Page 746 - Small Animal Clinical Nutrition 5th Edition

774 Small Animal Clinical Nutrition

VetBooks.ir Table 37-6. Distinguishing between acute and chronic kidney disease in dogs and cats on the basis of clinical and laboratory findings.*

Findings
Chronic kidney disease
Acute kidney disease
Clinical findings
Acute onset of clinical signs
(often over weeks to months)
(usually <seven days) Vague onset of clinical signs
Usually moderately to severely depressed Alert, responsive or only slightly depressed
Urine volume often decreased Polyuria/polydipsia more likely
Often good body condition May be thin
Kidneys enlarged, painful or may be normal Kidneys small, irregular or may be normal
Laboratory and diagnostic Normal or increased hematocrit; anemia may Nonregenerative anemia typical; hematocrit
imaging findings result from blood loss (e.g., gastrointestinal decreases progressively over time
hemorrhage)
Serum urea nitrogen and creatinine previously Serum urea nitrogen and creatinine previously
normal but increase progressively increased and typically remain stable
Normal to increased serum potassium Normal to decreased serum potassium,
especially in cats
Moderate to severe metabolic acidosis Mild to moderate metabolic acidosis
Urinary casts in some patients Usually no urinary casts
Proteinuria or glucosuria may result from acute Proteinuria often present, more likely due to
tubular necrosis glomerular disease
Bone density normal Bone density may be decreased
*Modified from Vaden SL. Differentiation of acute from chronic renal failure. In: Bonagura JD. Kirk’s Current Veterinary Therapy XIII.
Philadelphia, PA: WB Saunders Co, 2000; 856-858.

ring CKD (Table 37-7). In addition, sequelae of CKD (e.g.,
Table 37-7. Potential mechanisms in the pathogenesis of
chronic kidney disease. hypertension, proteinuria, metabolic acidosis and tubulointersti-
tial injury), changes in lipid metabolism and coagulation and
Altered lipid metabolism
Amyloidosis normal renal aging may contribute to progression. Although
Compensatory renal growth (hypertrophy) some of these mechanisms initially are adaptive when renal
Effects of renal aging function declines, they may ultimately lead to progressive renal
Glomerular hyperfiltration
Glomerular hypertension injury (Figure 37-2). In addition, these etiopathogenic mecha-
Hyperphosphatemia and secondary renal hyperparathyroidism nisms are not mutually exclusive and in some instances may act
Inadequate urinary concentration synergistically. Understanding these mechanisms helps guide
Increased renal ammoniagenesis
Metabolic acidosis selection of treatment for patients with CKD.
Renal oxidative stress Much of what we currently know about etiopathogenic
Systemic hypertension mechanisms in CKD comes from studies in which kidney dis-
Tubulointerstitial changes
ease was induced by reduction or ablation of renal mass. This
“remnant kidney model” causes progressive azotemia, mild pro-
teinuria and arterial hypertension. In rats, this model is charac-
deterioration of renal function that occurs over a period of terized by relentless progression to endstage kidney disease fol-
hours to days, whereas CKD occurs over a period of months to lowing the loss of a critical number of functioning nephrons
years. A careful medical history may reveal causes of acute kid- (i.e., approximately three-fourths of the functional renal mass).
ney disease (e.g., ingestion of a nephrotoxin such as ethylene Similarly, in human patients, progression from early to late
glycol). Patients with acute kidney disease generally are healthy stages of CKD has been reported regardless of the inciting
before sudden onset of lethargy, depression and vomiting, renal injury and whether the initiating cause is present or not
whereas clinical signs in CKD such as inappetence, weight loss (Ihle et al, 1989).
and polyuria/polydipsia occur more gradually. Patients with Some controversy has existed about whether similar progres-
acute exacerbation of CKD are common and may present a sive renal injury occurs in other species, because the remnant
diagnostic challenge. However, careful questioning of owners in kidney model has not been uniformly progressive in dogs and
these cases usually establishes a more chronic history. If it is still cats. Reduction of renal mass by 7/8 or less did not result in a
not possible to distinguish between acute and chronic disease, consistently progressive decline in GFR in studies in dogs and
renal biopsy may be helpful, particularly if results will alter cats (Polzin et al, 1991; Adams et al, 1994; Finco et al, 1998).
treatment or provide prognostic information that would help It is possible that progression was not observed in these studies
owners decide on a course of action. because the extent of the induced renal injury was insufficient
to alter glomerular hypertension or renal autoregulation or per-
Etiopathogenesis of Chronic Kidney Disease haps because only mild proteinuria occurred. In experimental
A variety of compensatory and adaptive responses are likely studies in dogs, reduction of renal mass resulted in glomerular
involved in the pathogenesis and progression of naturally occur- changes and proteinuria; the severity of these changes appeared