Page 748 - Small Animal Clinical Nutrition 5th Edition

776 Small Animal Clinical Nutrition

Systemic Hypertension
VetBooks.ir In dogs and cats, hypertension usually occurs secondary to
other diseases including kidney disease, obesity, hyperadreno-
corticism, hyperthyroidism, pheochromocytoma and diabetes
mellitus (Kobayashi et al, 1990; Rocchini et al, 1987; Brown et
al, 2007). However, CKD appears to be the disease most com-
monly associated with systemic hypertension (Brown et al,
2007).When considering hypertension in CKD,it is important
to note that CKD may cause hypertension and hypertension
can promote progression of CKD. Systemic hypertension can
also damage a number of other end organs, including the eyes,
central nervous system and cardiovascular system (Morgan,
1986). The IRIS scheme for staging CKD in dogs and cats
identifies substages based on magnitude of systemic blood pres-
Figure 37-3. Microscopic view of early stages of kidney disease. sure and risk of end-organ damage (Table 37-1).
(Above) Photomicrograph (hematoxylin-eosin stain) showing normal Impaired autoregulation occurs in dogs with ischemic acute
glomeruli, tubules and interstitium. (Below) Early progressive chronic kidney failure and reduced renal mass. In normal dogs, the renal
kidney disease. Photomicrograph (hematoxylin-eosin stain) showing
autoregulatory mechanism limits the effect of systemic blood
increased mesangial matrix, increased glomerular cellularity and
pressure changes on renal blood flow and GFR.This protection
increased interstitial infiltrates.
is achieved by adjusting preglomerular resistance so that renal
hemodynamics remain stable between mean systemic arterial
blood pressures of 70 to 150 mm Hg. Dogs with severe reduc-
tions in functional mass have impaired renal autoregulation
with elevations in renal arterial pressure. Impaired autoregula-
tion may lead to renal injury during systemic hypertensive
episodes and contribute to a progressive decline in kidney func-
tion (Brown et al, 1995; Polzin et al, 2005). Hypertension has
been associated with increased risk of uremic crisis and death in
dogs with CKD (Jacob et al, 2003).

Hyperphosphatemia and Secondary Renal
Hyperparathyroidism
Hyperphosphatemia and secondary renal hyperparathyroidism
have been incriminated as causes of progressive renal injury
(Felsenfeld and Llach, 1993; Lumlertgul et al, 1986). Sec-
ondary renal hyperparathyroidism, characterized by increased
PTH concentration, is an inevitable consequence of CKD
(Nagode and Chew, 1992; Nagode et al, 1996; Barber and
Elliott, 1998; Barber et al, 1999) (Figure 37-5). A study of cats
with spontaneous CKD found an overall prevalence of second-
ary renal hyperparathyroidism of 84% (Barber and Elliott,
1998). Hyperparathyroidism was present in 100% of cats with
endstage CKD and 47% of cats with biochemical evidence of
CKD, but no clinical signs. Secondary renal hyperparathy-
roidism may be present based on increased PTH concentra-
tions, even if serum phosphorus concentrations are within the
reference range.
The inciting event in the pathogenesis of secondary renal
hyperparathyroidism is phosphate retention (Figure 37-6).
Figure 37-4. Schematic showing the progressive effect of glomerular
capillary hypertension. Destruction of nephrons decreases phosphorus filtration with a
subsequent increase in serum phosphate, which stimulates
PTH release from the parathyroid gland (Burkholder, 2000;
stitial fibrosis. These mechanisms of glomerular and tubular Polzin et al, 2005). Hyperphosphatemia also decreases ionized
injury explain why even modest levels of proteinuria are associ- calcium concentration, which stimulates PTH secretion. In a
ated with more rapid progression of CKD in dogs (Jacob et al, normal kidney and in early CKD, one effect of PTH is to
2005) and cats (Syme et al, 2006). decrease phosphate resorption in the proximal tubules so that