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 25-28 September, 2018 | Singapore
of the underlying disease may resolve proteinuria; however, some patients will remain proteinuric due to the presence of irreversible damage. When proteinuria persists after elimination of the underlying disease
or when the latter neither can be identified nor be eliminated, therapy is merely symptomatic. Treatment goals include decreasing the magnitude of proteinuria to the reference range to minimize progressive
kidney damage, as well as preventing and treating
the secondary consequences of the protein loss (e.g., thromboembolism).
Azotemic patients require therapeutic intervention at a lower magnitude of proteinuria compared to non- azotemic patients. Current guidelines recommend treating non-azotemic patients when UPC ratio is ≥2.0, while azotemic dogs and cats are to be treated when UPC≥0.5 and UPC≥0.4, respectively.
Standard therapy
Dietary modification, angiotensin converting enzyme inhibition (ACEi) and angiotensin receptor blockade (ARBs) are the mainstay of therapy. Protein restriction
is one of the dietary modifications recommended for patients with protein losing nephropathy. Even though counterintuitive, increasing dietary protein amounts is associated with increased albuminuria and may result in decreased serum albumin concentration. ACEi and ARBs decrease the efferent glomerular arteriolar resistance, resulting in decreased glomerular transcapillary hydraulic pressure. Administration of ACEi and ARBs should be exercised with caution, especially in severely and acutely azotemic patients. Low dose aspirin (0.5 mg/kg, PO, q12- 24 hr) may also decrease proteinuria in dogs. It has been shown that glomerular damage may be prevented by thromboxane release inhibition, thus preventing platelet aggregation and neutrophil chemotaxis. An additional potential advantage of low dose aspirin therapy is decreasing the risk of thromboembolism, especially in animals with a decreased hypoantithrombinemia.
When kidney biopsy is obtained and there is evidence for immune complex deposition, immunosuppression should be initiated. Empirical application of immunosuppressive/anti-inflammatory therapy should
be considered for animals with severe, persistent, or progressive glomerular disease in which there is renal biopsy supported evidence of an immune pathogenesis and no identified contraindication to immunosuppressive therapy. For diseases associated with profound proteinuria, attendant hypoalbuminemia, nephrotic syndrome, and/or rapidly progressive azotemia, single drug or combination therapy consisting of rapidly acting immunosuppressive drugs is recommended.
Based on preliminary, uncontrolled clinical experience with mycophenolate and its low rate of serious complications, mycophenolate is recommended for therapy of dogs with glomerular disease of an apparent immune pathogenesis. Short-term administration of glucocorticoids may be recommended in fulminate cases where immediate immunosuppression is required if their use is adjusted to minimize their adverse effects. However, on the basis of current practice perceptions and anecdotal experience, the use of glucocorticoid therapy should be tapered to the minimally effective dose as quickly as possible due to predictable side effects (3).
Monitoring of proteinuria
When the degree of proteinuria is mild and therapeutic intervention is not indicated, periodic monitoring should include urinalysis, UPC ratio, and serum creatinine
and albumin concentration at least every 3-6 months. When therapy is applied, closer monitoring should be performed. In high-risk patients serum creatinine should be monitored 3-5 days after initiation of ACEi/ARBs to identify a significant decrease in glomerular filtration rate. Urinary protein to creatinine ratio should be monitored periodically and therapy should be adjusted. Due to day to day variation, not every change in UPC ratio would
be considered significant. At least a 35% or 80% change should be demonstrated when the UPC ratio is high (around 12) or low (around 0.5), respectively. In animals with progressive kidney disease, the magnitude of proteinuria may decrease in late stages of the disease due to a reduction in the number of remaining nephrons through which protein loss can occur.
1. Jacob F, Polzin DJ, Osborne CA, Neaton JD, Kirk CA, Allen TA, et al: Evaluation of the association between initial proteinuria and morbidity rate or death in dogs with naturally occurring chronic renal failure. J Am Vet Med Assoc. 2005 Feb;226(3):393-400.
2. Syme HM, Markwell PJ, Pfeiffer D, Elliott J: Survival of cats with naturally occurring chronic renal failure is related to severity of proteinuria. J Vet Intern Med 2006 May-June; 20(3):528-35.
3. Segev G, Cowgill LD, Heiene R, Labato MA, Polzin DJ. Consensus recommendations for immunosuppressive treatment of dogs with glomerular disease based on established pathology. J Vet Intern Med. 2013 Nov-Dec; Suppl 1:S44-54.

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