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Oliguria

Chapter · October 2018

DOI: 10.1002/9781119028994.ch95

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95

Oliguria
J.D. Foster, VMD, DACVIM
Friendship Hospital for Animals, Washington, DC, USA

Pathogenesis of Oligoanuria Table 95.1 Causes of oligoanuria.

Pathogenesis Potential causes

Urine output (UOP) is an important aspect of monitor-
ing the hospitalized patient, as it can provide valuable Decreased renal blood flow Hypovolemia or hypotension
information regarding kidney function and patency of Decreased cardiac output
the urinary tract, as well as helping to guide fluid ther- Renal artery stenosis or
apy. This is particularly true for the patient with renal thrombosis
disease. Normal urine production has been reported to Sepsis
be 1–2 mL/kg/h in dogs and cats [1–3]. Renal dysfunc-
Vasodilatory drugs
tion, such as acute kidney injury and chronic kidney
disease, typically includes impaired tubular solute reab- Tubular obstruction from Pyelonephritis
casts or cellular debris
sorption. This results in a solute diuresis and subsequent Acute interstitial nephritis
polyuria (>2 mL/kg/h UOP). Numerous definitions have Leptospirosis
been used for anuria and oliguria in veterinary patients. Acute tubular necrosis
Because most patients with renal disease will be polyuric,
Nephrotoxicity
UOP < 2 mL/kg/h indicates relative oliguria. UOP < 1 mL/
kg/h is considered absolute oliguria and anuria is defined Backflow of glomerular Ureteral, renal pelvis, or
as 0–0.5 mL/kg/h UOP. filtrate into renal urethral obstruction
interstitium Tubular obstruction from
While urine production is an important observance in
monitoring renal function, UOP cannot be used as a sur- casts and cellular debris
rogate for glomerular filtration rate (GFR). Rather, UOP Intrarenal renin-angiotensin Failure of NaCl reabsorption
is a function of GFR, tubular solute reabsorption, and system activation within proximal tubule
tubular solute secretion. Patients with complete anu- High chloride-containing
ria will have a GFR of 0 mL/kg/min, but the restoration intravenous fluid therapy
of UOP in these patients does not necessarily indicate Altered permeability of Glomerulonephritis
improvement in GFR. glomerular filtration barrier Vasculitis
Oligoanuric acute kidney injury can occur due to sev-
eral processes (Table 95.1) [4,5]. Dogs and cats with oli-
goanuric acute kidney injury (AKI) have higher mortality abdominal distension or pain, as well as urinary bladder
rates and as much as a 20-fold increased risk of death size. Assessment of patient hydration status and intra-
compared to polyuric animals [6,7]. vascular volume should be made and noted within the
patient’s medical record. Blood pressure measurement
and body weight are also very important to record.
Patient Assessment and Initial Diagnostics Initial diagnostics should include imaging to docu-
ment the size or volume of the urinary bladder (often
Oligoanuric patients should be evaluated with a thor- achievable with bedside ultrasound machines), PCV/TS,
ough physical examination with particular emphasis serum chemistry with electrolytes, and acid–base analy-
on detection of subcutaneous edema, cardiopulmonary sis. Urine should be collected for analysis prior to the ini-
auscultation, respiratory rate and effort, presence of tiation of fluid therapy; cystocentesis is preferred to also
Textbook of Small Animal Emergency Medicine, First Edition. Edited by Kenneth J. Drobatz, Kate Hopper, Elizabeth Rozanski and Deborah C. Silverstein.
© 2019 John Wiley & Sons, Inc. Published 2019 by John Wiley & Sons, Inc.
Companion Website: www.wiley.com/go/drobatz/textbook
602 Textbook of Small Animal Emergency Medicine

provide a sample for urine culture. The urine specific
gravity can be helpful to determine if a prerenal cause of
oligoanuria is present. Urine may be difficult to obtain in
anuric patients. Thoracic radiographs and/or ultrasound
should be performed in patients with any concern for
pulmonary edema or pleural effusion.
Managing the Oligoanuric Patient
The therapeutic approach to the oligoanuric patient is
dependent on their current volume and hydration status
(Figure 95.1). Hypovolemic patients should be treated
with boluses of isotonic replacement solutions, given
rapidly through an intravenous route (see Chapter 167).
Patients with decreased renal perfusion will have an
appropriate reduction in UOP secondary to activation
of the renin-angiotensin-aldosterone system. Therefore,
patients should be adequately hydrated with normal intra-
vascular volume prior to definitively declaring an oliguric
or anuric state. Patients that are cardiovascularly stable
but dehydrated should have their degree of dehydration
estimated from physical examination findings, and this
volume calculated and replaced over 6–8 hours (unless
cardiopulmonary disease is present that could create an
intolerance of such fluid rates) [5]. Once the patient has
been rehydrated, an appropriate UOP is 2–5 mL/kg/h
depending on the rate of intravenous fluid administra-
tion. A UOP less than 2 mL/kg/h would be considered
oliguria in a hydrated patient receiving intravenous fluids.

Assess
volume
status

Hypovolemic Normovolemic Hypervolemic

Give IV fluids Attempt Extracorporeal

Bolus IV fluids
to correct for pharmacologic renal
to restore
3–5% conversion to replacement
blood volume
dehydration polyuria therapy

UOP UOP

Furosemide
Yes No Yes No
bolus

UOP

Mannitol bolus Yes No

Continue IV
fluids to match
ins/outs UOP

Continue
furosemide until Consider
Yes No
envolemic, then fenoldopam
match ins/outs
UOP

Repeat mannitol
PRN, and match Yes No
ins/outs

Continue
fenoldopam until
euvolemic, then
match ins/outs

Figure 95.1 Therapeutic intervention for oligoanuria.


For euhydrated patients, an isotonic crystalloid of a
volume of fluid equal to 3–5% of body weight should be
administered because dehydration of less than 5% can-
not be detected clinically. If UOP fails to reach an appro-
priate magnitude (2–5 mL/kg/h), pharmacological con-
version to polyuria may be attempted (see below).
Oligoanuric patients who are hypervolemic often
show evidence of serous ocular and nasal discharge,
subcutaneous edema, pleural and abdominal effusion,
pulmonary edema, and arterial hypertension. Although
less commonly seen in veterinary oligoanuric patients,
conditions such as systemic inflammatory response
syndrome, vasculitis, sepsis, burns, trauma, or pancre-
atitis can result in intravascular volume depletion with
interstitial overhydration in humans (see Chapter 159)
[8]. Most patients have normal to increased intravascu-
lar and interstitial fluid volumes. Hypervolemic patients
with systemic hypotension should be treated with pres-
sors, and intravascular volume expansion should be per-
formed in any patient with a decreased effective circulat-
ing volume.
Monitoring UOP in comparison to volume of fluids
administered (sum of all IV and PO fluids, often referred
to as “ins/outs”) is very helpful in the assessment of oli-
goanuric patients. Aseptic placement of a urinary cathe-
ter and a closed collection system should be considered,
as it is more accurate, allows for more frequent assess-
ment of urine output, and protects hospital staff from
potential zoonotic agents compared to weighing urine
collected in pans and bedding. Hypervolemic patients
should be managed so their “outs” exceed their “ins.”
GI fluid losses through diarrhea or vomitus should be
estimated and included in this assessment. Euvolemic
patients should be managed with a neutral or minimally
negative total daily fluid balance. It has been documented
in people that a positive fluid balance is associated with
a worse prognosis in patients with AKI, greater risk of
developing AKI, and a poorer chance of return of renal
function following AKI [9,10].
The goal of fluid therapy is to maintain renal perfu-
sion. Several studies have shown that supraphysiological
rates of intravenous fluids fail to increase GFR in dogs
and cats [11,12]. Therefore, patients should have fre-
quent assessments and the fluid plan be adjusted to pre-
vent fluid accumulation.
Converting Oligoanuria to Polyuria
It is now accepted that pharmacological conversion from
an oligoanuric to a polyuric state is the mainstay of man-
agement in veterinary medicine. Studies in dogs and cats
are lacking, but it should be noted that numerous studies
in people have demonstrated that successful pharma-
95 Oliguria 603
cological induction of polyuria has no effect on patient
mortality [13]. Hypervolemia in an oligoanuric patient is
an indication for extracorporeal renal replacement ther-
apy, and referral for this treatment should be considered
early in the course of patient evaluation. In people, an
increase in urine output with diuretic use often delays
referral for dialysis, potentially at the expense of worse
clinical outcomes [14]. Currently, there is scant evidence
to show that pharmacological attempts at inducing poly-
uria are effective, or when it occurs that this carries an
improved survival and return of renal function in veteri-
nary patients with AKI.
Mannitol is an osmotic diuretic that decreases cellular
swelling and may help to wash out obstructive casts and
debris from the tubules. It may also serve as a free radi-
cal scavenger. Mannitol is administered as a intravenous
bolus of 0.25–1.0 g/kg, administered over 15–20  min-
utes. If an increase in UOP is achieved, mannitol can
be dosed intermittently q4–6 h or administered as a
CRI (60–120 mg/kg/h). Mannitol should not be given to
patients that are dehydrated because it can further exac-
erbate intracellular dehydration. Importantly, it is con-
traindicated if overhydration is present, and may worsen
pulmonary edema. Due to lack of evidence showing that
mannitol can help prevent AKI and potential risks of
hypervolemia secondary to administration, consensus
guidelines in people suggest that mannitol not be used
in patients with AKI [15]. It is still used in euvolemic vet-
erinary patients, but no publications have reported its
efficacy.
Furosemide is a loop diuretic, which inhibits the
Na-K-2Cl transporter in the thick ascending loop of
Henle. Experimental models have shown potential ben-
efits, including decreased renal oxygen consumption
and less ischemic damage. It should be noted that it is
the concentration of furosemide within the tubular fil-
trate and not the blood that determines the observed
effect [16]. Furosemide enters the tubular filtrate via
active secretion within the proximal tubule as well as
filtration of non-protein-bound furosemide across the
glomerular filtration barrier. Anuric patients with min-
imal to no tubular flow are unlikely to have furosem-
ide reach the site of activity, and therefore this drug is
often ineffective in increasing UOP in these patients.
Human patients who fail to respond to furosemide are
more likely to have progression and greater severity of
AKI [17]. Furosemide is typically administered as an
intravenous bolus or intramuscular dose of 1–4 mg/
kg. If an increased UOP is observed, the dose may be
repeated every 6–12 hours as needed, or a constant-rate
infusion may be administered. The function of the CRI
is to maintain serum concentrations sufficient to allow
continuous accumulation within the tubular filtrate.
Patients who fail to respond to a bolus of furosemide
604 Textbook of Small Animal Emergency Medicine
are unlikely to respond to a CRI, as they likely have ade-
quate serum concentrations for several hours following
bolus administration. It should be noted that in peo-
ple, consensus guidelines suggest that furosemide only
be used in early or established AKI for management of
fluid balance, hyperkalemia, and hypercalcemia, but
any putative role in amelioration of the AKI course is
unproven [18].
Renal dose dopamine has been advocated for the
management of oliguric AKI for its effects on renal
vasodilation. Human studies have shown limited to no
improvement in morbidity, mortality, or need for dialysis
in established AKI. Additionally, even at low doses, dopa-
mine is potentially toxic in critically ill patients and can
induce tachyarrhythmias and myocardial ischemia [19].
Based on these data, dopamine is not currently recom-
mended for treating AKI in humans or animals [20].
Fenoldopam is a selective postsynaptic dopamine
receptor (DA-1) agonist that causes more potent renal
vasodilation and natriuresis than dopamine. However,
it can also promote hypotension by decreasing systemic
vascular resistance. Fenoldopam has been shown to
increase UOP in healthy cats [21]. Compared to pla-
cebo, fenoldopam administration resulted in an increase
in GFR and fractional exertion of sodium in healthy
dogs [22]. Pharmacokinetic data exist for healthy dogs
[23]. A retrospective study of fenoldopam use for both
dogs and cats with AKI demonstrated no improvement
in survival or length of hospitalization in patients who
were administered fenoldopam compared to those who
were not [24].
Diltiazem is a calcium channel blocker that may
improve renal blood flow through afferent arteriolar
vasodilation, which may increase GFR and UOP [25]. It
may also be renoprotective by preventing the intracellu-
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The most significant complications of oligoanuria are
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