Uremic toxin

Under uremic toxins is understood twill own mostly nitrogenous substances including for the symptoms of uremia and nephropathy are responsible ( Urämiegifte ).

A toxin (from ancient Greek τοξικόν toxikón, German 'poison') is an often organic poison that is (naturally) synthesized by a living being. So all unnatural poisons do not count as toxins. The poisons effective in humans are divided into toxins and other poisons. The generic term for medically effective toxins is toxic . The adjective toxirenal means arising from kidney toxins . Under a toxicosis means the poisoning only by metabolites of the body. A Toxon is part of the diphtheria toxin , the paralysis caused and kidney damage. The toxicity or toxicity of the individual uremia poisons depends on their concentration in the tissue.

Uremic toxins cause renal insufficiency . Not all kidney failure is due to kidney disease. Nephrotoxins , by definition, always cause kidney disease , with or without kidney failure.

Pathophysiology

The urinary substances are normally excreted via the kidneys . The concentration of these substances in the blood can rise if there is a decrease in the glomerular filtration rate, e.g. B. in acute kidney failure or in chronic kidney failure or there is an increase in tubular reabsorption.

The uremic toxins with low or medium molar mass can be partially removed by dialysis . This is accompanied by an improvement in the symptoms of uremia. In the case of persistent symptoms of uremia, the high protein binding and the resulting low renal clearance of uremia toxins are held responsible.

Low or medium molar mass toxins

A selection of uremia toxins with their respective effects is listed below:

urea: End product of the urea cycle , marker for the severity of renal insufficiency; as a uremia toxin , it inhibits NaK2Cl cotransport in the erythrocytes
Creatinine: in high concentrations it leads to hemolysis
uric acid: if the protective factor is suspected, the damage in uremia is low
heat stable acidic peptide: Molar mass from 1000 to 2000 Da , responsible for insulin resistance in uremia
Pseudouridine: Inhibition of the uptake of glucose in uremia
Hippuric acid: Inhibition of the uptake of glucose in uremia
Calcitriol toxin: inhibits the synthesis of calcitriol , binds specifically to the calcitriol receptor and leads to calcitriol resistance.
Cyanate: by carbamylation it reacts with the amino groups of lysine residues
AGE: Condensation products of primary amines with aldoses . They release cytokines, increase blood coagulation and are responsible for late vascular complications, e.g. B. in diabetes mellitus. They are associated with β ₂ -microglobulin amyloidosis .
Indoxyl sulfate: It leads to the progression of renal insufficiency by sclerotherapy of the glomerula . Inhibition of erythropoiesis and the transport mechanisms of the hepatocytes (e.g. Multispecific Organic Anion Transporter ( MOAT ) for the transport of bile). It is also responsible for the itching in uremia.
Homocysteine: atherogenic uremia toxin
Sperm: Erythropoiesis inhibitors
Methylguanidine: is considered to be a factor in uremic polyneuropathy . Also hemolysis, inhibition of pancreatic secretion , inhibition of iron uptake in bone marrow cells , inhibition of DNA synthesis in the lymphocytes .
Guanidine succinate: Thrombocytopathy , uremic polyneuropathy
Nitric oxide: Thrombocytopathy
para-cresol: Inhibition of phagocytosis of granulocytes
Parathyroid hormone: Inhibits insulin secretion and erythropoiesis. Related to bone marrow fibrosis . The increased absorption and accumulation of calcium in the entire organism leads to a variety of disorders.
β2-microglobulin: Dialysis-associated amyloidosis
Malnutrition factor: Physiologically excreted in the urine; in animal experiments it inhibits food intake.

diagnosis

For reasons of cost and time, routine laboratory medicine usually only determines the plasma concentrations of urea and creatinine.

therapy

The most effective reduction in uremia toxins is an improvement in kidney function or adequate dialysis treatment.

Individual evidence

^ Franz Volhard : Die double-sided haematogenic kidney diseases , in: Gustav von Bergmann , Rudolf Staehelin (Ed.): Handbook of Internal Medicine, 2nd edition, Springer-Verlag, Berlin, Heidelberg 1931, Volume 6, pp. 548 and 776.
^ Ulrich Kuhlmann, Joachim Böhler, Friedrich C. Luft , Mark Dominik Alscher , Ulrich Kunzendorf (eds.): Nephrology, 6th edition, Georg Thieme Verlag , Stuttgart, New York 2015, ISBN 978-3-13-700206-2 , P. 422.
^ Wilhelm Dultz: DGB Foreign Words Lexicon , German Book Association , Berlin, Darmstadt, Vienna 1965, 491.
^ Harrison's internal medicine , 19th edition, Georg Thieme Verlag , Stuttgart 2016, ISBN 978-3-88624-560-4 , p. 2227 f.
↑ Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney Diseases, Schattauer Verlag , Stuttgart, New York 2003, ISBN 3-7945-2177-3 , p. 31 f.
↑ Hanns-Wolf Baenkler et al .: Internal Medicine , publisher: MLP AG , Thieme Verlag , Stuttgart 2001, ISBN 3-13-128751-9 .

[1] Franz Volhard : Die double-sided haematogenic kidney diseases , in: Gustav von Bergmann , Rudolf Staehelin (Ed.): Handbook of Internal Medicine, 2nd edition, Springer-Verlag, Berlin, Heidelberg 1931, Volume 6, pp. 548 and 776.

[2] Ulrich Kuhlmann, Joachim Böhler, Friedrich C. Luft , Mark Dominik Alscher , Ulrich Kunzendorf (eds.): Nephrology, 6th edition, Georg Thieme Verlag , Stuttgart, New York 2015, ISBN 978-3-13-700206-2 , P. 422.

[3] Wilhelm Dultz: DGB Foreign Words Lexicon , German Book Association , Berlin, Darmstadt, Vienna 1965, 491.

[4] Harrison's internal medicine , 19th edition, Georg Thieme Verlag , Stuttgart 2016, ISBN 978-3-88624-560-4 , p. 2227 f.

[5] Helmut Geiger, Dietger Jonas, Tomas Lenz, Wolfgang Kramer (eds.): Kidney Diseases, Schattauer Verlag , Stuttgart, New York 2003, ISBN 3-7945-2177-3 , p. 31 f.

[6] Hanns-Wolf Baenkler et al .: Internal Medicine , publisher: MLP AG , Thieme Verlag , Stuttgart 2001, ISBN 3-13-128751-9 .