Oliguria

Mobeen Z. Haider; Ahsan Aslam.

Author Information and Affiliations

Last Update: December 13, 2022.

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Continuing Education Activity

Oliguria is a frequently encountered clinical condition that can arise due to either
prerenal, renal, or post-renal abnormalities. It has various etiologies and management is
dependent on the underlying cause(s). In order to avoid renal failure, the providers
should not only keep in view the etiology and management of oliguria but also the
various risk factors and precipitating factors as well. This activity reviews the
evaluation and management of oliguria and highlights the role of the interprofessional
team in improving care for patients with this condition.
Objectives:
 Identify the etiology of oliguria.
 Describe the appropriate evaluation steps for assessing oliguria.
 Summarize the management options for oliguria.
 Explain the importance of collaboration and communication amongst the
interprofessional team to enhance delivery of care for patients with oliguria.
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Introduction
Oliguria is defined as urinary output less than 400 ml per day or less than 20 ml per
hour and is one of the earliest signs of impaired renal function.[1] It had been described
early in the literature when Hippocrates identified the prognostic importance of the
urinary output. It was in the second century that Galen proposed its significance to
indicate renal function.[2] Later on, renal failure accompanied by oliguria was described
by Heberden as ‘ischuria renalis.’[3][4] According to the Acute Dialysis Quality
Initiative group, a patient with urinary output <0.3 ml/kg/h for at least 24 hours can be
defined to be oliguric.[5]
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Etiology
Oliguria can be the result of various causes that can be apparent or
subclinical.[1] Oliguria can arise as a result of the normal physiological response of the
body or due to an underlying pathology affecting the kidney or urinary tract. The human
body has a normal physiological mechanism of conserving fluids and electrolytes in
episodes of hypovolemia. These mechanisms are under close neurohormonal control
and are completely reversible without any subsequent injury to the kidneys.[6] The
various etiologic factors can be broadly classified into prerenal, renal, and postrenal
causes depending upon the pathophysiology.
Prerenal Causes:
 Hypovolemia: decreased effective blood volume secondary to less fluid intake,
bleeding, gastrointestinal fluid loss (diarrhea, vomiting, or nasogastric suction),
renal losses (diuretics or glycosuria), third-spacing of fluid (ascites, pleural
effusion), trauma, surgery, burns, sepsis, anaphylaxis, hepatic failure, nephrotic
syndrome, vasodilatory drugs or anesthetic agents.
 Pump Failure: Myocardial failure secondary to myocardial infarction,
pulmonary embolism, cardiac tamponade, and congestive heart failure.
 Vascular: Renal-artery or renal-vein occlusion due to thrombosis,
thromboembolism, severe stenosis, disrupted renal autoregulation secondary to
the administration of angiotensin-converting–enzyme (ACE) inhibitors.
Renal or Intrinsic Causes:
 Vasculitis, glomerulonephritis, scleroderma, malignant hypertension, or
interstitial nephritis.
 Acute tubular necrosis (ATN) due to ischemia and nephrotoxic substances,
including drugs (e.g., gentamicin, kanamycin, mercury, cisplatin), radiographic
contrast agents.
Postrenal Causes:
 Upper urinary tract obstruction due to ureteral obstruction of one or both sides.
 Lower urinary tract obstruction (more common), including bladder-outlet
obstruction due to BPH, tumor, drugs, etc.[1]
In the postoperative course, as a result of the release of vasopressin as well as the
sympathetic stimulation, transient oliguria may be observed.[3][7]
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Epidemiology
Oliguria is a commonly prevalent condition in hospitalized patients and requires close
follow up.[8] Episodes of oliguria are observed in nearly half of patients admitted to the
intensive care unit (ICU).[3][9] Chronic oliguria is commonly seen in patients on long
term dialysis.[8]
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Pathophysiology
The most common prerenal cause is reduced blood flow to the kidney secondary to
intravascular volume depletion, heart failure, sepsis, or as a side effect of medication.
Oliguria secondary to prerenal causes usually resolves with the restoration of normal
renal perfusion. As a result of the decreased renal blood flow, various neurohormonal
pathways are activated, that result in the increased production of renin, angiotensin,
aldosterone as well as catecholamines and prostaglandins. Activation of these pathways
leads to increased water and salt reabsorption resulting in the production of low
quantities of concentrated urine while maintaining adequate glomerular filtration rate
(GFR) and renal blood flow (RBF) to meet the metabolic requirements of the kidneys.
In case fluid corrections are not done, decremental reductions in GFR and RBF will
result in acute renal failure (ARF).
Renal causes of oliguria arise as a result of tubular damage. As a result of the tubular
damage, the kidney loses its normal function i.e., production of urine while excreting
the waste metabolites. In addition to this, direct damage to the renal tubules leads to a
back leak of filtered uremic metabolites from the tubular lumen into the bloodstream.
Hence, in these cases, decreased production of urine leads to oliguria.
In post-renal causes, urine production is normal, but as a result of an obstruction in the
urinary tract, urine output is greatly diminished.[8]
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History and Physical

In a patient with oliguria, a detailed history is required with a focus on past medical
history (diabetes, hypertension, heart disease, autoimmune disease, etc.), family history
as well as the current medications (potential nephrotoxins).
The patient should be inquired about their occupation, hobbies, and recent travel as
well. A thorough physical exam should be carried out to assess the hydration status of
the patient (skin turgor, mucous membranes) as hemodynamic status can help in the
identification of pre-renal causes of oliguria. Alternating episodes of oliguria and
polyuria point towards a diagnosis of intermittent urinary tract obstruction.[1] Palpation
of the urinary bladder may reveal a distended bladder secondary to urinary retention in
acute cases. A bedside urinary bladder ultrasound may also be helpful and can
instantaneously determine if there is the retention of urine.
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Evaluation
After a detailed history is obtained and thorough physical examination is performed,
baseline investigative workup should be done, including serum creatinine, urea, serum
electrolytes, and blood urea nitrogen. In addition to these, urine analysis should be done
along with a renal tract/abdominal ultrasound. Urine collection should be done before
fluid replacement and drug administration.[1] Certain cases require specific laboratory
investigations, including an autoimmune profile (ANA, ANCA, complement
levels).[3] An urgent and proper investigation of the patient with oliguria is necessary in
order to identify any potentially reversible precipitating factor. Prompt investigation and
correction avoid the progression of the patient to a state of acute renal failure that is
associated with its own risks as well as higher morbidity and mortality.[10] The
evaluation of the hemodynamic status of the patient may require invasive monitoring of
the central venous pressure (CVP) or the pulmonary capillary wedge pressure in cases
where the measurements cannot be done with non-invasive methods. Such invasive
monitoring may be needed in more critically ill patients.
Urinalysis can aid in distinguishing the causes of oliguria as well. The specific gravity
of the urine is >1.02 in prerenal and <1.01 in renal causes. Urinary sodium
concentration (mmol/liter) value is <20 in prerenal causes whereas it is >40 in renal
etiologies. Similarly, fractional excretion of sodium (%) is <1% in prerenal and >1% in
renal causes. The ratio of urinary to plasma creatinine is >40 in prerenal causes,
whereas <20 in renal causes. Urine osmolality is >500 in prerenal and <350 in renal
etiologies, and the ratio of urine to plasma osmolarity is >1.5 in prerenal and <1.1 in
renal etiologies.[11] The blood urea nitrogen (BUN) to creatinine ratio is >20:1 in
prerenal disease and <10:1 in renal diseases.[8]
It is due to the fact that the resorptive abilities of the kidney remain normal in prerenal
causes. Urinary sediments can also aid in differentiating the prerenal and renal causes of
oliguria. Urine samples from patients with prerenal failure often have hyaline and fine-
granular casts, whereas brown granular casts with tubular epithelial cells are seen in
patients with renal causes.[1]
Renal ultrasound with doppler of renal vasculature can help in the assessment of renal
perfusion through the Doppler-based renal resistive index (RI). Imaging, including renal
tract ultrasound and CT scan of the abdomen, can help in the identification of the post-
renal causes of oliguria. In cases of obstructive uropathy, dilatation of the urinary tract
may or may not be present. The dilatation is specifically absent in cases with
malignancy, severe dehydration, and the patients who present early for medical
attention.[1]
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Treatment / Management
A stepwise approach is recommended in the diagnosis and treatment of patients with
oliguria. Treatment depends mainly on the underlying etiology.
In post renal causes of oliguria, attention should be directed to underlying
etiology. Sometimes only simple measures are required to manage those causes, for
example, catheter irrigation in case of a clogged urinary catheter, or manipulation in
case of a kinked catheter, etc. A bedside bladder ultrasound may be helpful to detect
urinary retention and to guide if an indwelling urinary catheter is needed. A urology
consultation might be helpful in cases of urinary retention due to BPH, tumors, or
stones.
Hemodynamic Stabilization:
The first step is the hemodynamic stabilization of the patient. The amount of fluid is
calculated on an individual basis.[1] It should be noted that although hemodynamic
stabilization is necessary, volume overloading should be avoided at all costs and treated
with diuresis or renal replacement therapy if indicated.[12] Starch products can lead to
tubular damage and hence should be avoided. For a large volume replacement, balanced
crystalloids are recommended. The target for hemodynamic stabilization is achieving
the mean arterial pressure (MAP) of 65-70 mmHg in non-hypertensive patients. In
addition to all the therapeutic modalities, close hourly monitoring of urine output is
extremely important to gauge treatment accordingly.[3]
Diuretic Therapy:
If fluid resuscitation fails to resolve the oliguria, diuretic therapy should be initiated
utilizing a standardized approach. A furosemide stress test (FST) can be done in order to
assess the patient’s response to diuresis. It should be noted that a diuretic challenge
should only be given once the patient is euvolemic. Failure of resolution of oliguria with
the above step(s) should raise suspicion for evaluation for acute kidney injury (AKI).
FST is a standardized test to assess the functional integrity of the tubules and aids in the
risk stratification as well as decision making. FST is said to be nonresponsive if 1.0-1.5
mg/kg of furosemide produces a urine output of 100 ml/h in the first two hours.
Nonresponsive FST is associated with a higher stage of AKI. Some studies suggest
using 100-200 mg of furosemide initially, and if there is no response, doubling the dose
may be considered. If this fails to bring any significant improvement adding a thiazide
diuretic can also be considered.[1]
One of the most important prerequisites of FST is that the patient should not be
hypovolemic, and the heart rate, as well as the blood pressure, should be closely
monitored. A recent study has shown that 75% of the patients who are nonresponsive to
FST require renal replacement therapy as compared to only 13.6% of patients who are
FST responsive.[13] A patient responsive to diuretics should be managed
accordingly.[3][14] If diuretic therapy fails to improve the clinical condition, it should
be discontinued.[1]
Renal Replacement Therapy:
In oliguric patients, secondary to renal etiology treatment is mainly focused on
supportive care and potential renal replacement therapy to manage the fluid and
electrolyte balance to avoid the development of complications.[1]
Dietary Recommendations:
In addition to focusing on fluid and electrolyte management, adequate protein and
caloric intake are necessary. High rates of protein catabolism (200–250 g/day) are
observed in patients with ARF, sepsis, or rhabdomyolysis.[1]
Pharmacological Modifications:
The treatment for oliguria should be continued keeping in view the guidelines of AKI
treatment. All nephrotoxic drugs should be discontinued, and drugs excreted by the
renal system should be carefully reviewed, and their doses should be adjusted.[3] Drugs
metabolized by kidneys should be avoided. These drugs include doxorubicin,
allopurinol, aminoglycosides, azathioprine, cephalosporins, clofibrate, digoxin,
diazepam, meperidine, procainamide, propoxyphene, propranolol, and sulfonamides. In
case these drugs are necessary, a dose modification must be done in accordance with the
degree of renal injury.[1]
It should be kept in mind that in the setting of oliguria, fluid resuscitation does put the
patient at risk of fluid overload, which in turn leads to worsening AKI. As a result,
overcompensation with fluid is associated with higher mortality when urine output is
the determining factor for fluid replacement.[15] Signs of fluid overload include
peripheral edema, increased CVP, and increased IVC diameter.[16][17] In diuretic
responsive patients with fluid overload, diuretic medications are used to manage the
fluid overload. On the other hand, in patients who are nonresponsive to diuretics, renal
replacement therapy can be used.[3][12]
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Differential Diagnosis
While evaluating a patient with oliguria, the following differential diagnosis must be
kept in mind, and evaluation should be done accordingly:
 Pre-renal azotemia: (hemodynamic status of the patient, urine analysis, and
doppler based renal resistive index).
 Acute glomerulonephritis: (Renal biopsy, complement levels)
 Oliguric acute tubular necrosis: (urine analysis)
 Non-oliguric acute tubular necrosis: (urine output measurement, urine analysis)
 Urinary tract obstruction: (urine sediment, renal ultrasonography, non-contrast
CT scan)
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Prognosis
Oliguria is one of the first indicators of acute renal injury.[8] Oliguric episodes that
occur outside the hospital are usually due to a single cause and are mostly reversible
with a good prognosis. On the other hand, oliguric patients admitted to the hospitals
usually have severe renal insufficiency due to several underlying precipitating factors.
As a result, they have a worse prognosis than that of non-hospitalized patients. Patients
admitted in the intensive care unit develop oliguria later in the course of their illness and
are secondary to multiple organ failure.[18][19] Hospitalized patients with oliguria have
significantly higher morbidity as well as mortality.[1]
Oliguric patients are at higher risk of developing acute renal failure (ARF). 30 to 70
percent of patients with ARF develop infections that are associated with higher
morbidity and mortality.[1] However, the mortality risk due to oliguria is not
completely attributable to the development of ARF.[4]
The duration and intensity of oliguria have a great impact on prognosis. As the intensity
of oliguria worsens to <0.5 ml/kg/h, the mortality rises significantly.[4]
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Complications
In patients with acute oliguria, one of the most common functional derangements that
are observed is the sudden fall in the GRF, leading to acute renal failure. It results in
rapid increment in plasma urea and creatinine levels, metabolic acidosis with
hyperkalemia, other electrolyte abnormalities, and volume overload. This warrants an
expedited hospital admission for management and hence avoidance of the cascade of
life-threatening events. Life-threatening complications include:
 Electrolyte imbalance: Hyperkalemia, metabolic acidosis, salt, and water
retention leading to pulmonary edema, ascites, or pleural effusions,
hyperphosphatemia, or hypocalcemia.
 Neurologic: drowsiness, confusion, somnolence, hyperreflexia, seizures, and
coma.
 Cardiovascular: As a result of the fluid and salt imbalance, congestive heart
failure, pulmonary edema, and hypertension usually occur. In some cases,
 hypotension may be seen, which is a manifestation of other concomitant
illnesses such as sepsis. Electrocardiographic (ECG) changes due to
hyperkalemia can be seen. In about a quarter of cases, arrhythmias may occur
due to electrolyte imbalance. Pericarditis is also seen rarely and is a
manifestation of uremia.
 Gastrointestinal: nausea, vomiting, ileus, gastrointestinal hemorrhage, gastritis.
 Respiratory: Kussmaul breathing due to metabolic acidosis.
 Musculoskeletal: muscle weakness or paralysis.
 Pharmacological: As a result of the renal injury, the metabolism of various drugs
is slowed down, leading to an increased risk of toxicity. It warrants dose
modification for drugs.
 Infectious: Increased risk of urogenital tract and respiratory infections as a result
of damage to the normal barriers, uremia, and inappropriate antibiotic usage.
Prevention of infectious complications requires close monitoring of the patient.
 Hematological: Acute renal failure leads to anemia due to decreased
erythropoiesis and partly due to hemolysis, with hematocrit values between 20
and 30 percent.[1]
Early detection of the complications warrants meticulous monitoring and helps in
avoiding the development of life-threatening complications.
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Consultations
The primary care provider should consult a nephrologist for an expert opinion as well as
a dietician or nutritionist for advice on maintaining appropriate protein and caloric
intake. Radiologist consultation may be required in order to properly assess renal
perfusion through the Doppler-based renal resistive index (RI).[1] In addition to this,
pharmacy consult is necessary to look for the potential nephrotoxic effects of a
prescription or any other medication that is primarily renally excreted so that
appropriate dosage modification can be made.[20]
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Deterrence and Patient Education

The patient should be educated about the importance of maintaining adequate hydration
and instructed to avoid the use of any medication without consulting the physician,
especially NSAIDs, which are one of the commonly used medications available over the
counter for pain relief. The patient should be recommended to follow the provider’s
advice and get regularly followed up by their physician as well as a nephrologist if the
physician suggests.
Prolonged fasting and excessive exercise should be avoided as they can worsen oliguria
and can lead to rhabdomyolysis. Any catheterized patient should be adequately educated
about their catheter care. Monitoring the urine output is one of the determining factors
for therapeutic intervention. The patient should be instructed about monitoring the
quantity and appearance of urine. The patient should report any color changes, frothing,
and sediment formation. In addition, to focus on fluid and electrolyte management,
adequate protein and caloric intake is necessary.[1]
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Pearls and Other Issues

PREDISPOSING RISK FACTORS FOR OLIGURIA:[8]
The following factors have shown to predispose the patient to the development of
oliguria:
 Old age
 Intravascular volume depletion
 Prior history of renal disease
 Vasoconstrictive drugs e.g., NSAIDs, tacrolimus, cyclosporine
 Nephrotoxic agents e.g., radiocontrast media, aminoglycosides,
chemotherapeutic agents
 Comorbidities e.g., diabetes, congestive heart failure, liver disease
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Enhancing Healthcare Team Outcomes

Studies have suggested that early recognition and management play a key role in the
prognosis of patients with oliguria; hence close monitoring should be done in patients
with urine output less than 0.5 ml/kg/hour for a period of two consecutive hours.[5]
Radiographic agents used for various diagnostic imaging studies can precipitate oliguria
and acute renal failure, particularly due to their vasoconstrictive effect of renal blood
circulation. In a catheterized patient presenting with oliguria, catheter dysfunction
should be ruled out.[21] Oliguric episodes in hospitals are usually associated with
volume depletion, peri-operative course, diagnostic procedures, and medications.[1]
Special care should be taken to avoid any potential nephrotoxic drugs to a patient with
oliguria. These drugs include but are not limited to nonsteroidal anti-inflammatory
drugs (NSAIDs), aminoglycosides, radiographic contrast agents, general anesthetics,
angiotensin-converting–enzyme (ACE) inhibitors, amphotericin B, and numerous
chemotherapeutic drugs.[20] In addition to all the therapeutic modalities, close, hourly
monitoring of urine output is extremely necessary to gauge treatment.[3]
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