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Uremic Gastropathy

Chapter · January 2014

DOI: 10.1007/978-3-319-40560-5_1632

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Elisabete Rios Francisco Beca

Hospital de São João Stanford Medicine
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Chapter Title Uremic Gastropathy

Copyright Year 2014
Copyright Holder Springer-Verlag Berlin Heidelberg
Corresponding Author Family Name Rios
Particle
Given Name Elisabete
Suffix
Division/Department Department of Pathology
Organization/University Centro Hospitalar de São João
Street Alameda Prof. Hernâni Monteiro
Postcode 4200-319
City Porto
Country Portugal
Division/Department Faculty of Medicine
Organization/University University of Porto
Street Alameda Prof. Hernâni Monteiro
Postcode 4200-319
City Porto
Country Portugal
Organization/University Institute of Pathology and Molecular
Immunology of The University Of Porto
City Porto
Country Portugal
Email culex.rios@gmail.com
Author Family Name Beça
Particle de
Given Name Francisco Ferro
Suffix
Division/Department Department of Pathology
Organization/University Centro Hospitalar de São João
Street Alameda Prof. Hernâni Monteiro
Postcode 4200-319
City Porto
Country Portugal
Division/Department Faculty of Medicine
Organization/University University of Porto
Street Alameda Prof. Hernâni Monteiro
Postcode 4200-319
City Porto
Country Portugal
Organization/University IPATIMUP – Institute of Pathology and
Molecular Immunology of the University of
Porto
City Porto
Country Portugal
Email fbeca@dfci.harvard.edu
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1
U

2 Uremic Gastropathy heartburn, and postprandial fullness, are common 29

in these patients, although they may have no 30

3 Elisabete Rios1,2,4 and Francisco Ferro symptoms (Nardone et al. 2005). Uremic fetor 31

4 de Beça1,2,3 (ammonia or urine-like odor to the breath) also 32

1
5 Department of Pathology, Centro Hospitalar de may be present. Endoscopic and histological 33

6 São João, Porto, Portugal lesions are more frequent in symptomatic patients 34
2
7 Faculty of Medicine, University of Porto, Porto, but may also be present in asymptomatic subjects 35

8 Portugal (Khazaei et al. 2008). Hemorrhagic gastropathy 36

3
9 IPATIMUP – Institute of Pathology and is the most prevalent lesion, particularly in 37

10 Molecular Immunology of the University of patients receiving chronic hemodialysis or in the 38

11 Porto, Porto, Portugal setting of acute renal failure. It is mostly due to 39

4
12 Institute of Pathology and Molecular mucosal lesions, with gastroduodenal erosions 40

13 Immunology of The University Of Porto, and/or peptic ulcers detected in up to 67 % of 41

14 Porto, Portugal patients (Walker et al. 2004). Other uncommon 42

disorders such as esophagitis, gastric 43

angiodysplasia, and inflammatory gastric polyps 44

15 Synonyms have also been described (Sotoudehmanesh et al. 45

2003). 46

16 Uremic gastritis Underlying mechanisms and factors contrib- 47

uting to the development of these gastropathies 48

remain unclear. In acute renal failure (ARF), 49

17 Definition gastropathy is thought to be more likely related 50

to physiologic stress, with additional factors that 51

18 Uremic gastropathy is a term commonly used to increase the risk of bleeding such as NSAIDs, 52

19 describe the upper gastrointestinal signs and his- liver disease, and other comorbidities (Walker 53

20 topathologic changes associated with uremia, et al. 2004). Hypergastrinemia, gastrointestinal 54

21 secondary to renal failure. dysmotility, and acid secretion alterations are 55

22 The clinical spectrum of upper gastrointestinal considered to be key factors in the pathophysiol- 56

23 disorders in the uremic patients varies widely, ogy of gastrointestinal lesions in patients with 57

24 since it might be influenced by several factors, chronic renal failure (CRF). Possible mecha- 58

25 such as the severity of renal function impairment, nisms for dysmotility include increased levels of 59

26 the stress level of the patients, and the assigned hormones involved in the modulation of gastro- 60

27 treatment. Gastrointestinal (GI) bleeding and intestinal motility (e.g., cholecystokinin, gastrin, 61

28 dyspeptic symptoms, such as anorexia, vomiting, and neurotensin) and other humoral disorders 62

H.V. Krieken (ed.), Encyclopedia of Pathology,

DOI 10.1007/978-3-642-04978-1, # Springer-Verlag Berlin Heidelberg 2014
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U 2 Uremic Gastropathy

63 (hypercalcemia, hypokalemia, and acidosis), that Sotoudehmanesh et al. (2003) reported that 110

64 are mainly ascribed to the reduced renal clearance male gender had higher risk of uremic 111

65 as well as autonomic nervous system dysfunction. gastropathy. 112

66 The mechanisms that lead to hypergastrinemia are • Site 113

114

67 commonly attributed to reduced renal clearance Up to 67 % of uremic patients lesions occur in 115

68 but may also be due to a feedback mechanism the stomach and duodenum, with gastric 116

69 from gastric acid neutralization with gastric lesions predominantly in the antrum (approx. 117

70 ammonia, a breakdown product of urea that is 50 %). 118

71 higher in gastric mucus among patients with • Treatment 119

120

72 advanced renal failure (Nardone et al. 2005). Treatment of uremic gastropathy relies on the 121

73 This concept has been used as substrate by resolution of uremia, which can be accom- 122

74 several investigators (Khazaei et al. 2008) to plished by medical treatment for associated 123

75 explain the high susceptibility of these patients metabolic and electrolyte abnormalities, such 124

76 to colonization of Helicobacter pylori (HP). as anemia, hyperkalemia, hypocalcaemia, 125

77 These linkage stems from the notion that HP hyperparathyroidism, and iron deficiency. 126

78 possesses a powerful urease, which converts When these treatments fail, renal replacement 127

79 urea to ammonia and, thus, provides protection therapy with hemodialysis, peritoneal dialysis, 128

80 against the low pH of the gastric environment. or renal transplantation is the treatment of 129

81 Since uremic patients have an increased level of choice. 130

82 gastric urea in gastric mucus, they might be more Other therapeutic interventions include 131

83 susceptible to HP infection. However, the dietary changes and hemostatic procedures, 132

84 reported prevalence of HP infection and its rela- in case of uremic bleeding. 133

85 tionship to upper GI pathologic changes in ure- • Outcome 134

135

86 mic patients have been controversial. While some Uremic gastropathy can be a significant cause 136

87 studies have demonstrated a higher prevalence of of morbidity and mortality, likely due to the 137

88 HP infection in uremic patients (Khazaei et al. considerable risk of complicated upper GI 138

89 2008), others have determined that the preva- lesion in uremic patients, namely, acute 139

90 lence of the infection is less than in the general upper GI bleeding, despite its rarity. Increased 140

91 population (Day et al. 2003). prevalence of peptic ulcers after renal trans- 141

plantation is reported historically, having 142

accounted for approximately 4 % of deaths 143

92 Clinical Features (Walker et al. 2004). However, the use of 144

acid-suppression therapies and corticoste- 145

93 • Incidence roid-sparing immunosuppressive regimens 146

94 The reported prevalence of uremic gastropathy has reduced the frequency of this 147

95 in the uremic patients is quite varied, there complication. 148

96 being a wide range of between 7 % and 100 %

97 (Nardone et al. 2005; Khazaei et al. 2008).
98
99 • Age Macroscopy 149

100 Prevalence of uremia and subsequently ure-

101 mic gastropathy among different age groups Upper gastrointestinal endoscopy features are 150

102 is largely unknown. Several reports demon- variable and include erythema, multiple small 151

103 strate it can affect both adults and children, petechial hemorrhages, erosions, ulcerations, 152

104 being more prevalent in older adults (Khazaei and nodularity in either the stomach or duodenum 153

105 et al. 2008). or, less frequently, in the esophagus (Walker et al. 154
106
107 • Sex 2004; Khazaei et al. 2008). Gastric and duodenal 155

108 Uremia is slightly more prevalent in men than angiodysplastic lesions as well as gastric polyps 156

109 in women (male-to-female ratio, 1.2:1). have also been reported (Sotoudehmanesh et al. 157
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Uremic Gastropathy 3 U
158 2003). Hypertrophic folds in mucosa of the cor- Differential Diagnosis 182

159 pus may frequently be associated with successful

160 kidney transplantation (Day et al. 2003). Normal The main disease to consider in establishing 183

161 findings on endoscopy can occur with uremic a differential diagnosis, especially based on 184

162 gastropathy; nevertheless, histological evaluation biopsy specimens, is chronic gastritis. A firm 185

163 of blindly collected biopsies can identify epithe- diagnosis can only be made when supportive 186

164 lial lesions within normal-appearing mucosa. clinical data (such as known history of uremia) 187

are available. 188

165 Microscopy
References and Further Reading 189

166 Characteristic findings of uremic gastropathy

167 include foveolar hyperplasia, multinucleated Day, D. W., Jass, J. R., Price, A. B., Shepherd, N. A., 190
Sloan, J. M., Talbot, I. C., Warren, B. F., Williams, 191
168 parietal cells with vacuolation and fragmentation
G. T., et al. (2003). Morson and Dawson’s gastroin- 192
169 of the cytoplasm, and extension of parietal cells testinal pathology (4th ed.). Malden: Blackwell 193
170 into the antrum and even the duodenum. This Science. 194

171 may be related to long-term steroid therapy and Khazaei, M. R., Imanieh, M. H., & Hosseini Al-Hashemi, 195
G. (2008). Gastrointestinal evaluation in pediatric kid- 196
172 the trophic effects of hypergastrinemia. In addi-
ney transplantation candidates. Iranian Journal of Kid- 197
173 tion, heterotopic calcification within the gastric ney Diseases, 2, 40–45. 198
174 mucosa may occur. Helicobacter pylori organ- Nardone, G., Rocco, A., Fiorillo, M., Del Pezzo, M., 199

175 isms may be seen on H&E staining in some Autiero, G., Cuomo, R., Sarnelli, G., Lambiase, A., 200
Budillon, G., & Cianciaruso, B. (2005). Gastroduode- 201
176 cases; identification is enhanced with special
nal lesions and Helicobacter pylori infection in dys- 202
177 stains (Giemsa, Diff-Quik, immunohistochemis- peptic patients with and without chronic renal failure. 203
178 try, or silver stain). The increased incidence Helicobacter, 10, 53–58. 204

179 of CMV infection should be considered in Sotoudehmanesh, R., Ali Asgari, A., Ansari, R., & 205
Nouraie, M. (2003). Endoscopic findings in end-stage 206
180 patients receiving immunosuppression therapy
renal disease. Endoscopy, 35, 502–505. 207
181 (Day et al. 2003). Walker, W. A., Durie, P. R., Kleinman, R., & Walker- 208
Smith, J. A. (2004). Pediatric gastrointestinal disease, 209
pathophysiology, diagnosis and management (4th ed.). 210
Philadelphia: BC Decker. 211

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