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 was first described in the literature when Hippocrates identified the prognostic importance of urinary output. It was in the second century that Galen proposed this indicator as a marker of 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 is considered oliguric.[5]

Etiology

Oliguria can result from various causes, some apparent and others subclinical.[1] Oliguria can result from the body's normal physiological response or from an underlying pathology affecting the kidneys 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 on the underlying 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,s 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, or 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 (eg, gentamicin, kanamycin, mercury, cisplatin), and 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 vasopressin release and sympathetic stimulation, transient oliguria may be observed.[3][7]

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]

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 decreased renal blood flow, various neurohormonal pathways are activated, resulting in increased production of renin, angiotensin, aldosterone, catecholamines, and prostaglandins. Activation of these pathways leads to increased water and salt reabsorption, resulting in the production of small volumes of concentrated urine while maintaining adequate glomerular filtration rate (GFR) and renal blood flow (RBF) to meet the kidneys' metabolic requirements. If fluid corrections are not made, decremental reductions in GFR and RBF will result in acute renal failure (ARF).

Renal causes of oliguria result from tubular damage. As a result of tubular damage, the kidney loses its normal function, ie, the production of urine and the excretion of waste metabolites. In addition, direct damage to the renal tubules leads to a backflow 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 obstruction of the urinary tract greatly diminishes urine output.[8]

History and Physical

In a patient with oliguria, a detailed history is required, focusing on past medical history (diabetes, hypertension, heart disease, autoimmune disease, etc.), family history, and current medications (potential nephrotoxins).

The patient should also be asked about their occupation, hobbies, and recent travel. A thorough physical exam should be performed to assess the patient's hydration status (skin turgor, mucous membranes), as hemodynamic status can help identify 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 distension secondary to urinary retention in acute cases. A bedside urinary bladder ultrasound may also be helpful and can instantaneously determine whether there is urinary retention.

Evaluation

After a detailed history is obtained and a 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 appropriate investigation of the patient with oliguria is necessary to identify any potentially reversible precipitating factor. Prompt investigation and correction can 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 patient's hemodynamic status may require invasive monitoring of central venous pressure (CVP) or pulmonary capillary wedge pressure when noninvasive measurements are unavailable. Such invasive monitoring may be needed in more critically ill patients.

Urinalysis can also aid in distinguishing the causes of oliguria. The specific gravity of the urine is >1.02 in prerenal and <1.01 in renal causes. The urinary sodium concentration (mmol/liter) 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 it is <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 disease.[8] 

This is because the kidney's resorptive capacity remains 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 the renal vasculature can help assess renal perfusion using the Doppler-based renal resistive index (RI). Imaging, including renal tract ultrasound and abdominal CT, can help identify 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 patients who present early for medical attention.[1]

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 the 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. A bedside bladder ultrasound may be helpful in detecting urinary retention and in guiding whether an indwelling urinary catheter is needed. A urology consultation might be helpful for 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] Although hemodynamic stabilization is necessary, volume overload should be avoided at all costs and treated with diuresis or renal replacement therapy if indicated.[12] Starch products can cause tubular damage and should therefore be avoided. For 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 therapeutic modalities, close hourly monitoring of urine output is extremely important for adjusting 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 performed to assess the patient’s response to diuresis. It should be noted that a diuretic challenge should be given only after 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 that assesses the functional integrity of the tubules and aids in risk stratification and decision-making. FST is said to be nonresponsive if 1.0 to 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 starting with 100-200 mg of furosemide; if there is no response, doubling the dose may be considered. If this fails to yield significant improvement, adding a thiazide diuretic may also be considered.[1]

One of the most important prerequisites for FST is that the patient should not be hypovolemic, and that heart rate and 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 with a renal etiology, treatment is primarily supportive, with potential renal replacement therapy to manage fluid and electrolyte balance and avoid complications.[1]

Dietary Recommendations

In addition to 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 Therapy

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 kidneys should be carefully reviewed and their doses adjusted.[3] Drugs metabolized by the kidneys should be avoided. These drugs include doxorubicin, allopurinol, aminoglycosides, azathioprine, cephalosporins, clofibrate, digoxin, diazepam, meperidine, procainamide, propoxyphene, propranolol, and sulfonamides. If these drugs are necessary, the dose must be modified in accordance with the degree of renal injury.[1]

It should be kept in mind that in the setting of oliguria, fluid resuscitation puts the patient at risk of fluid overload, which in turn leads to worsening AKI. As a result, overcompensation with fluids is associated with higher mortality when urine output determines 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, diuretics are used to manage it. On the other hand, in patients who are nonresponsive to diuretics, renal replacement therapy can be used.[3][12]

Differential Diagnosis

When evaluating a patient with oliguria, the following differential diagnosis should be kept in mind, and the evaluation should be conducted 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)

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 to the intensive care unit develop oliguria later in the course of their illness, which is 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 associated with oliguria is not entirely attributable to the development of ARF.[4]

The duration and intensity of oliguria have a great impact on prognosis. As the severity of oliguria worsens to <0.5 ml/kg/h, mortality increases significantly.[4]

Complications

In patients with acute oliguria, one of the most common functional derangements that is observed is the sudden fall in the GRF, leading to acute renal failure. It results in a rapid increase 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 result from electrolyte imbalances. 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 patient monitoring.
• 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 complications warrants meticulous monitoring and helps avoid the development of life-threatening complications.

Consultations

The primary care provider should consult a nephrologist for an expert opinion, as well as a dietitian or nutritionist, for advice on maintaining appropriate protein and caloric intake. Radiologist consultation may be required to properly assess renal perfusion using the Doppler-based renal resistive index (RI).[1] In addition, a pharmacy consultation is necessary to assess the potential nephrotoxic effects of a prescription or other medication that is primarily renally excreted, so that appropriate dosage modification can be made.[20]

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 advised to follow the provider’s advice and be regularly followed by their physician and, if the physician suggests, a nephrologist.

Prolonged fasting and excessive exercise should be avoided as they can worsen oliguria and lead to rhabdomyolysis. Any catheterized patient should receive adequate education on 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 fluid and electrolyte management, adequate protein and caloric intake are necessary.[1]

Pearls and Other Issues

Predisposing Risk Factors for Oliguria

The following factors have been shown to predispose the patient to the development of oliguria:

• Old age
• Intravascular volume depletion
• Prior history of renal disease
• Vasoconstrictive drugs eg, NSAIDs, tacrolimus, cyclosporine
• Nephrotoxic agents, eg, radiocontrast media, aminoglycosides, chemotherapeutic agents
• Comorbidities eg, diabetes, congestive heart failure, liver disease [8]

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 performed in patients with urine output less than 0.5 ml/kg/hour for 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 on 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, perioperative course, diagnostic procedures, and medications.[1]

Special care should be taken to avoid any potential nephrotoxic drugs in 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 therapeutic modalities, close hourly monitoring of urine output is essential to gauge treatment.[3]

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References

1.

Klahr S, Miller SB. Acute oliguria. N Engl J Med. 1998 Mar 05;338(10):671-5. [PubMed: 9486997]

2.

Marketos SG, Eftychiadis AG, Diamandopoulos A. Acute renal failure according to ancient Greek and Byzantine medical writers. J R Soc Med. 1993 May;86(5):290-3. [PMC free article: PMC1294008] [PubMed: 8505754]

3.

Klein SJ, Lehner GF, Forni LG, Joannidis M. Oliguria in critically ill patients: a narrative review. J Nephrol. 2018 Dec;31(6):855-862. [PMC free article: PMC6244549] [PubMed: 30298272]

4.

Glassford NJ, Bellomo R. The Role of Oliguria and the Absence of Fluid Administration and Balance Information in Illness Severity Scores. Korean J Crit Care Med. 2017 May;32(2):106-123. [PMC free article: PMC6786718] [PubMed: 31723625]

5.

Rimmelé T, Kellum JA. Oliguria and fluid overload. Contrib Nephrol. 2010;164:39-45. [PubMed: 20427992]

6.

Hoffman MD, Weiss RH. Does Acute Kidney Injury From an Ultramarathon Increase the Risk for Greater Subsequent Injury? Clin J Sport Med. 2016 Sep;26(5):417-22. [PMC free article: PMC4900946] [PubMed: 26657822]

7.

Bell S, Ross VC, Zealley KA, Millar F, Isles C. Management of post-operative acute kidney injury. QJM. 2017 Nov 01;110(11):695-700. [PubMed: 27803367]

8.

Lesko J, Johnston JP. Oliguria. AACN Clin Issues. 1997 Aug;8(3):459-68. [PubMed: 9313381]

9.

Macedo E, Malhotra R, Bouchard J, Wynn SK, Mehta RL. Oliguria is an early predictor of higher mortality in critically ill patients. Kidney Int. 2011 Oct;80(7):760-7. [PubMed: 21716258]

10.

Edelstein CL, Ling H, Schrier RW. The nature of renal cell injury. Kidney Int. 1997 May;51(5):1341-51. [PubMed: 9150442]

11.

Basile DP, Anderson MD, Sutton TA. Pathophysiology of acute kidney injury. Compr Physiol. 2012 Apr;2(2):1303-53. [PMC free article: PMC3919808] [PubMed: 23798302]

12.

Joannidis M, Druml W, Forni LG, Groeneveld ABJ, Honore PM, Hoste E, Ostermann M, Oudemans-van Straaten HM, Schetz M. Prevention of acute kidney injury and protection of renal function in the intensive care unit: update 2017 : Expert opinion of the Working Group on Prevention, AKI section, European Society of Intensive Care Medicine. Intensive Care Med. 2017 Jun;43(6):730-749. [PMC free article: PMC5487598] [PubMed: 28577069]

13.

Lumlertgul N, Peerapornratana S, Trakarnvanich T, Pongsittisak W, Surasit K, Chuasuwan A, Tankee P, Tiranathanagul K, Praditpornsilpa K, Tungsanga K, Eiam-Ong S, Kellum JA, Srisawat N., FST Study Group. Early versus standard initiation of renal replacement therapy in furosemide stress test non-responsive acute kidney injury patients (the FST trial). Crit Care. 2018 Apr 19;22(1):101. [PMC free article: PMC5909278] [PubMed: 29673370]

14.

Joannidis M, Klein SJ, John S, Schmitz M, Czock D, Druml W, Jörres A, Kindgen-Milles D, Kielstein JT, Oppert M, Schwenger V, Willam C, Zarbock A. [Prevention of acute kidney injury in critically ill patients : Recommendations from the renal section of the DGIIN, ÖGIAIN and DIVI]. Med Klin Intensivmed Notfmed. 2018 Jun;113(5):358-369. [PubMed: 29594317]

15.

Ostermann M, Straaten HM, Forni LG. Fluid overload and acute kidney injury: cause or consequence? Crit Care. 2015 Dec 27;19:443. [PMC free article: PMC4699346] [PubMed: 26707872]

16.

Chen KP, Cavender S, Lee J, Feng M, Mark RG, Celi LA, Mukamal KJ, Danziger J. Peripheral Edema, Central Venous Pressure, and Risk of AKI in Critical Illness. Clin J Am Soc Nephrol. 2016 Apr 07;11(4):602-8. [PMC free article: PMC4822669] [PubMed: 26787777]

17.

Mullens W, Abrahams Z, Francis GS, Sokos G, Taylor DO, Starling RC, Young JB, Tang WHW. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J Am Coll Cardiol. 2009 Feb 17;53(7):589-596. [PMC free article: PMC2856960] [PubMed: 19215833]

18.

Wardle EN. Acute renal failure and multiorgan failure. Nephron. 1994;66(4):380-5. [PubMed: 8015638]

19.

Cumming AD. Sepsis and acute renal failure. Ren Fail. 1994;16(1):169-78. [PubMed: 7514310]

20.

Solomon R, Werner C, Mann D, D'Elia J, Silva P. Effects of saline, mannitol, and furosemide on acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994 Nov 24;331(21):1416-20. [PubMed: 7969280]

21.

Schetz M, Hoste E. Understanding oliguria in the critically ill. Intensive Care Med. 2017 Jun;43(6):914-916. [PubMed: 27620297]

Disclosure: Mobeen Haider declares no relevant financial relationships with ineligible companies.

Disclosure: Ahsan Aslam declares no relevant financial relationships with ineligible companies.