Zusammenfassung
Unter Urämie versteht man die Gesamtheit aller Effekte der chronischen Niereninsuffizienz infolge einer verminderten Ausscheidung von Stoffen, die beim Gesunden renal eliminiert werden. Akut äußert sich die Urämie in einer Symptomatik mit Übelkeit, Perikarditis, Pleuritis und zentralnervösen Störungen bis zum Koma. Die akute Urämie ist durch Nierenersatzverfahren behandelbar. Daneben gibt es chronische Störungen vieler Organsysteme, die auch unter der Dialysetherapie weiter voranschreiten. Diese sind durch eine in zeitlicher Hinsicht oder im Hinblick auf das Molekulargewichtsspektrum unzureichende Clearance des Nierenersatzverfahrens bedingt. Urämische Toxine können Metabolite aus dem Intermediär- und Nukleinsäurestoffwechsel oder Proteine sein, es kann sich aber auch um Stoffe handeln, die unter den Bedingungen des urämischen Milieus chemisch modifiziert werden. Sie spielen für alle Langzeitkomplikationen der Niereninsuffizienz eine Rolle: chronische Entzündung, Herz-Kreislauf-Veränderungen, Immundefekt, Malnutrition, Anämie, Knochenstoffwechselstörung sowie Polyneuropathie. Die therapeutischen Möglichkeiten sind begrenzt, in der Regel sind die Komplikationen jedoch durch eine erfolgreiche Nierentransplantation reversibel.
Abstract
Uremia describes the consequences of intoxication in chronic renal failure with substances that are renally cleared in healthy individuals. Acute uremia is a syndrome of gastrointestinal symptoms, pericarditis, pleuritis, and central nervous system alterations ending with coma. These symptoms can be resolved by renal replacement therapy. In addition, chronic uremia can result in damage of multiple organ systems, which continues to advance despite dialysis therapy. This is caused by retention of toxins that cannot be adequately removed due to insufficient treatment time or a molecular weight range hampering elimination. Uremic toxins can be generated by the energy or nucleic acid metabolism, they can be proteins or large molecules that are altered chemically by the uremic milieu. Chronic uremia can influence the majority of long-term complications of chronic renal failure: systemic microinflammation, cardiovascular disease, immunodeficiency, malnutrition, anemia, bone metabolism, and polyneuropathy. There are few therapeutic options other than kidney transplantation.
Literatur
Aguilera A et al (2004) Eating behavior disorders in uremia: a question of balance in appetite regulation. Semin Dial 17:44–52
Auffray C et al (2007) Monitoring of blood vessels and tissues by a population of monocytes with patrolling behavior. Science 317:666–670
Chiang CK, Tanaka T, Inagi R et al (2011) Indoxyl sulfate, a representative uremic toxin, suppresses erythropoietin production in a HIF-dependent manner. Lab Invest 91:1564–1571
Del Vecchio L, Locatelli F, Carini M (2011) What we know about oxidative stress in patients with chronic kidney disease on dialysis – clinical effects, potential treatment, and prevention. Semin Dial 24:56–64
Foley RN, Parfrey PS, Sarnak MJ (1998) Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis 32:112–119
Girndt M et al (2002) Anti-inflammatory interleukin-10 genotype protects dialysis patients from cardiovascular events. Kidney Int 62:949–955
Girndt M, Sester M, Sester U et al (2001) Defective expression of B7-2 (CD86) on monocytes of dialysis patients correlates to the uremia-associated immune defect. Kidney Int 59:1382–1389
Girndt M, Sester U, Kaul H, Köhler H (1998) Production of proinflammatory and regulatory monokines in hemodialysis patients shown at a single cell level. J Am Soc Nephrol 9:1689–1696
Haaber AB, Eidemak I, Jensen T et al (1995) Vascular endothelial cell function and cardiovascular risk factors in patients with chronic renal failure. J Am Soc Nephrol 5:1581–1584
Kielstein JT et al (1999) Asymmetric dimethylarginine plasma concentrations differ in patients with end-stage renal disease: relationship to treatment method and atherosclerotic disease. J Am Soc Nephrol 10:594–600
Locatelli F et al (2009) Effect of membrane permeability on survival of hemodialysis patients. J Am Soc Nephrol 20:645–654
Longenecker JC et al (2002) Traditional cardiovascular disease risk factors in dialysis patients compared with the general population: the CHOICE study. J Am Soc Nephrol 13:1918–1927
Mak RH, Cheung W, Cone RD, Marks DL (2006) Mechanisms of disease: Cytokine and adipokine signaling in uremic cachexia. Nat Clin Pract Nephrol 2:527–534
Nangaku M, Eckardt KU (2006) Pathogenesis of renal anemia. Semin Nephrol 26:261–268
Pupim LB, Caglar K, Hakim RM et al (2004) Uremic malnutrition is a predictor of death independent of inflammatory status. Kidney Int 66:2054–2060
Ridker PM, Cushman M, Stampfer MJ et al (1997) Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 336:973–979
Rocco MV et al (2011) The effects of frequent nocturnal home hemodialysis: the Frequent Hemodialysis Network Nocturnal Trial. Kidney Int 80:1080–1091
US Renal Data System (2010) USRDS 2009 Annual Data Report: atlas of end-stage renal disease in the United States. National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda/MD
Ulrich C, Heine GH, Seibert E et al (2010) Circulating monocyte subpopulations with high expression of angiotensin-converting enzyme predict mortality in patients with end-stage renal disease. Nephrol Dial Transplant 25:2265–2272
Ulrich C, Seibert E, Heine GH et al (2011) Monocyte angiotensin converting enzyme expression may be associated with atherosclerosis rather than arteriosclerosis in hemodialysis patients. Clin J Am Soc Nephrol 6:505–511
Vanholder R, Baurmeister U, Brunet P et al (2008) A bench to bedside view of uremic toxins. J Am Soc Nephrol 19:863–870
Wahl P, Wolf M (2012) FGF23 in chronic kidney disease. Adv Exp Med Biol 728:107–125
Zimmermann J, Herrlinger S, Pruy A et al (1999) Inflammation enhances cardiovascular risk and mortality in hemodialysis patients. Kidney Int 55:648–658
Interessenkonflikt
Der korrespondierende Autor gibt an, dass kein Interessenkonflikt besteht.
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Girndt, M. Klinische Probleme der Urämie. Internist 53, 817–822 (2012). https://doi.org/10.1007/s00108-011-3013-2
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00108-011-3013-2