Uremia

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Classification according to ICD-10
N19 Unspecified renal insufficiency
R39.2 Extrarenal uremia
ICD-10 online (WHO version 2019)

The word uremia (from Latin urina , German 'urine', and ancient Greek αἷμα haĩma , German 'blood' ) means “urine in the blood”, that is, the increased occurrence of urinary substances in the blood due to missing or insufficient kidney function ( renal insufficiency ). The consequence of this inadequate purification of the blood is urine poisoning by harmful urine components ( uremia toxins , nephrotoxins ). One also speaks of retention uremia and, when the end products of nitrogen metabolism predominate, of azotemic uremia .

The full clinical picture of uremia can occur acutely (5–10 days after acute kidney failure ) or chronic (developing over years in chronic kidney failure ).

Cerebral disorders in chronic arterial hypertension with states of confusion (as in cerebral sclerosis ) even without renal insufficiency were previously referred to as pseudouremia .

causes

Renal uremia can occur in two ways: When glomerular filtration decreases, too little plasma is cleaned of the urinary substances. Your serum levels rise. If, on the other hand, the tubular reabsorption increases, the plasma level of the urinary substances also increases. A decrease in the glomerular filtration rate and an increase in the tubular reabsorption rate can lead to uremia.

Not every kidney disease leads to uremia. Not all uremia is due to kidney disease. The extrarenal kidney syndromes according to Wilhelm Nonnenbruch should be considered here, i.e. kidney failure even without kidney disease. The cardiorenal syndrome and the hepatorenal syndrome should be mentioned here, for example . In 1949, Nonnenbruch described extrarenal uremia even in patients with anuria . In 1953, in the German edition of ICD-6 (International Statistical Classification of Diseases and Related Health Problems), extrarenal uremia was coded with N 899. Today it is classified in the ICD-10 with R 39.2.

In addition, with certain metabolic disorders, the pathologically increased formation of uremia toxins, regardless of kidney function, also leads to uremia ( overproduction uremia ).

Symptoms

The main clinical features are therapy-resistant itching ( uremic pruritus ) and the signs of enterocolitis . This is often associated with problems of the gastrointestinal tract such as nausea , vomiting and bleeding due to inflammation of the stomach lining ( gastritis ) and intestinal inflammation ( colitis ). In the heart, uremia can cause inflammation of the pericardium, which can be caused by rubbing of the pericardium audible with the stethoscope . Heart failure (cardiac insufficiency) can again result as a complication . As the disease progresses, hyperkalaemia (excess potassium) with subsequent cardiac arrhythmias can develop. A pulmonary edema ( "water in the lungs") with shortness of breath and central cyanosis (bluish violet to discoloration of the skin, mucous membranes, lips and / or fingernails) occurs in some cases.

Since urea can damage nerves in higher concentrations , it can lead to neurological disorders such as uremic encephalopathy (pathological changes in the brain), which can range from personality changes, sleep disorders , states of agitation and slowing down to coma . Also, peripheral nerves can be disturbed, which clinically as polyneuropathy (disease of the entire outer nervous system) FIG. The hematopoiesis (blood formation) is disturbed, leading to anemia (anemia) leads. The odor of urine ( foetor uraemicus ) in the air we breathe is also noticeable - but it only occurs when urease-containing bacteria are present in the mouth.

therapy

Uremia as a clinical picture usually occurs in stage IV of chronic renal failure , the treatment of which is aimed at ameliorating the uremia. The therapeutic focus is on improving kidney function. In chronic renal failure, ACE inhibitors , AT1 antagonists and other antihypertensive drugs such as calcium antagonists and beta blockers are used.

Dialysis, also popularly known as "blood washing" (as hemodialysis , hemofiltration or peritoneal dialysis ) is a therapeutic option for advanced kidney disease and is based on the creatinine value, the urea concentration in the serum, the serum potassium , calcium and phosphate and on the clinical symptoms.

In addition, a strict diet has been prescribed so far , e.g. B. To avoid excessive protein , potassium (from fruit juices, fruit) and phosphate intake (from cola, pizza). Current studies, however, question both the value of strictly restricting protein intake and the value of a low-phosphate diet.

In the case of extrarenal uremia , as an alternative to renal replacement therapy, in addition to treating the underlying diseases , the use of water tablets ( diuretics ) can also be considered. All diuretics reduce the tubular reabsorption iatrogenically and thus increase the rate of formation of secondary urine with a corresponding excretion of uremic toxins.

In the event of a pathologically increased formation of uremia toxins, an attempt must be made to reduce this overproduction through an appropriate diet, with medication or with other methods.

See also

literature

  • Walter H. Hörl: Uremia - What is it . In: NEPHRO NEWS . No. 5/10 , 2010, pp. 1-8 ( article ).

Individual evidence

  1. ↑ Alphabetical directory for the ICD-10-WHO version 2019, volume 3. German Institute for Medical Documentation and Information (DIMDI), Cologne, 2019, p. 912
  2. ^ Franz Volhard : The double-sided hematogenous kidney diseases (Bright's disease) , Springer-Verlag, 1st edition, Berlin, Heidelberg 1918, 576 pages plus appendix, reprint from III. Volume of the "Handbook of Internal Medicine" (edited by L. Mohr and Rudolf Staehelin ), ISBN 978-3-662-42272-4 , pp. 168-258.
  3. ↑ H. Straub, K. Beckmann: General Pathology of Water and Salt Metabolism and Urine Preparation , in: Textbook of Internal Medicine , 4th Edition, 2nd Volume, published by Julius Springer, Berlin 1939, p. 50.
  4. ↑ H. Straub, K. Beckmann: General Pathology of Water and Salt Metabolism and Urine Preparation , in: Textbook of Internal Medicine , 4th Edition, Springer-Verlag, 2 volumes, Volume 2, Berlin 1939, p. 51.
  5. ^ Wilhelm Nonnenbruch : The bilateral kidney diseases - Brightii disease , Ferdinand Enke Verlag , Stuttgart 1949, p. 128.
  6. ↑ Handbook of the international statistical classification of diseases, damage to health and causes of death , publisher: Federal Statistical Office , Wiesbaden 1953, Volume 3: Detailed German systematics , pp. 76 and 96.
  7. ↑ Bernd Graubner: German Institute for Medical Documentation and Information (DIMDI): Alphabetical directory ICD-10-GM 2013 , 10th revision, version 2013, Deutscher Ärzte-Verlag , Cologne 2013, ISBN 978-3-7691-3509-1 , P. 1206.
  8. ↑ Franz Volhard : The bilateral hematogenous kidney diseases . In: Gustav von Bergmann , Rudolf Staehelin (eds.): Handbook of Internal Medicine , 2nd edition, Springer-Verlag, Berlin, Heidelberg 1931, Volume 6, pp. 195 and 723.
  9. ↑ Gerd Herold : Internal Medicine 2020 , self-published, Cologne 2019, ISBN 978-3-9814660-9-6 , p. 642.
  10. ↑ Gerd Herold : Internal Medicine 2020 , self-published, Cologne 2019, ISBN 978-3-9814660-9-6 , p. 642.
  11. ↑ Amitava Majumder, Anne Paschen: Medical working techniques. In: Jörg Braun, Roland Preuss (Ed.): Clinic Guide Intensive Care Medicine. 9th edition. Elsevier, Munich 2016, ISBN 978-3-437-23763-8 , pp. 29-93, here: pp. 62-66 ( dialysis method ).
  12. ↑ Bruno Cianciaruso, u. a .: Effect of a low- versus moderate-protein diet on progression of CKD: follow-up of a randomized controlled trial . In: American Journal of Kidney Diseases . 54, No. 6, December 2009, ISSN  1523-6838 , pp. 1052-1061. doi : 10.1053 / j.ajkd.2009.07.021 . PMID 19800722 .
  13. ^ Steven M. Brunelli: The Association between Prescribed Dietary Phosphate Restriction and Mortality among Hemodialysis Patients . In: CJASN . electronic publication before printing; December 2010, 2011 ( article ).