Renal
Efficacy
Chronic renal insufficiency
The basis of dietary treatment of dogs with chronic renal insufficiency is the combination of phosphorus and protein restriction and a high intake of the omega-3 fatty acid, eicosapentaenoic acid (EPA). The efficacies of the three nutrients as only variable have only been investigated in dogs with chronic renal insufficiency as induced by partial nephrectomy. In this animal model, the progression of renal failure is inhibited by phosphorus restriction (Finco et al., 1992), protein restriction (Finco et al., 1994) and a high intake of EPA (Brown et al., 2000). A limited intake of phosphorus reduces calcification of the insufficient kidney (Finco et al., 1992), whereas protein restriction particularly inhibits the development of microscopically detectable lesions (Finco et al., 1994) and lowers the morbidity and mortality in relation to uremic syndrome (Polzin et al., 1984). The protective effect of EPA possibly is explained by stimulation of the blood flow through the kidney (Brown et al., 2000) and inhibition of inflammatory reactions in the kidney (Bauer, 2007).
The efficacy of a diet low in phosphorus and protein and high in omega-3 polyunsaturated fatty acids has been demonstrated in dogs with spontaneous, chronic renal insufficiency (Jacob et al., 2002). In the trial that lasted 24 months, there were 17 control patients and 21 test patients fed a normal maintenance food and a kidney diet, respectively. The kidney diet reduced the incidence of uremia and lowered the concentration of serum creatinine. Within the duration of the clinical trial, feeding the kidney diet reduced mortality from 94% to 52%. The therapeutic diet had phosphorus and protein contents that are similar to those of SANIMED Renal. Apart from protein restriction, urea synthesis is further inhibited by the high content of beet pulp in SANIMED Renal. In the colon, the beet pulp stimulates the conversion of ammonia into bacterial protein so that less ammonia reaches the liver (Middelbos et al., 2007).
The extra characteristics of SANIMED Renal are a low sodium content, positive base excess and a high level of vitamin E. Chronic renal insufficiency can lead to glomerular hypertension (Brown et al., 1998), which apart from the high EPA-content (Brown et al., 2000) is further beneficially influenced by the low level of sodium (Chandler, 2008). In patients with kidney failure, the excretion of metabolically generated acids may be diminished, causing a tendency towards acidosis (Langston, 2008). The positive base excess of SANIMED Renal contributes to the prevention of acidosis. There are indications that chronic renal failure is associated with increased oxidative stress which stimulates the progression of the condition (Brown, 2008). The addition of extra vitamin E to the diet may reduce the oxidative damage (Tain et al., 2007) and thereby retard the progression of kidney disease.
Liver insufficiency
The most important goal of dietary treatment of liver patients is prevention of the development of encephalopathy. Accumulation of ammonia through a diminished conversion into urea probably is the main cause of hepatic encephalopathy. The supply of ammonia, and thereby its accumulation, can be reduced by a diminished protein breakdown in the liver and a reduced uptake of ammonia by the colonic wall (Bauer, 1996; Center, 1998). The low protein content of SANIMED Renal reduces the magnitude of protein degradation. The high level of beet pulp in the diet stimulates the incorporation of ammonia into bacterial protein within the lumen of the colon so that less ammonia enters the circulation (Middelbos et al., 2007). The low amount of sodium in SANIMED Renal contributes to the control of portal hypertension and ascites (Michel, 1995).
Ammonium urate, calcium oxalate and cystine urolithiasis
SANIMED Renal is suitable for patients in order to prevent urolithiasis in the form of ammonium urate, calcium oxalate and cystine. Dietary treatment to prevent recurrence of urolithiasis is aimed at lowering the concentrations of the stone-forming components in urine and steering the urinary pH towards a range that counteracts stone development (Bartges et al., 2004). SANIMED Renal meets these prerequisites.
The formation of ammonium urate and cystine is promoted by acidic urine (Osborne et al., 1989) and this indirectly also holds for calcium oxalate. A low urinary pH stimulates calcium excretion which raises the concentration of calcium in urine (Gevaert et al., 1991) and thus increases the risk of formation of calcium oxalate. Dissolution and formation of crystals of calcium oxalate is not dependent on pH within its physiological range. SANIMED Renal will induce an average urinary pH of 6.9, which is in the neutral zone.
The amount of protein in the diet reduces the concentration of ammonium in urine (Bartges et al., 1995) and also that of cystine in patients with cystinuria (Osborne et al., 1999). Because the amino acid glycine is the substrate for oxalate synthesis, it is acceptable that the low protein content of SANIMED Renal diminishes the production of oxalate. The low level of calcium in the diet contributes to a low urinary calcium concentration which antagonizes the formation of calcium oxalate. The low protein content implies a low amount of purines and consequently a diminished synthesis of urate in patients.
SANIMED Renal counteracts hypercalciuria and hyperoxaluria which renders it effective in the prevention of development of calcium oxalate urolithiasis in dogs (Stevenson et al., 2004). The low protein content of SANIMED Renal and the induction of a neutral urinary pH will antagonize the formation of ammonium urate (Bartges et al., 1995) and cystine (Osborne et al., 1999).