Page 781 - Small Animal Clinical Nutrition 5th Edition

Chronic Kidney Disease 809

other patient factors such as presence of CKD in this Table 1. Results of initial laboratory evaluation including CBC, serum
case. In dogs, administration of an angiotensin-con-
VetBooks.ir verting enzyme (ACE) inhibitor usually is the initial Parameters Day 1 Reference ranges
biochemistries and urinalysis.
treatment of choice for hypertension. Because ACE
inhibitors preferentially dilate the efferent arteriole, Hematocrit (%) 46 37-62
Total white blood cell
21.5
count (x 1,000/µl)
5.4-16.6
they have the potential to decrease glomerular filtra- Segmented neutrophils (x 1,000/µl) 18.92 3.24-10.7
tion rate and worsen azotemia. Therefore starting at a Bands (x 1,000/µl) 0.215 0.0-0.25
lower dose and gradually increasing it over time while Lymphocytes (x 1,000/µl) 1.29 0.75-5.65
monitoring renal function may be helpful. Monocytes (x 1,000/µl) 1.075 0.1-1.19
2. It is difficult to definitively localize the proteinuria as Glucose (mg/dl) 119 89-135
Urea nitrogen (mg/dl)
67
8-27
of renal origin from CKD vs. postrenal from the UTI. Creatinine (mg/dl) 1.6 0.6-1.4
5.2
2.6-6.0
UTIs add plasma proteins to the urine after glomeru- Phosphorus (mg/dl) 10.1 9.5-11.6
Calcium (mg/dl)
lar filtration, thus postrenal proteinuria is recognized Total protein (g/dl) 6.5 5.4-7.2
by the presence of proteinuria with hematuria and Albumin (g/dl) 2.8 2.7-3.8
18-24
19
pyuria. The urine sediment examination only revealed Total CO (mmol/l) 4.6 3.5-5.5
2
Potassium (mg/dl)
hematuria without pyuria, most likely because of cur- Amylase (IU/l) 985 338-1,007
rent antibiotic administration. Therefore, postrenal Lipase (IU/l) 1,245 268-1,796
proteinuria was less likely. The proteinuria was con-
firmed to be of renal origin by follow-up urinalyses
that showed persistence of proteinuria despite resolution of the UTI.
Proteinuria occurs as a result of CKD; however, it may also play a role in the pathogenesis of progressive CKD. In one study,
an initial UPC ≥1 in dogs with CKD was associated with greater risk of having a uremic crisis or dying compared with dogs that
had a UPC <1. Dogs with proteinuria should be fed a reduced-protein food designed for patients with CKD, whether azotemia
exists or not (Box 37-2). Patients should be monitored periodically (e.g., every two to four weeks initially) to determine the opti-
mal quantity of dietary protein that maintains lean body mass and decreases magnitude of proteinuria, as measured by UPC
ratios. Patients should receive enough calories to achieve and maintain ideal body weight and condition. Administration of an
ACE inhibitor also is indicated for dogs with proteinuria due to glomerular disease. In a study of dogs with naturally occurring
idiopathic glomerulonephritis, treatment with enalapril was associated with significant improvement compared with dogs that
c
received a placebo. Both groups also received low-dose aspirin and a veterinary therapeutic renal food. Resorption of excessive
amounts of protein from the tubular filtrate in dogs with CKD and proteinuria may damage the tubules resulting in progressive
tubulointerstitial injury. (See Renal Oxidative Stress in the Etiopathogenesis section.)
3. This dog does not have active pancreatitis. However, long-term management should include feeding foods with relatively less fat
that avoid excessive protein because both are stimuli for pancreatic secretion. Feeding a moderate-fat food (≤15% dry matter
[DM]) has been recommended for patients recovering from pancreatitis, whereas a low-fat food (≤10% DM) may be more
appropriate for those with concurrent obesity or hypertriglyceridemia. Clinical studies have not evaluated effects of feeding dif-
ferent amounts of fat on recurrence of pancreatitis. One approach is to feed less fat than the patient was eating when the most
recent episode of pancreatitis occurred.
4. Patients with multiple disorders can be challenging to manage, especially when treatment for one condition may not be ideal for
a concurrent disease. Feeding a veterinary therapeutic renal food is indicated for this patient.These foods often contain increased
amounts of fat, which would not be ideal for a patient at risk for pancreatitis. One approach for this patient would be to recom-
mend a renal food with the lowest fat content. In general, dry foods contain less fat; therefore, feeding a dry food may be prefer-
able as long as the dog is able to maintain hydration. If the patient does not respond well to a commercially available food, an
alternative would be to formulate a homemade food. In these cases, it is recommended to seek input from a board-certified clin-
ical nutritionist who can help design a nutritionally balanced maintenance food tailored for that patients’ particular needs.

Progress Notes
Enrofloxacin (5 to 7 mg/kg per os twice daily for six to eight weeks) was recommended to treat possible pyelonephritis.This antimi-
crobial was selected because the organism was susceptible based on urine culture and sensitivity results. A low number of organisms
most likely grew on the initial urine culture because the dog was receiving a low dose of antimicrobial at the time urine was collect-
ed. A follow-up urine culture was recommended one week after beginning treatment, one week after completing antimicrobial
treatment and once monthly for three months thereafter to ensure eradication of infection.
Additional treatment included administration of an ACE inhibitor, H -receptor antagonist and a veterinary therapeutic renal
2
d
food.Benazepril (0.25 to 0.5 mg/kg orally once or twice daily) was begun to manage hypertension and proteinuria.To avoid poten-
tial for worsening azotemia, it was recommended to begin at the lowest dose once daily and gradually increase while monitoring
e
serum creatinine and urea nitrogen concentrations. Cimetidine (5 to 10 mg/kg orally, twice daily) was prescribed to help manage
possible uremic gastritis. All dry versions of commercially available veterinary therapeutic renal foods from major companies con-