Page 762 - Small Animal Clinical Nutrition 5th Edition

790 Small Animal Clinical Nutrition

ever, until results of such studies are available, it has been rec-
VetBooks.ir ommended that modest dietary avoidance of salt be encouraged
in human patients with CKD, especially if they have hyperten-
sion and/or proteinuria (Jones-Burton et al, 2006).
The long-term effects of altering dietary sodium intake alone
in cats and dogs with naturally occurring CKD have not been
reported. Feeding veterinary therapeutic renal foods with
decreased sodium (0.18 to 0.3% DM sodium in cats and 0.17%
DM sodium in dogs) has been associated with increased sur-
vival time compared with feeding maintenance foods that con-
tain more sodium (0.4 to 1.1% DM sodium in cats and 0.4%
DM sodium in dogs) (Ross et al, 2006; Jacob et al, 2002; Elliott
et al, 2000). Several reports describe short-term effects (seven
days to six months) of feeding differing amounts of sodium on
Figure 37-11. Survival of dogs with experimentally induced chronic renal function in dogs and cats (Buranakarl et al, 2004; Greco
kidney disease fed low-protein foods with different levels of phos-
et al, 1994; Luckschander et al, 2004; Kirk et al, 2006; Xu et al,
phorus. Note that survival was much improved in dogs consuming
2009). In healthy adult cats (mean age = seven years), feeding
the low-phosphorus food. (Adapted from Brown SA, Crowell WA,
Barsanti JA, et al. Beneficial effects of dietary mineral restriction in foods containing 1.11% DM sodium was not associated with
dogs with marked reduction of functional renal mass. Journal of the increased serum concentrations of urea nitrogen, creatinine or
American Society of Nephrology 1991; 1: 1169-1179.) phosphorus, compared with feeding foods containing 0.55%
DM sodium for six months (Xu et al, 2009). In this study, data
from nine cats with serum creatinine values >1.5 mg/dl were
evaluated; there were no significant differences between groups
based on dietary sodium intake. Urine concentrating ability for
these nine cats was not reported; however, mean urine specific
gravity for all cats at the beginning of the study ranged from
1.049 to 1.053. In a study in cats with induced kidney disease,
three different amounts of sodium (0.34, 0.68 and 1.35% DM)
were fed for seven days (Buranakarl et al, 2004). Feeding the
lowest amount of sodium was associated with increased urinary
potassium loss and reduced GFR (Buranakarl et al, 2004).The
effects of high salt intake (1.19% DM sodium) for three
months were evaluated in six cats with naturally occurring
CKD (azotemia with urine specific gravity <1.035) (Kirk et al,
2006). The CKD cats fed the high-salt food had significant
and progressive increases in blood urea nitrogen, serum creati-
nine and serum phosphorus compared with results from cats
consuming food with 0.37% DM sodium (Kirk et al, 2006).
Two of the cats were removed from the study after beginning
Figure 37-12. Proposed relationship between dietary potassium the high-sodium food due to decreased food intake; this did not
intake, excessively acidifying foods and feline chronic kidney affect results of statistical analysis or study conclusions.
disease. A number of studies examined the interaction of dietary so-
dium with other ions, including chloride.The full expression of
(Figure 37-7). In human patients with CKD, the anti-protein- sodium chloride-sensitive hypertension in people depends on
uric effect of angiotensin-converting enzyme (ACE) inhibition the concomitant administration of both sodium and chloride
was strongly dependent on dietary sodium restriction; increased (Kurtz et al, 1987; Boegehold and Kotchen, 1989; Luft et al,
sodium intake virtually abolished the anti-proteinuric effect of 1990). In experimental models using rodents with sodium
the ACE inhibitor lisinopril (Heeg et al, 1989). Administration chloride-sensitive hypertension and in clinical studies with
of ACE inhibitors has been associated with decreased protein- small numbers of hypertensive people, blood pressure and vol-
uria in dogs and cats (Grauer et al, 2000; King et al, 2006; ume were not increased by a high dietary sodium intake provid-
Mizutani et al, 2006). The role of dietary sodium on beneficial ed with anions other than chloride. Furthermore, high chloride
effects of ACE inhibition has not been evaluated in dogs and intake without sodium has less effect on blood pressure than
cats; however, most patients in these studies were also fed vet- does sodium chloride intake (Kurtz et al, 1987; Boegehold and
erinary therapeutic renal foods, which likely contained Kotchen, 1989; Kotchen et al, 1981). The failure of non-chlo-
decreased amounts of sodium. Additional clinical studies are ride sodium salts to produce hypertension or hypervolemia may
needed to evaluate the role of salt in progression of CKD; how- be related to their failure to expand plasma volume because the