Abstract
Gastrointestinal (GI) mucosal lesions are common in chronic kidney disease (CKD), end-stage renal disease (ESRD), and in post-renal transplant period. However, etiology of mucosal lesions pre- and post-transplant is very different. Gastropathy in non-transplant ESRD patients usually develops because of uremia, chronic anemia, and fluctuations in the gastric blood supply during hemodialysis, eventually leading to uremic gastritis. Gastropathy in post-transplant patients tends to be associated with immunosuppressive therapies.Helicobacter pylori infection is more prevalent in uremic patients than in post-transplant patients. Uremia can also lead to uremic arteriolopathy and autonomic nervous system dysfunction, which can present with GI symptoms mimicking uremic gastropathy. Post-transplantation immunosuppressive therapies have been linked to GI mucosal lesions as well. These lesions carry a poor prognostic factor disrupting the function of the GI tract, which in turn affects the pharmacokinetics of the immunosuppressive drugs eventually leading to poor graft survival and increased mortality. Mycophenolate mofetil is one of the agents more associated with intestinal erosions.Recognizing uremic gastropathy and intervening early helps prevent post-transplant GI complications. Acid controlling therapies can be an effective prophylaxis against both gastropathies. Using enteric-coated formulation for immunosuppressive agents may slow down the mucosal insult. Treatment of H. pylori in both patient populations may help prevent further mucosal injury. Lastly, timely screening for symptoms may help start treatment early and prevent progression to serious gastropathy.
Highlights
BackgroundUremic patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) as well as renal transplant recipients have been historically susceptible to gastrointestinal (GI) mucosal lesions [1,2]
Acid controlling therapies can be an effective prophylaxis against both gastropathies
The selected publications were analyzed in order to better understand the pathophysiology and management options of both uremic gastropathy and gastropathy induced by post-renal transplant immunosuppressive therapy
Summary
Uremic patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) as well as renal transplant recipients have been historically susceptible to gastrointestinal (GI) mucosal lesions [1,2]. Khedmat et al compared H. pylori infection and endoscopic findings in uremic patients with controls [3] They observed a higher number of gastric and duodenal mucosal lesions as well as H. pylori infection in patients with uremia when compared to those with normal renal function. They observed that gastric or duodenal ulcers were significantly higher in patients who had the infection but were not treated when compared to those who had the infection but received treatment (5 vs 1; p=0.05) and when compared to those without the infection (5 vs 0; p=0.05) They concluded that patients with H. pylori infection should be treated to avoid long-term complications from gastric or duodenal PUD subsequent to renal transplantation
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