Page 391 - Cote clinical veterinary advisor dogs and cats 4th
P. 391
168 Chronic Kidney Disease, Occult (Asymptomatic)
• Hemodynamic azotemia (e.g., dehydration, Advanced or Confirmatory Testing • A gradual (over several weeks) and methodical
hypotension) typically distinguished from • Urine protein/creatinine ratio: pathologic introduction to the renal diet often results
VetBooks.ir with hemodynamic azotemia, inadequately ratio > 0.5 [dogs], > 0.2-0.4 [cats]; urinary Drug Interactions
proteinuria (urine protein/creatinine [UPC]
in a higher compliance rate.
CKD by urine specific gravity (concentrated
concentrated with CKD).
sediment is inactive, and culture is negative)
• Intrinsic azotemia with inadequately concen-
therapeutic target.
trated urine may be due to kidney disease provides prognostic information as well as a • Nephrotoxic drugs (e.g., aminoglycosides)
or drug combinations (e.g., nonsteroidal
(most commonly) or to dehydration (i.e., • Glomerular filtration rate (GFR) mea- antiinflammatory drugs [NSAIDs] plus
hemodynamic azotemia) combined with surement: can confirm inadequate GFR, ACE inhibitors) should be avoided whenever
extrarenal impairment of urine concentration. particularly when azotemia is absent or cause possible, and if a nephrotoxic drug is used,
○ Drug therapy (e.g., diuretics, glucocorticoids) of impaired urine concentration is unclear. clients should be counseled to discontinue
○ Osmotic diuresis (e.g., diabetes mellitus) Iohexol clearance, creatinine clearance, and if signs of illness become manifest.
○ Impaired medullary concentration gradient nuclear scintigraphy are most commonly • Dosage adjustment of most drugs is unneces-
(e.g., hypoadrenocorticism, portosystemic used. sary at this stage of CKD.
shunting) • CKD in cats may complicate the diagnosis of • Phosphate binders can interfere with absorp-
○ Central diabetes insipidus concurrent hyperthyroidism by suppressing tion of orally administered medications,
○ Nephrogenic diabetes insipidus (e.g., total thyroxine. Additional thyroid testing especially antibiotics and fat-soluble vitamins.
hypercalcemia, pyometra, pyelonephritis) may be warranted if total thyroxine (T 4 ) value
• Postrenal azotemia (e.g., urinary obstruc- is normal but hyperthyroidism suspected Recommended Monitoring
tion, rupture) is generally differentiated clinically (p. 503). • Stable patients with incidental CKD should
from kidney disease by dysuria or imaging be monitored every 3-6 months.
and biochemical findings consistent with TREATMENT • Evaluations should include body weight,
uroperitoneum, respectively. CBC (or at least packed cell volume), serum
Treatment Overview biochemistry profile with electrolytes, and
Initial Database The treatment goal is to slow progression of BP measurement.
• CBC: usually unremarkable; occasionally kidney disease. • Clinical manifestations of hypokalemia,
mild anemia hyperphosphatemia, anemia, and hyperten-
• Serum biochemistry profile: azotemia, Acute General Treatment sion may not occur until they result in severe
hyperphosphatemia, hypokalemia, metabolic Because patients are asymptomatic, acute clinical manifestations; early interventions
acidosis, and hypercholesterolemia occur to treatment is not needed. can be based on detection by routine
various degrees. screening.
• Urinalysis: frequently isosthenuric or mini- Chronic Treatment • Urinalysis +/− urine protein/creatinine ratio
mally concentrated specific gravity (dogs < • For patients with proteinuria, renin- every 6-12 months.
1.030; cats < 1.035). Active sediment may angiotensin-aldosterone system (RAAS) • Urine culture should be performed if
indicate UTI. Proteinuria should be quanti- inhibition (e.g., angiotensin-converting suspicion of lower or upper urinary tract
fied by urine protein/creatinine ratio. enzyme [ACE] inhibition, angiotensin recep- infection exists.
• Urine culture may be indicated to rule out tor blockade) reduces proteinuria in cats and
infection. dogs and slows progression of kidney disease PROGNOSIS & OUTCOME
• Symmetric dimethylarginine (SDMA): this in dogs (enalapril or benazepril 0.25-0.5 mg/
relatively new blood test may detect CKD kg PO q 12-24h initially) (pp. 51 and 390). • Some animals with incidental CKD may
earlier than creatinine and is less affected • As kidney disease progresses, animals may remain stable and free of clinical signs for
by loss of lean body mass. If occult CKD is decompensate (show overt signs caused by years, but others progress more rapidly.
suspected but creatinine is normal, SDMA CKD). For specific therapeutic recommenda- • There are no reliable predictors of the rate of
may be useful (p. 1381). tions, see p. 169. progression of kidney disease, except perhaps
• Thyroid hormone assay (elderly cats): rule the presence of proteinuria (as quantified by
out hyperthyroidism as concurrent disorder. Nutrition/Diet UPC) and body condition score (for dogs).
○ Some of the clinical signs of hyperthyroid- • Diets specifically formulated for dogs and
ism (particularly polyuria and polydipsia) cats with kidney disease slow progression of PEARLS & CONSIDERATIONS
can mimic those of CKD. CKD:
○ Correction of hyperthyroidism can ○ The level of kidney dysfunction at which Comments
exacerbate azotemia. a renal diet should be introduced is con- • Occult CKD may progress slowly or rapidly;
○ In cats that have both hyperthyroidism troversial. It may be best to transition to the course of progression cannot be predicted.
and CKD, treatment emphasis is placed a renal diet that is palatable to the patient Advanced age, higher plasma creatinine and
on the disease most responsible for clinical when renal disease is occult or mild, rather phosphorus levels, and proteinuria generally
signs (p. 503). than waiting until the animal is overtly are associated with more rapid progression.
• BP (p. 1065): hypertension (systolic BP > ill (uremic). As with rate of progression, survival time is
160-179 mm Hg, diastolic BP > 95-119 mm ○ The low-solute characteristics of most highly varied and likely influenced by owners’
Hg) present in 20% of cats with CKD; may renal diets may reduce the urine volume decisions for euthanasia at various stages of
cause end-organ damage (especially heart, modestly in some patients with polyuria. disease.
eyes, central nervous system, kidneys). ○ There are many different brands of renal • If anesthesia or potentially nephrotoxic drugs
• Abdominal radiographs and/or ultrasound: diet, and acceptance of different formula- (e.g., ACE inhibitors) must be used, ensure
may further elucidate cause of or factors tions varies with the individual patient. adequate hydration and monitor carefully
contributing to CKD (e.g., obstructing ○ Homemade renal diets may also be used for deterioration in renal function.
or partially obstructing nephroliths or but should be formulated by a board-
ureteroliths, renal neoplasia, polycystic certified veterinary nutritionist. Technician Tips
disease, perinephric pseudocysts). Alterations ○ Maintaining adequate caloric intake The technician can help clients develop a plan
of shape, size, and echogenicity of kidneys and avoiding protein malnutrition is for a gradual transition from a maintenance
are common. paramount. diet to a renal diet.
www.ExpertConsult.com