Page 808 - Small Animal Clinical Nutrition 5th Edition
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838        Small Animal Clinical Nutrition



                  nia and bromsulphalein retention. Other non-Dalmatian  miniature schnauzers with ammonium urate uroliths associat-
        VetBooks.ir  breeds that appear to have a significantly higher incidence of  ed with portal vascular anomalies. In these dogs, urine uric acid
                                                                      concentrations were approximately 50 mg/kg body weight/day
                  urate urolithiasis based on quantitative urolith analyses are
                                                                      and urine ammonia concentrations were approximately 1.5
                  miniature schnauzers, Shih  Tzus and  Yorkshire terriers
                  (Osborne et al, 1995).                              mM/kg body weight/day while the dogs consumed a growth-
                    Urate uroliths from non-Dalmatian dogs have been recog-  type food.When two of these dogs consumed a purine-restrict-
                  nized most frequently in males. Uroliths have been detected  ed food, urine uric acid concentrations were approximately 17
                  throughout the lifespan of affected dogs; however, they were  mg/kg body weight/day and urine ammonia concentrations
                  most frequently detected in dogs three to six years of age.  were approximately 0.6 mM/kg body weight/day.
                    Regardless of cause, severe hepatic dysfunction may predis-  Not all dogs with portal systemic anomalies develop concur-
                  pose dogs to urate lithogenesis, especially ammonium urate  rent ammonium urate urolithiasis. Definition and characteriza-
                  uroliths. Observations and evidence derived from experimental  tion of other factors responsible for promoting or inhibiting
                  models suggest that prolonged consumption of foods with  urate lithogenesis in affected dogs require further investigation.
                  markedly restricted levels of protein may be associated with for-  We have observed urate urocystolith formation in miniature
                  mation of urate uroliths in dogs (Kruger and Osborne, 1986).  schnauzers and Yorkshire terriers with hepatic microvascular
                  Biochemical and histologic evaluation of these dogs suggests  dysplasia. Dogs with this disorder do not have macrovascular
                  that long-term consumption of foods severely restricted in pro-  shunts. Rather, intrahepatic microvascular shunting apparently
                  tein may induce hepatocellular dysfunction and concomitant  occurs. Clinical signs and biochemical abnormalities are similar
                  hyperuricemia. Hepatic cirrhosis has also been associated with  to those seen in dogs with macroscopic vascular shunts. When
                  urate uroliths in dogs and other species (Rothuizen and van den  affected dogs consumed a growth-type food, urinary uric acid
                  Ingh, 1980). However, foods with severely restricted protein  excretion was approximately 30 mg/kg body weight/24 hours,
                  levels and other causes of hepatic dysfunction have been  urinary ammonia excretion was approximately 1.25 mmol/kg
                  uncommon causes of ammonium urate urolithiasis. None-  body weight/24 hours and urinary pH was less than 6.5 pH
                  theless, their significance relative to ammonium urate lithogen-  units. When dogs were fed a purine-restricted food, urinary
                  esis deserves further study.                        uric acid excretion was approximately 16 mg/kg body
                                                                      weight/24 hours, urinary ammonia excretion was approximate-
                  Dogs with Portal Vascular Anomalies or Hepatic      ly 0.5 mmol/kg body weight/24 hours and urinary pH was
                  Microvascular Dysplasia                             greater than 7.0 pH units.
                  Ammonium urate uroliths have frequently been observed in  Not all dogs with portal systemic anomalies or hepatic
                  dogs with portal vascular anomalies. These uroliths occur in  microvascular dysplasia develop concurrent ammonium urate
                  males and females and usually have been detected before dogs  urolithiasis. Definition and characterization of other factors
                  reach three years of age (Rothuizen and van den Ingh, 1980;  responsible for promoting or inhibiting urate lithogenesis in
                  Marretta et al, 1981; Hardy and Klausner, 1983; Kruger and  affected dogs require further investigation.
                  Osborne, 1986).
                    Direct communication between the portal and systemic vas-  Dietary Risk Factors
                  culature shunts blood around the liver. Severe hepatic atrophy  Concentrations of lithogenic substances in urine depend on urine
                  and diminished hepatic function may occur as a result. Hepatic  volume. Because commercial dry foods are associated with pro-
                  dysfunction in turn is associated with reduced hepatic conver-  duction of less urine compared with moist foods,consumption of
                  sion of uric acid to allantoin and reduced conversion of ammo-  dry foods is likely a risk factor for urate urolith formation.
                  nia to urea. The predisposition of dogs with portal vascular  Dalmatian dogs consuming foods containing more than 20%
                  anomalies to urate urolithiasis is probably associated with con-  dry matter (DM) protein, and protein sources high in purines
                  comitant hyperuricemia, hyperammonemia, hyperuricuria and  and purine precursors (Table 39-3) are at increased risk for
                  hyperammonuria (Kruger and Osborne, 1986; Hardy and  urate lithogenesis. Because urate uroliths associated with portal
                  Klausner, 1983). Serum uric acid concentrations in 15 dogs  vascular anomalies are often diagnosed in dogs less than one
                  with portal vascular anomalies evaluated at the University of  year of age, it is probable that they were consuming foods with
                  Minnesota Veterinary Teaching Hospital were increased (val-  increased protein content.
                  ues ranged from 1.2 to 4.0 mg/dl) (Hardy and Klausner, 1983).  Urine acidity is a risk factor for urate lithogenesis because the
                  Concurrent hyperuricuria, hyperammonuria, hyperuricemia  solubility of most purines, especially ammonium urate, is pH-
                  and hyperammonemia were observed in an 18-month-old  dependent. Therefore, consumption of foods that promote
                  Bernese mountain dog with recurrent ammonium urate  aciduria (e.g., high-protein foods or those with other acidifying
                  uroliths associated with a portal vascular anomaly (Kruger and  ingredients) may be a risk factor.
                  Osborne, 1986). This dog had a urine uric acid concentration
                  of 42 mg/kg body weight/day and a urine ammonia concentra-
                  tion of 3.2 mM/kg body weight/day while the dog was fed a  BIOLOGIC BEHAVIOR
                  protein-restricted food. Hyperuricuria, hyperammonuria,
                  hyperuricemia and hyperammonemia were observed in three  Purine uroliths have the potential to undergo spontaneous dis-
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