Functional oliguria R34

Oliguria was already described at a time when Hippocrates recognized the prognostic importance of urine excretion. In the 2nd century, Galen suggested using urine excretion as an indicator of renal function.

In 1802, William Heberden described suppression of urine output as "ischiuria renalis" (Turner 2015).

Between the two World Wars, Reinwein published a paper on oliguria associated with high specific urine weight. Nonnenbruch summarized oligoanuria in extrarenal renal syndrome in 1942 (Mohr 1968).

Functional oliguria is the reduction of daily urine output to < 500 ml caused by a functional reduction of the glomerular filtration rate (Herold 2022). The tubular apparatus is morphologically intact (Guder 1989). In the Anglo-Saxon world, the term oliguria is used only from a urine output of < 400 ml / d (Kasper 2015).

Oliguria may occur in the context:

- prerenal renal failure due to exsiccosis as so-called functional oliguria (Braun 2022)

- intra- or postrenal renal failure (Scheurlen 2013)

- of a chronic renal insufficiency (Braun 2022)

Functional oliguria occurs in up to 80% as the cause of oliguria / anuria (Braun 2022).

It is particularly found in the elderly, as there is often a decreased sense of thirst in the elderly (Gesenhues 2020).

The cause of functional oliguria is exsiccosis with resulting hypovolemia (Scheurlen 2013).

• Hypovolemia due to e.g.
  • Fluid losses from:
    • gastrointestinal tract e.g. vomiting, diarrhea etc.
    • Skin e. g. due to evaporation, burns etc.
    • Respiratory system e.g. due to evaporation (Kasper 2015).
    • increased urine excretion in case of e.g. glucosuria (Haider 2021)
  • due to fluid accumulation in the:
    • Peritoneum
    • Interstitium
    • Gastrointestinal tract
  • severe bleeding (Kasper 2015)
  • after prolonged thirst (Herold 2022)
  • medicinal by e.g. diuretics
  • in case of bilateral renal artery occlusion (very rarely occurring, e.g., in the context of a dissecting aortic aneurysm [Braun 2022])
  • in the context of certain diseases such as:
    • Diabetes insipidus (Kasper 2015)
    • Sepsis
    • pump failure of the heart (Haider 2021)
  • trauma-related
  • during surgical interventions (Haider 2021)

Decreased renal blood flow results in activation of neurohormonal signaling pathways leading to increased production of:

• Renin
• Angiotensin
• Aldosterone
• Catecholamines
• Prostaglandins

These trigger increased reabsorption of water and salt, resulting in the formation of a decreased amount of concentrated urine. For a period of time, this allows the glomerular filtration rate (GFR) and adequate renal blood flow (RBF) to be maintained. Without appropriate fluid correction, GFR and RBF will decline in the further course, leading to the occurrence of acute renal failure (Haider 2021).

Non-specific symptoms such as:

• general weakness
• fatigue
• Postural dizziness
• Thirst

In the further course may be added:

• abdominal or thoracic pain
• confusion
• unconsciousness
• peripheral cyanosis
• muscle weakness in patients with additional hypokalemia (Kasper 2015)
• Fever (Gesenhues 2020).
• dark urine color (Brown 2022)
• history of alternating oliguria and polyuria (indicates intermittent obstruction of the urinary tract = postrenal failure [Haider 2021])

A detailed history with emphasis on any pre-existing conditions, especially arterial hypertension, diabetes mellitus, cardiac disease, nephrolithiasis, autoimmune disease is important in patients with functional oliguria, as well as medication history (Haider 2021).

Physical examination:

• dry mucous membranes (Scheurlen 2013)
• standing skin folds
• decreased jugular venous pressure
• orthostatic hypotension (when standing up there is a drop in blood pressure of > 10 - 20 mmHg)
• cold extremities (Kasper 2015)
• Blood pressure:

In hypertonic dehydration, blood pressure remains normal for a long time. In hypotonic dehydration, on the other hand, arterial hypotension occurs early with the significant tendency to collapse (Gesenhues 2020).

CVD measurement

Depending on the hemodynamic status of the patient, monitoring of central venous pressure may be necessary (Haider 2021).

Sonography with Doppler

• Exclusion of the kidneys and urinary tract for urinary retention (Braun 2022).
• Determination of the renal resistance index to assess renal perfusion (Haider 2021).
• Possibly existing indications of ascites, pleural effusion, etc.

Typical laboratory values in functional oliguria compared with acute kidney injury (AKI) are:

• Serum urea elevated (also seen in oliguria due to AKI).
• creatinine only slightly elevated (significantly elevated in AKI)
• Specific gravity > 1.025 g / l (in AKI < 1.015 g / l)
• Osmolality > 1,000 mosm / kg (in AKI < 600 mosm / kg) (Herold 2022).
• Urine to plasma osmolality ratio > 1.5 (in AKI < 1.1 (Haider 2021)
• urinary sodium concentration < 20 mmol / l (in AKI > 20 mmol / l [Bergmann2013])
• Fractional sodium excretion < 1 % (in AKI > 1 % (Haider 2021)
• Serum concentration urea / creatinine > 30 (in AKI < 20 [Häussler 2006]).

Other laboratory abnormalities may include:

• increased hematocrit
• Increased total protein
• Plasma osmolality increased
• Urea usually strongly elevated (creatinine only moderately)
• ADH secretion increases
• the renin- angiotensin- aldosterone system is stimulated (Scheurlen 2013)
• Blood gas analysis (BGA):

Metabolic acidosis with decreased bicarbonate may be present (Kasper 2015).

• Neutrophil gelatinase - associated lipocalin (NGAL):

Egal et al. showed in a 2016 study that NGAL can differentiate between functional oliguria and acute renal failure (Egal 2016).

• Oliguria due to acute renal failure or chronic renal insufficiency.
• Anuria (where the daily urine output is < 100 ml / d [Herold 2022])

If oliguria is not treated, it may develop into acute renal failure (Herold 2022).

Severe functional oliguria can lead to hypovolemic shock (Kasper 2015).

The treatment of functional oliguria depends on the severity of the hypovolemia. In mild cases, oral fluid administration is usually sufficient.

In severe cases, i.v. fluid substitution with isotonic saline (0.9% NaCl) is indicated.

Patients with hypernatremia should instead receive a hypotonic solution such as 5% dextrose if water loss alone has occurred, or hypotonic saline (½ to ¼ normal saline) if water plus NaCl loss has occurred.

In metabolic acidosis with loss of bicarbonate, i. v. substitution of bicarbonate is indicated (Kasper 2015).

Blood loss: Patients with severe hemorrhage, should receive red cell concentrates, with hematocrit not exceeding 35% (Kasper 2015).

Urineoutput: Urine output is recommended to be monitored hourly in severe cases (Haider 2021).

Diuretics: If the oliguria does not resolve with the above fluid administration, the furosemide stress test (FST) is indicated for accurate assessment of renal function and further prognosis. The FST is one of the newer dynamic function markers (Kindgen- Milles 2020).

For this, the patient must first be euvolaemic. The test itself should be performed under constant monitoring of heart rate and blood pressure.

The patient receives a short infusion of 1 - 1.5 mg / kg bw furosemide.

If a diuresis of > 100 ml / h subsequently occurs, this indicates a GFR of > 20 ml / min and makes a progression of acute renal failure unlikely (Kindgen- Milles 2020). In this case, therapy with diuretics should be continued (Haider 2021).

If the above. Diuresis does not start within the first 2 h p. i., it is recommended to administer 100 - 200 mg furosemide. If this is also unsuccessful, a thiazide diuretic can still be tried. If all attempts are unsuccessful, diuretics should be discontinued (Haider 2021).

In patients with secondary renal oliguria, treatment focuses on supportive measures and - if necessary - renal replacement therapy (Haider 2021).

Functional oliguria usually disappears after timely restoration of renal perfusion (Haider 2021).

If the patient does not respond to a furosemide stress test (see "Therapy"), he will require renal replacement therapy in up to 75% (Haider 2021).

A significantly worse prognosis with increasing mortality is found with an intensity of oliguria < 0.5 ml / kg / h (Haider 2021).

1. Bergmann H et al (2013) Clinical anesthesiology and intensive care: hemofiltration - hemodialysis - hemopheresis. Springer Verlag Berlin / Heidelberg / New York / London / Paris / Tokyo / Hong Kong / Barcelona / Budapest 4.
2. Braun J et al (2022) Clinical guide to internal medicine. Elsevier Urban and Fischer Publishers 398
3. Egal M et al. (2016) Neutrophil Gelatinase- Associated Lipocalin as a Diagnostic Marker for
4. Acute Kidney Injury in Oliguric Critically Ill Patients: A Post-Hoc Analysis. Nephron (134) 81 - 88
5. Gesenhues S et al (2020) Practice guide to general medicine. Elsevier Urban and Fischer Publishers 766, 775.
6. Guder W G et al (1989) German Society for Clinical Chemistry Merck- Symposium: Pathobiochemistry and functional diagnostics of the kidney. Springer Verlag Berlin / Heidelberg / New York / London / Paris / Tokyo / Hong Kong / Barcelona / Budapest 128
7. Haider M Z et al (2021) Oliguria. StatPearls Publishing LLC. PMID: 32809573 Bookshelf ID: NBK560738
8. Häußler, U., & Keller, F. (2006). Renal diseases. In: Facharztwissen Urologie. Springerverlag Berlin / Heidelberg 623 - 633.
9. Herold G et al (2022) Internal medicine. Herold Publishers 599, 637
10. Kasper D L et al (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 289 - 293, 297 - 298.
11. Kindgen- milles D et al (2020) New renal function tests: renal functional reserve and furosemide test. Med Klin Intensivmed Notfmed 1 / 20
12. Mohr L et al (1968) Handbook of internal medicine. Eighth volume: renal diseases. Springer Verlag Berlin 944
13. Scheurlen G et al (2013) Differential diagnosis in internal medicine. Springer Verlag Berlin / Heidelberg / New York / London / Paris / Tokyo 506.
14. Turner N et al (2015) Oxford textbook of clinical nephrology. Oxford University Press 1831