Page 761 - Small Animal Clinical Nutrition 5th Edition

Chronic Kidney Disease 789

overload and edema. If sodium intake is inadequate, negative
VetBooks.ir sodium balance develops with resultant declines in extracellular
fluid volume, plasma volume and GFR. Also, excessive dietary
sodium intake may increase the absorptive workload on surviv-
ing nephrons, increasing oxygen consumption and contributing
to hypoxia and increased production of damaging ROS. (See
Antioxidants below.)
Limiting dietary sodium intake has been recommended for
patients with CKD because of its potential to help manage
concomitant hypertension; however, this has not been critically
evaluated in dogs and cats with CKD. Systemic hypertension
has been reported in 9 to 93% of dogs and 19 to 65% of cats
with CKD (Elliott et al, 2001; Syme et al, 2002; Brown et al,
2007). The mechanism for hypertension in renal parenchymal
disease is not well understood. It has been postulated that
reduced intrarenal blood flow activates the renin-angiotensin-
aldosterone system, which leads to chronic expansion of the
extracellular fluid and elevations in blood pressure. Other pos-
sible mechanisms include secondary renal hyperparathyroidism
and reduced levels of renal vasodilators such as prostaglandins.
Kidney disease may cause hypertension, and the kidneys may
suffer the consequences of uncontrolled hypertension. The
mechanism by which hypertension damages the kidney is not
completely understood (Klahr, 1989). Canine CKD patients Figure 37-10. Photomicrographs of the renal cortex from cats with
with major reduction of functional renal mass have impaired experimentally induced chronic kidney disease. (Above) Renal tissue
from a cat fed a low-phosphorus food (0.42% DM phosphorus).
renal autoregulation as evidenced by increased renal arterial pres-
Mineralized foci are not seen in this kidney (hematoxylin-eosin stain).
sure. Dysfunctional autoregulation may result in further renal (Below) Renal tissue from a cat fed a food with normal phosphorus
damage during hypertensive episodes, which contribute to a pro- levels (1.56% DM phosphorus). Mineralization (black foci), fibrosis
gressive decline in kidney function (Brown et al, 1995). Dogs and mononuclear cell infiltrates are extensive compared with that
with surgically induced CKD with more pronounced hyperten- seen on a renal photomicrograph from a cat eating the lower phos-
phorus food (von Kossa’s stain). (Reprinted with permission from
sion had significantly lower GFR values, higher UPC ratios and
Ross LA, Finco DR, Crowell WA. Effect of dietary phosphorus restric-
increased renal lesions (Finco, 2004). Hypertension has been tion on the kidneys of cats with reduced renal mass. American
associated with increased risk of uremic crisis and death in dogs Journal of Veterinary Research 1982; 43: 1023-1026.)
with naturally occurring CKD (Jacob et al, 2003). In cats with
CKD, however, hypertension has not been associated with
decreased survival (Elliott et al, 2001; Syme et al, 2006; Jepson et
al,2007).Based on other studies,increased dietary sodium intake
has not been associated with increased blood pressure in healthy
cats, dogs, cats with induced kidney disease, or cats with natural-
ly occurring CKD (Buranakarl et al, 2004; Greco et al, 1994;
Luckschander et al, 2004; Kirk et al, 2006).
Currently, the role of sodium intake in progression of CKD
is a topic of considerable interest in human medicine and has
been mentioned in dogs and cats with CKD (Polzin, 2007;
Chandler, 2008). Sodium may be directly nephrotoxic and
restricting sodium intake may be beneficial in CKD, independ-
ent of its effect on blood pressure (Cianciaruso et al, 1998; Ritz
et al, 2006; Jones-Burton et al, 2006; Sanders, 2004; Weir and
Fink, 2005; Verhave et al, 2004). Potential mechanisms for the
negative effects of salt in patients with CKD include: 1)
increased TGF-β expression in renal endothelial cells, which
may lead to renal fibrosis, 2) increased oxidative stress and 3)
increased proteinuria. Angiotensin II or increased dietary salt
intake may independently increase production of TGF-β
(Sanders, 2004). Increased production of TGF-β, in turn,
results in increased renal oxidative stress by production of ROS