Evaluation of Urinary Protein Electrophoresis and Albuminuria in Dogs with Hyperadrenocorticism, and Relationship to Systemic Arterial Blood Pressure
ACVIM 2008
C.Z. Cavalcante1; M.M. Kogika1; M.L. Santoro2; A. Bacic1; S.I. Miyashiro1; J.P. Sault1; D.M.N. Simões1; C.S. Prosser1
1School of Veterinary Medicine, University of São Paulo, Brazil; 2Institute Butantan, São Paulo, Brazil

Hyperadrenocorticism (HAC) is a common endocrinopathy in dogs; chronic hypercortisolemia may promote several complications including glomerulonephritis (GN) and systemic arterial hypertension, and this latter per se may also cause secondary GN or worsening of previous glomerular disease. Loss of albumin in urine is characteristic of glomerular diseases. The aim of the current study was to investigate proteinuria, qualitatively and quantitatively, and whether hypertension is associated with increased albuminuria, in dogs with naturally occurring HAC. The qualitative study of proteinuria was performed by sodium dodecyl sulphate polyacrilamide gel electrophoresis (SDS-PAGE) stained with Comassie blue, and for the quantitative evaluation urine protein-to-creatinine (UPC) ratio, normalized albumin (nUAlb) concentration, and urinary albumin-to-creatinine (UAC) ratio (using a competitive canine albumin capture ELISA) were determined.

Thirty dogs of various breeds (6 male, 24 female) with documented HAC, ranging in age from 5 to 13 y-old were subdivided in two groups as follows: group I composed of 13 dogs with hypertension (systolic pressure > 180 mmHg) and group II consisted of 17 normotensive dogs. None of the dogs had received anti-hypertensive drugs. Results were compared with data of 30 clinically healthy dogs (controls). All data of HAC dogs (groups I and II) compared with controls were statistically different. Hypertension in dogs with HAC did not affect the magnitudes of proteinuria or albuminuria when compared to normotensive HAC dogs (mean ± SEM, respectively), concerning UPC ratio (3.68 ± 1.21 vs 2.22 ± 0.76; P > 0.05), nUAlb concentration (0.13 ± 0.03 vs 0.11 ± 0.05 mg/mL; P > 0.05) and UAC ratio (0.92 ± 0.31 vs 1.03 ± 0.52; P > 0.05). Also the comparison of molecular weights of urinary proteins of HAC dogs of groups I and II showed no difference; low molecular weight was considered for bands < 60 kDa (LMW--region B) and high molecular weight proteins for bands > 60 kDa (HMW--region A, which albumin is included). UPC ratio determinations for each region, LMW--region B (1.10 ± 0.51 vs 0.47 ± 0.15; P > 0.05) and HMW--region A (2.58 ± 0.85 vs 1.74 ± 0.63; P > 0.05), also demonstrated no significant difference.

In conclusion, dogs with hyperadrenocorticism showed tubular lesions detected by increased number of LMW proteins bands (tubular proteinuria) as well as glomerular lesions characterized by the presence of albuminuria and HMW proteins bands in urine, independently of systemic arterial hypertension, suggesting that blood pressure did not influence consistently the intensity of urinary protein loss or glomerular damage, and chronic hypercortisolemia is likely to be the main cause of the development of kidney disease.

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Marcia Kogika

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