Page 745 - Small Animal Clinical Nutrition 5th Edition

Chronic Kidney Disease 773

is by first detecting evidence of changes in renal function (e.g., azotemia usually have either isosthenuria (urine specific gravity
VetBooks.ir azotemia, proteinuria) that arise as a result of renal lesions of 1.008 to 1.013) or minimally concentrated urine (specific
gravity <1.025). However, as previously noted, some patients
(Lees, 2004). Looking for subtle changes (e.g., gradually
with CKD may retain the ability to produce concentrated urine.
increasing serum creatinine over time, progressive decline in
urine concentrating ability or presence of mild proteinuria) is Postrenal azotemia should be suspected in patients with
helpful for identifying CKD at earlier stages (Lees, 2004). stranguria, dysuria, pollakiuria, abdominal pain, ascites,
Earlier diagnosis of CKD allows earlier therapeutic interven- firm/painful urinary bladder, subcutaneous swelling or discol-
tion, which could slow or halt disease progression. oration of the perineum or a history of recent abdominal trau-
ma. Palpable urethroliths or masses in the urethra, urinary blad-
Localizing Azotemia der or prostate gland also suggest a postrenal cause of azotemia.
Azotemia is present by the time CKD is diagnosed in most Complete absence of urine production (i.e., anuria) most often
dogs or cats.Increased serum concentrations of urea nitrogen or is caused by lower urinary tract obstruction, although it may
creatinine may result from prerenal,renal or postrenal disorders. occur in some cases of acute kidney disease (e.g., ethylene glycol
Prerenal azotemia may be caused by catabolic states (e.g., treat- toxicosis). An attempt should be made to pass a urinary catheter
ment with corticosteroids), consumption of a high-protein if there is any question regarding patency of the lower urinary
food, gastrointestinal hemorrhage, dehydration, hypovolemia tract. However, the ability to pass a urinary catheter does not
or decreased cardiac output. Renal structure remains normal definitively exclude urethral obstruction. Urine specific gravity
and the kidneys are capable of normal function if the prerenal often is not helpful for distinguishing between renal and postre-
insult is corrected before permanent damage occurs. Renal nal azotemia because urinary tract obstruction may cause renal
azotemia is caused by kidney disease and generally occurs when tubular dysfunction and interfere with urine concentrating abil-
75% of nephrons are nonfunctional. Renal azotemia should be ity. Abdominal ultrasonography is helpful for detecting masses
further classified as either acute or chronic because of differ- and accumulation of fluid when urinary tract obstruction or rup-
ences in treatment and prognosis. Postrenal azotemia is caused ture is suspected. Abdominal fluid analysis in patients with
by disorders that impair elimination of urine from the body uroabdomen reveals a modified transudate or exudate character-
(e.g., urinary tract obstruction or rupture). Sites most often ized cytologically by neutrophils, macrophages and mesothelial
affected are the urethra and urinary bladder, and less often, cells; bacteria may be seen if there is urinary tract infection. If
ureters and kidneys. For upper urinary tract disease to cause uroabdomen is suspected, a sample of abdominal fluid should be
postrenal azotemia, bilateral renal or ureteral disease must be submitted for measurement of creatinine and potassium con-
present (unless the patient has concomitant kidney disease). As centrations so these values can be compared to concomitant
with prerenal disorders, renal function in patients with postre- serum concentrations. Measurement of urea nitrogen concen-
nal azotemia is normal initially; development of irreversible tration in abdominal fluid often equals that of serum or blood
renal injury depends on severity, duration and nature of the dis- and is therefore not helpful in patients with uroabdomen.
order impairing urine outflow. Contrast urethrocystography is indicated when rupture or
One of the most useful tests for distinguishing between pre- obstruction of the urethra or urinary bladder is likely; whereas,
renal and renal azotemia is analysis of urine obtained before any excretory urography is indicated when rupture of the upper uri-
treatment, especially fluid therapy. Patients with azotemia and nary tract is suspected. If available, urethrocystoscopy may also
evidence of adequate urine concentration (i.e., specific gravity be used to confirm rupture of the bladder or urethra.
>1.030 in dogs and >1.040 in cats) usually have prerenal disor- Response to treatment may help localize azotemia. In gener-
ders. There are two exceptions to this rule: 1) some cats with al, pre- and postrenal azotemia resolve rapidly within one to
CKD may have renal azotemia and still retain urine concentrat- three days after the underlying cause is corrected. In contrast,
ing ability (specific gravity >1.040); it may be many months renal azotemia usually decreases more slowly, persists after
before they finally develop concurrent azotemia and inadequate appropriate treatment or recurs soon after discontinuation of
concentrating ability, 2) some dogs with glomerular disease may treatment. Note that severe or prolonged pre- or postrenal
develop azotemia initially and then lose concentrating ability; azotemia may cause renal injury, which eventually leads to per-
this “glomerulotubular imbalance” should be suspected in dogs manent kidney disease. It is also possible for renal azotemia to
that have significant proteinuria, azotemia and urine specific exist concomitantly with either pre- or postrenal disorders; this
gravity values greater than 1.030. When azotemia is initially possibility should be suspected in patients that do not respond
identified, it’s important to determine if the patient has received to treatment as expected.
any treatment that may interfere with urine concentrating abil-
ity such as intravenous fluids, diuretics or corticosteroids. Also, Differentiating Between Acute and Chronic Kidney
disorders that may cause prerenal azotemia but concomitantly Disease
decrease urine specific gravity must be excluded; examples After renal azotemia is confirmed, additional evaluation is indi-
include hypoadrenocorticism, diabetic ketoacidosis, hypercal- cated to distinguish between acute and CKD (Vaden, 2000).
cemia, hepatic disease and pyometra. Hypoadrenocorticism may Careful review of history, physical examination findings and
be easily misdiagnosed as acute kidney failure because of similar laboratory evaluation results usually distinguishes between
clinical and laboratory findings. Dogs and cats with renal acute and CKD (Table 37-6). Acute kidney disease is a rapid