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söndag 11 mars 2012

Munuaissairauden lopputilan riski keliaakikolla

Lopputilan riski on aika myöhäinen riski. Keliaakikolla on munuaissairauden lopputilanriskejä.

Gut. 2012 Jan;61(1):64-8. Epub 2011 Aug 3. Increased risk of end-stage renal disease in individuals with coeliac disease.

The prevalence of end-stage renal disease (ESRD) is increasing worldwide. Although increased levels of coeliac disease (CD) autoantibodies are often seen in renal disease, the importance of biopsy-verified CD for the risk of future ESRD is unclear. The aim of this study was therefore to investigate the risk of future ESRD in individuals with CD.
This was a population-based prospective cohort study. 29,050 individuals with CD (Marsh III) were identified through small-intestinal biopsy reports obtained between July 1969 and February 2008 in Sweden's 28 pathology departments. ESRD was defined as the need for renal dialysis or renal transplant in accordance with the international classification of disease and procedure codes in Swedish patient registers. Using Cox regression, the risk of ESRD in individuals with CD compared with age- and sex-matched reference individuals was estimated.
During follow-up, 90 individuals with CD developed ESRD (expected count 31). This corresponded to a HR for ESRD of 2.87 (95% CI 2.22 to 3.71, p<0.001). Adjusting for diabetes mellitus had only a marginal effect on the risk estimate (HR 2.52, 95% CI 1.92 to 3.31). Excluding individuals with any urinary/renal disorder before study entry, the HR for ESRD in CD was 2.47 (95% CI 1.80 to 3.40). When restricting the outcome measure to ESRD confirmed by independent data from the Swedish Renal Registry (SRR), the risk estimate increased to 3.20 (95% CI 2.39 to 4.28).

CONCLUSION: This study indicates that individuals with biopsy-verified CD suffer increased risk of subsequent ESRD.

Päivitys 4.9.2012 Tämä artikkeli pitäisi suomentaa . 

IgA nefropatia

Epäilen gluteeniyliherkkyyden olevan yksi syy IgA nefropatiaan ja epästabiiliin verenpaineeseen.




Celiac disease (CD) is a chronic intestinal disorder caused by intolerance to gluten. It is characterized by immune-mediated enteropathy, associated with maldigestion and malabsorption of most nutrients and vitamins. Prevalence of clinically overt CD varies from 1/270 in Finland to 1/5,000 in North America. CD is typically diagnosed in early childhood around two years of age. The main symptoms are: stomach pain, gas and bloating, diarrhea, weight loss, anemia, edema, bone or joint pain. Latent CD may be found around 40 years of age. Since CD can be asymptomatic, most subjects are not diagnosed or may present with atypical symptoms. Patients with atypical CD present with extraintestinal symptoms like immunoglobulin A (IgA)-nephropathy, hemosiderosis of the lungs and a variety of neurological disorders. Furthermore, severe inflammation of the small intestine can be present with no gastrointestinal symptoms; antibodies and typical small intestinal changes can be found. The exact cause of celiac disease is unknown but it is thought to be primarily immune-mediated (tissue-transglutaminase autoantigen); the disease is often inherited. The disease is associated with HLA-DQ2/DQ8 genes. However, 20% of the healthy population carry these genes. Therefore, no genetic test which could identify celiac disease-causing genes is currently available. In predisposed patients, the ingestion of gluten-containing food such as wheat and rye induces a flat jejunal mucosa with infiltration of lymphocytes. Early diagnosis is desirable since many symptoms can resolve after initiation of a gluten-free diet, and since CD causes growth retardation in untreated children as well as atypical symptoms such as infertility or neurological symptoms. Diagnosis requires endoscopy with jejunal biopsy. Identification of tissue-transglutaminase antibodies is important to confirm the diagnosis and rule out diseases which can mimic celiac disease. Differential diagnosis includes: collagenous colitis,Whipple's disease, Crohn's disease of the small intestine, autoimmune enteropathy, graft versushost disease (see these terms), tropical sprue, viral enteritis, giardiasis, AIDS, small intestinal lymphoma, carbohydrate intolerance, cow's milk intolerance, and radiation damage. There is no need for genetic screening since CD can be treated by a specific diet. Management consists in lifelong withdrawal of dietary gluten, which leads to significant clinical and histological improvement. However, complete normalization of histology can take years. Patients usually enjoy a good quality of life and have a normal life expectancy.

Expert reviewer(s)

  • Pr Wolfgang F. CASPARY
  • Dr Wolfgang HOLTMEIER