) ;
  • Chang-woo, Lee (Department of Veterinary Clinical Pathology, College of Veterinary Medicine, Seoul National University)
  • Published : 2003.12.01
Download PDF
⟨ Previous Next ⟩

Abstract

The purpose of this study is to evaluate urine protein-to-creatinine ratio as a parameter for early detection of nephrotic syndrome and as a parameter for monitoring effectiveness in early course of treatment. Nine healthy dogs were sensitized by intravenous injection with 1 $\mu$g of endotoxin and 5 mg of native bovine serum albumin. After 1 week, 120 mg of cationized bovine serum albumin was injected intravenously 5 times a week. Among nine dogs, five dogs were confirmed as having developed glomerulonephritis and nephrotic syndrome by increase of urine protein-to-creatinine ratio(>1.0), hypoalbuminemia (<1.5 g/dl), hypercholesterolemia (> 240 mg/dl) and azotemia (BUN>40 mg/dl). During the induction of glomerulonephritis and the progression to nephrotic syndrome, the increase of urine protein-to-creatinine ratio was firstly detected. 1 to 4 weeks later, hypoalbuminemia, hypercholesterolemia, and azotemia were detected. Prednisolone (2.2 mg/kg, bid) was administered orally to the dogs with induced nephrotic syndrome. In early stage of treatment, the increase of serum albumin and decrease of serum cholesterol were detected. 1 to 4 weeks later, decrease of urine protein-to-creatinine ratio was detected. It was concluded that urine protein-to-creatinine ratio is a useful parameter for early detection of nephrotic syndrome, and serum albumin and cholesterol are useful parameters for the monitoring in early course of treatment in nephrotic syndrome.

이 연구의 목적은 실험적으로 유발한 면역매개성 사구체 질환이 신증후군으로 진행하는 과정과 치유과정에서 단백뇨 배설에 근거한 조기진단 및 치유과정의 감시에 대한 평가를 하는 것이다. 두당 endotoxin 1 $\mu$g과 native bovine serum albumin 5mg 을 9두의 건강한 개에 정맥주사하여 감작시키고, 그 후 1주일부터 양이온화한 bovine serum albumin 120mg을 주 5회 반복 정맥주사한 결과 5두에서 면역매개성 사구체신염과 신증후군이 발생하였다. 사구체신염이 발생한 실험동물에서는 요단백질/ 크레아티닌 비의 증가 (>1.0), 저알부민혈증 (< g/이), BUN 증가 (>40 mg/dl), 부종 등이 나타났다. 이것은 임상병리학적으로 평가 가능한 면역매개성 사구체시염 및 신증후군 모델견이 제작되었음을 제시하는 것이었다. 사구체신염의 유발과 신증후군의 진행과정에 요단백질/크레아티닌 비의 증가가 저알부민혈증, BUN 증가, 고콜레스테롤혈증보다 1-4주 먼저 출현하였다. 사구체신염에 의해 신증후군이 유발된 실험동물 모두에서 prednisolone 을 2.2 mg/kg씩 1일 2회 경구투여한 결과 혈중 알부민 농도의 증가와 콜레스테롤 농도의 감소가 먼저 일어나고, 그 후 1-4 주에 요단백질/크레아티닌 비가 감소하기 시작하였다. 종합적으로 볼때, 면역매개성 사구체신염성 신증후군의 조기진단에는 요 단백질/크레아티닌 비가 유리한 지표로, 그리고 초기 치유과정의 감시에는 혈청 알부민, 콜레스테롤이 더 유리한 임상 지표로 이용될 수 있음을 확인하였다.

Keywords

References

  1. Bastford SR, Mihatsch MJ, Rawiel M, et al. Surface charge distribution is a determinant of antigen deposition in the renal glomerulus: studies employingcharge-hybndmolecules. Clin Exp Immunol 1991; 86: 471-477 https://doi.org/10.1111/j.1365-2249.1991.tb02955.x
  2. Center SA, Wilkinson E, Smith CA. 24-Hour urine protein/creatinine ratio in dogs with protein-losing nephropathies. J Am Vet Med Assoc 1985; 187: 820-824.
  3. Center SA, Smith CA, Wilkinson E. Clinicopathologic, renal immunofluorescent, and light microscopic features of glomerulonephritis in the dog: 41 cases (1975-1985). J Am Vet Med Assoc 1987; 190: 81-90
  4. Cook AK, Cowgill LD. Clinical and pathological features of protein-losing glomeruar disease in the dog: a review of 137 cases (1985-1992). J Am Anim Hosp Assoc 1996; 32: 313-322
  5. Finco DR. Kidney function. In: Kaneko, J.J., John, W.H., Michael, L.B., ed. Clinical biochemistry of dompstic animals, 5th ed. Sandiego: Academic press. 1997: 441-484
  6. Forrester SD, Lees GE. Urogenital system-Disease of the kidney and ureter. In: Birchard, S.J. and Shering, R.G., ed. Small Animal Practice. Ohio: WB Saunders. 1994: 799-820
  7. Grauer GF, DiBartola SP. Glomerular disease. In: Ettinger, S.J. and Feldman, E.C., ed. Textbook of Veterinary internal medicine, 4th ed. Philadelphia: WB Saunders, 1995: 1760-177
  8. Grauer GF, Thomas CB, Eicker SW. Estimation of quan-titative proteinuria in the dog, using the urine protein-to-creatinine ratio from a random, voided sample. Am J Vet Res 1985; 46: 2116-2119
  9. Kanwar YS. Biophysiology of glomerular filtration and proteinuria. Lab Invest 1984; 51: 7-21
  10. Kaysen GA, Myers BD, Couser WG, Felts JM. Mechanisms and consequences of proteinuria. Lab Invest 1986; 54: 479-498 https://doi.org/10.1111/1523-1747.ep12259296
  11. Lott JA, Stephan VA, Pritchard KA. Evaluation of the coomassie brilliant blue G-250 method for urinary protein. Clin Chem 1983; 29: 1946-1950
  12. Macdougall DF, Cook T, Steward AP, Cattell V. Canine chronic renal disease: prevalence and types of glomerulon-ephritis in the dog. Kidney Int 1986, 29: 1144-1151 https://doi.org/10.1038/ki.1986.120
  13. Wright NG, Mohammed NA, Eckersall PD, Nash AS. Experimental immune complex glomerylonephritis in dogs receiving cationised bovine serum albumin. Res Vet Sci 1985; 38: 322-328