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. Author manuscript; available in PMC: 2011 Jun 30.
Published in final edited form as: Ther Apher Dial. 2010 Aug 31;15(1):1–9. doi: 10.1111/j.1744-9987.2010.00851.x

Review of Helicobacter pylori Infection and Chronic Renal Failure

Mitsushige Sugimoto 1, Yoshio Yamaoka 1,2
PMCID: PMC3126920  NIHMSID: NIHMS305194  PMID: 21272246

Abstract

Chronic renal failure patients receiving hemodialysis and continuous ambulatory peritoneal dialysis often encounter gastrointestinal troubles over their long treatment period. Helicobacter pylori infection has close association with development of peptic ulcer, gastric cancer and gastric lymphoma, and is thought to be one of the major risk factors for gastrointestinal troubles in dialysis patients. However, it is unclear whether H. pylori infection is directly associated with progression of renal dysfunction and prognosis of chronic renal failure patients. Recent consensus shows that the prevalence of H. pylori infection in chronic renal failure patients is significantly lower than in subjects with normal renal function. In the natural history of H. pylori infection in hemodialysis patients, the prevalence of infection decreases as dialysis periods progressed, in particular within the first four years after the start of treatment. However, the chance of natural eradication becomes rare for patients receiving dialysis treatment for a long time. Moreover, chronic renal failure patients with H. pylori infection have a higher incidence of gastroduodenal diseases, and therefore, are recommended to receive eradication therapies, especially for those receiving treatment for a long time and with higher risks of complication. Intensive endoscopic check-ups for the prevention of gastrointestinal events and the discovery of peptic ulcer and neoplastic diseases at an early phase may be required.

Keywords: Chronic renal failure, Continuous ambulatory peritoneal dialysis, Eradication therapy, Helicobacter pylori, Hemodialysis, Peptic ulcer

Chronic renal failure (CRF) patients receiving hemodialysis treatment consist of more than 1.1 million people in the world, and the size of this population is expanding at a rate of 7% per year according to the progress in medical and dialysis machine technique (1). Although heart failure, angina pectoris, hypertension, parathyroid-related disease, amyloidosis, renal anemia and infection are well known to occur by receiving hemodialysis and continuous ambulatory peritoneal dialysis (CAPD) for long periods (2), those patients also often suffer from gastrointestinal troubles including peptic ulcer, hemorrhage, abdominal symptoms, constipation, diarrhea, ileus, and perforation (3–12).

Helicobacter pylori is a spiral-shaped, microaerophilic Gram-negative flagellate bacterium that was isolated in 1983 from gastric biopsy specimens of patients with chronic gastritis (13). The gastric mucosa of approximately 50% of the world's population is infected with H. pylori, and the infection levels exceed 70% in some developing areas (14,15). Helicobacter pylori infection plays a crucial role in the development of gastrointestinal diseases, such as peptic ulcer, gastric hyperplastic polyps, gastric adenoma, gastric cancer, and gastric mucosa associated-lymphoid tissue lymphoma, both in individuals with normal renal function and in chronic renal failure patients receiving hemodialysis and CAPD (Tables 1 and 2) (4–9,16,18–32,34,36–45,47–60).

TABLE 1.

List of previous reports: association of Helicobacter pylori infection prevalence and patients with hemodislysis

Year Author Period (months) Patient (n) Control (n) Character of Control PU GIF
1989 Offerhaus GJA (16) NA 44% (50) 45% (40) Healthy + −
1990 Wee A (17)† NA 31% (322) NA NA +
1991 Davenport A (18) 38 (1–76) 34% (76) 30% (247) Healthy NA −
1991 Loffeld RJ (19) 4 (2–16) 43% (30) 38% (344) Healthy NA −
1995 Jasperson D (20) NA 23% (34)a 37% (127) Symptoms + +
1995 De Vecchi AF (21) NA 59% (29) 72% (29) Symptoms + −
1996 Luzza F (22) 74 ± 63 73% (103) 78% (103) Symptoms NA −
1996 Seyrek N (23) 23 ± 2 14% (91) 23% (35) Healthy NA −
1996 Krawczyk W (24) 28 ± 12 62% (21) 64% (22) Dyspepsia − +
1996 Abu Farsakh NA (25) 18 (1–108) 57% (28)a 73% (100) NA +
1997 Hruby Z (26) 52 ± 54 35% (25) 44% (16) Dyspepsia NA +
1997 Ozgur O (27) 29 ± 29 60% (47) 64% (100) Symptoms + +
1998 Munoz de Bustillo E (28) 40 ± 42 64% (52) NA + + +
1999 Yildiz A (29) 33 ± 28 66% (47) 73% (55) Healthy NA −
1999 Fabirizi F (30) NA 56% (228) 53% (158) Healthy NA −
1999 Araki H (31)† 91 ± 62 46% (63) 66% (64) Healthy + +
1999 Gut G (32) 21 ~ 22 57% (44) 55% (45) Dyspepsia − +
1999 Boran M (33) 52 ± 21 50% (50) NA NA +
2000 Huang JJ (34) 28 (1–156) 47% (70) 60% (42) Dyspepsia + +
2001 Wang YL (35) 53 50% (80) 60% (80) Dyspepsia + +
2002 Nakajima F (36) 47 ± 58 28% (51)a 56% (25) CRF (non-HD) + +
2002 Fabbian F (37) 51 ± 58 13% (38) NA − 4-
2002 Tsukada K (38) 76.5−57.4 30% (47)a 56% (55) Dyspepsia + +
2003 Sotoudehmanesh R (5) 14 ± 29 59% (206) NA + +
2003 Marsenic O (39)‡ NA 9% (22) NA − +
2004 Lopez T (40) 56 ± 61 42% (86) NA NA −
2004 Sezer S (4) 67 ± 48 10% (163) NA − +
2004 Nakajima F (41) 57 ± 62 37% (138) 62% (138) Healthy NA −
2004 Al-Mueilo SH (42) NA 63% (44) 63% (60) Dyspepsia + +
2004 Trimarchi H (43) 19 ~ 20 28% (29) NA NA −
2005 Blusiewicz K (44) NA 63% (30) 71% (31) Dyspepsia + +
2006 Lentine (45) 28 25% (97) NA NA −
2007 Khedmat H (9) 47 ± 11 63% (73)b 35% (305) Dyspepsia + +
2007 Itatsu T (46) NA 40% (77) NA Symptoms NA +
2008 Gioe FP (47) 42–85 53% (142) 45% (132) Symptoms − −
2009 Sugimoto M (48) 59 ± 0.4 49% (539)a 79% (400) Symptoms + +
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a

P < 0.05 when significantly lower compared with control subjects;

b

P < 0.05 when significantly higher compared with control subjects.

†

Paper contains hemodialysis and CAPD patients

‡

Paper contains hcmodialysis and CRF patients.

Treatment period was determined as median (range) or mean ± SE or SD according to reports. Gastrointestinal endoscopy (GIF)-positive (+) indicates that GIF was performed in the study, and peptic ulcer-positive (+) meant reports included peptic ulcer in both/either patient group and/or control group with normal renal function. CAPD, continuous ambulatory peritoneal dialysis; CRF, chronic renal failure; PU, peptic ulcer; NA, not available.

TABLE 2.

List of previous reports: association with Helicobacter pylori infection prevalence and patients with CAPD and Tx

Treatment Year Author Period (month) Patient (n) Control (n) Character of Control PU GIF
CAPD
1995 De Vecchi AF (21) NA 53% (38)a 79% (38) Symptoms + −
1997 Antoniou S (49) (1–108) 64% (39) NA NA −
2001 Aguilera A (50) 18 ± 13 33% (48) NA − −
2005 Lui SL (51) 54 ± 42 26% (136) NA NA −
2008 Altay M (52) 21 ± 18 27% (64) NA NA −
TX
1991 Davenport A (18) 45 (6–219) 29% (202) 30% (247) Healthy NA −
1997 Hruby Z (26) 41 ± 35 62% (29) 44% (16) Dyspepsia NA +
1997 Ozgur O (27) 51 ± 40 70% (54) 64% (100) Symptoms + +
1999 Yildiz A (29) 38.6% (57) 73% (55) Healthy NA −
2007 Khedmat H (9) 52 ± 16 40% (25) 35% (305) Dyspepsia + +
CRF
1990 Shousha S (53) 24% (50)a 42% (120) Symptoms − +
1991 Ala-Kaila K (54) 17% (89) NA NA −
1993 Neithercut WD (55) 48% (23) NA NA +
1995 Jaspcrson D (20) 24% (59)a 37% (127) Symptoms + +
1997 Moustafa FE (56) 40% (70) NA NA +
1999 Misra V (57) 56% (50)a 78% (50) Healthy − +
2000 Emir S (58) 63% (16) NA + +
2002 Schoonjans R (59) 46% (28) NA − −
2004 Strid H (60) 26% (31) NA NA −
2004 Nakajima F (41) 53.3 (30) 62% (138) Healthy NA −
2007 Khedmat H (9) 66% (71)b 35% (305) Dyspepsia + +
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a

P < 0.05 when significantly lower compared with control subjects;

b

P < 0.05 when significantly higher compared with control subjects.

Treatment period was determined as median (range) or mean ± SE or SD according to reports. Gastrointestinal endoscopy (GIF)-positive (+) indicates that GIF was performed in the study, and peptic ulcer-positive (+) meant reports included peptic ulcer in both/either patient group and/or control group with normal renal function. CAPD, continuous ambulatory peritoneal dialysis; CRF, chronic renal failure; PU, peptic ulcer; NA, not available; Tx, kidney transplant.

Patients with chronic renal failure often have gastrointestinal symptoms caused not only by H. pylori infection, but also by high urea levels, decline of gastrointestinal motility, amyloid protein deposition (59,60), and decreased sensory disturbance. Therefore, the quality of life in patients with chronic real failure is usually poor, which affects their nutrition status leading to the development of malnutrition, which is a potent predictor of morbidity and mortality. Moreover, patients with chronic renal failure may have higher risks of gastric mucosal damages compared with individuals with normal renal function because of systemic and/or local chronic circulatory failure (61,62), hypergastrinemia (32), high ammonia levels (55), and enhanced inflammation. Especially, 25–75% of those patients suffer from a number of gastrointestinal lesions and complications including gastric erosions, peptic ulcers, angiodysplasia and gastrointestinal bleeding (3–12,17).

It is unclear about the actual condition of gastroduodenal diseases in hemodialysis and CAPD patients related with H. pylori infection, because previous reports have controversial results due to small sample size and short observation periods. In this review article, we therefore initially reviewed the association between H. pylori infection and chronic renal failure, the natural history of H. pylori infection according to the treatment periods, and then summarize the H. pylori eradication therapy for chronic renal failure patients.

Helicobacter pylori infection in patients receiving hemodialysis and CAPD

Helicobacter pylori infection has an influence on intake of proton pump inhibitors (PPI) and antibiotics and eradication therapy of H. pylori. The prevalence of H. pylori infection in chronic renal failure patients receiving CAPD or hemodialysis was shown to be equal or lower compared to subjects with normal renal function in various different geographic populations irrespective to presence/absence of gastric symptoms (4–9,16,18–32,34,36–45,47–60) (Table 1). Recently, in the investigation of 539 Japanese hemodialysis patients with treatment periods of mean 8.4 ± 0.3 years, the prevalence of H. pylori infection was reported to be 48.6% ([95% CI: 44.3–52.9%]), which was significantly lower than in dyspepsia patients with normal renal function (78.5% [74.1–82.4%], 314/400, P < 0.001) and individuals with normal renal function receiving annual health exams (69.4% [60.3–77.5%], 84/121, P < 0.001) (48). Moreover, the prevalence of H. pylori infection in hemodialysis patients is significantly lower (27.5%) compared with non-hemodialysis chronic renal failure patients (56.0%) (36), and the prevalence in individuals with normal renal function is similar with patients receiving hemodialysis treatment for less than 1-year period (48). These data suggest that hemodialysis treatment, but not uremia by chronic renal failure itself, plays a role in the lower prevalence of H. pylori infection. The start of hemodialysis treatment is thought trigger the decrease in the prevalence of H. pylori infection.

Previously, eight studies showed significantly lower prevalence of H. pylori infection in patients receiving hemodialysis (8/36 studies, 22.2%) (20,21,25,36,38,48,53,57) compared with controls and one study has found a significantly lower prevalence of H. pylori infection in patients receiving CAPD (1/5 studies, 20.0%) (21); whereas only one study reported that Iranian hemodialysis patients (63.0%) and chronic renal failure patients (66.2%) had significantly higher prevalence of H. pylori infection compared with normal individuals (27.5%) (Table 1) (9). However, since the prevalence of H. pylori infection in the Iranian population is reported to be more than 60% in other reports (63,64), further studies are required to clarify this discrepancy in the Iranian population. In a combined analysis using previous reports (4–9,16,18–32,34,36–45,48–60), the prevalence of H. pylori infection in patients receiving chronic hemodialysis and CAPD are 43.9% ([95% CI: 42.2–45.6%], 1435/3 272) and 34.8% ([29.6–40.2%], 113/325), respectively, which is significantly lower than in individuals with normal renal function both with and without gastrointestinal symptoms (49.8% [48.0–51.7%], 1476/2961, P < 0.001).

There is variation in H. pylori infection rates among different countries. It may, therefore, be better to evaluate the infection rate in various countries. In East Asian countries, the prevalence of H. pylori infection in patients receiving chronic hemodialysis is 44.5% ([95% CI: 41.5–47.6%], 474/1065), which is significantly lower than in individuals with normal renal function (54.0% [50.9–57.1%], 560/1038, P < 0.001). On the other hand, because the prevalence of H. pylori in other areas, such as Europe, Middle East, and South Asia has a wide variation, it is difficult to evaluate the prevalence of H. pylori infection in those areas.

The prevalence of H. pylori infection in patients receiving a kidney transplant was 39.0% ([33.9–44.2%], 143/367) (Table 2). Kidney transplant patients with sufficient renal function at present also have a lower H. pylori infection rate, as well as hemodialysis and CAPD patients. This may be explained by a situation in which most patients received hemodialysis and/or CAPD anytime before kidney transplantation.

The evaluation of an association between H. pylori infection and causes of chronic renal failure is limited. The prevalence in patients whose chronic renal failure was caused by diabetic nephropathy (60.1%) is reported to be significantly higher than that in chronic glomerulonephritis patients (46.1%) irrespective of the decreased immune system of diabetes patients (48). This suggests that disorders of the immune system, such as severe diabetic nephropathy, does not lose the maintenance of H. pylori infection.

Treatment periods of hemodialysis and H. pylori infection

Only a few reports have evaluated the relationship between H. pylori infection and dialysis treatment periods, and the mean dialysis duration in H. pylori-positive patients was significantly shorter than in uninfected patients (28,29,36,41,48). Munoz de Bustillo et al. (28) reported that mean hemodialysis periods in H. pylori negative patients receiving dialysis was 66.5 months, which was significantly longer than in positive patients (24.7 months). Nakajima et al. (36) reported that the prevalence of H. pylori infection markedly decreases when the treatment duration is two years or more. Recently, when the treatment period of hemodialysis and the H. pylori infection rate were simply measured at one time in a hospital, the infection rate was reported to gradually decrease according to dialysis treatment periods until four years after starting hemodialysis followed by a plateau (Table 3) (48). The prevalence of H. pylori infection is inversely associated with treatment periods of hemodialysis and the decreasing pattern is characteristic (Table 3). However, there are no data on the relationship between H. pylori infection and the time course of CAPD treatment periods.

TABLE 3.

Changes in Helicobacter pylori infection rate at the beginning, two years later, and 4 years later among total patients, chronic glomerulonephritis (CGN) patients, and patients with diabetes and others (48)

Total CGN Diabetes Others
Beginning 51.7% 48.8% 64.0 %b 48.8%
2 years later 42.9%a 41.3% 47.2% 46.5%
4 years later 38.3%a 38.2% 41.6% 32.6%
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a

P < 0.05 (vs. Beginning);

b

P < 0.05 (vs. CGN and others groups).

Others included lupus nephritis, polycystic kidney, chronic pyelonephritis and nephrosclerosis.

The follow-up survey of H. pylori infection

To investigate whether H. pylori infection was actually eradicated after beginning hemodialysis treatment, a follow-up survey using the same dialysis patients with H. pylori infection is required. When the natural history of H. pylori infection was investigated using more than 300 patients for a 4 year-follow up survey, although nobody received eradication therapy, the prevalence of H. pylori infection was reported to be 51.6% at first year, 42.9% two years later, and 38.3% four years later, indicating that the infection rate gradually decreased during dialysis treatment (Table 3). In other words, 26.7% of dialysis patients naturally cured H. pylori infection over four years. Patients who received hemodialysis and CAPD are expected to eradicate H. pylori not only naturally but also by environmental improvement and H. pylori eradication.

The mechanisms of lower prevalence of H. pylori infection in hemodialysis and CAPD patients

There are at least three explanations as to why dialysis patients have low prevalence of H. pylori infection: (i) Patients receiving dialysis have higher levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, IL-8 and tumor necrosis factor (TNF)-α, from activated inflammatory cells infiltrating the gastric mucosa (65). As a result, gastric atrophy progresses, accompanied by increased pH, and finally H. pylori are not able to live in gastric mucosa (66). (ii) Blood urea levels as well as urea nitrogen levels in gastric secretions are higher in dialysis patients than in patients with normal renal function, and high urea levels may inhibit H. pylori growth in the stomach (67). (iii) H. pylori infection might be cured upon antibiotic treatment, both because antibiotics are commonly used during the initial treatment periods and most dialysis patients had many chances of bacterial infection during the treatment, and because antibiotic concentrations are higher and more prolonged in patients with renal failure than in individuals with normal renal function. Importantly, there was no significant difference in the prevalence of H. pylori infection between patients with normal renal function and patients receiving less than one year of dialysis treatment (48). Therefore, urea concentration and antibiotic usage are unlikely to be contributors in decreasing the prevalence of infection. One possible explanation for decreased H. pylori prevalence is therefore up-regulation of pro-inflammatory cytokine resulting from dialysis enhanced severe inflammation of gastric mucosa, and progression to gastric atrophy. However, further studies to investigate the histopathology of gastric inflammation and atrophy are necessary.

Necessity of H. pylori eradication therapy for chronic renal failure patients

The prevalence of peptic ulcer in hemodialysis and CAPD patients with H. pylori infection is higher than in individuals with normal renal function (9). Moreover, the incidence of tumor death is 2–4 times higher in dialysis patients than in the general population, and it is known that the most frequently detected malignant tumor is gastric cancer (68).

For hemodialysis and CAPD patients, one of the severe gastroduodenal events is a hemorrhage from gastroduodenal lesions. Because most chronic renal failure patients receive anti-coagulant drugs and/or anti-platelet drugs for prevention of hypertension and brain infarction, and thus anti-coagulant drugs, such as heparin sodium, are usually used during hemodialysis treatment, hemorrhage from gastroduodenal lesions easily occurs in such patients and often causes fatal blood loss. Moreover, gastric mucosa is known to be fragile in hemodialysis and CAPD patients. Therefore, to prevent hemorrhage from gastrointestinal diseases, intragastric pH in patients receiving hemodialysis and CAPD should be kept at a higher level by doses of acid inhibitory drugs (e.g. proton pump inhibitors) and by limiting doses of anticoagulant drugs.

One important question is whether H. pylori eradication therapies are necessary for H. pylori-infected hemodialysis and CAPD patients to prevent gastroduodenal disease development. As described above, more than one-third of the patients receiving approximately four years of dialysis treatment have naturally cured H. pylori infections, especially in hemodialysis patients (48). However, the frequency of peptic ulcer in patients receiving dialysis treatment is known to be higher in H. pylori infected patients than in uninfected patients, as observed in patients with normal renal function (48). We therefore recommend eradication therapies for H. pylori-infected hemodialysis patients and for patients receiving hemodialysis treatment. Moreover, it is better to eradicate at an early time for patients with a higher risk of disease development, such as past history of peptic ulcer and/or gastroduodenal hemorrhage, usage of several kinds of anticoagulants and non-steroidal anti-inflammatory drugs (NSAIDs, Fig. 1).

FIG. 1.

FIG. 1

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The schema of natural history of Helicobacter pylori infection in hemodialysis patients and treatment strategy.

Present condition otH. pylori eradication therapy for patients with chronic renal failure

One of the merits for H. pylori eradication therapy in hemodialysis and CAPD patients is that they keep a high plasma concentration of PPI and antibiotics even with low doses of drugs, although overdose of drugs must be carefully checked. On the other hand, one of the demerits for H. pylori eradication therapy in hemodialysis and CAPD patients is that there is a possibility that those patients are often infected with antibiotic-resistant strains since they have many occurrences of antibiotic intake due to an impaired immune system. In fact, 36.4% of patients with end-stage renal disease are reported to have clarithromycin-resistant strains, which is significantly higher than in non-uremic controls (15.2%) (69).

As summarized in Table 4 (4,28,31,32,35,38,46,70–75), each eradication regimen previously reported use of different PPIs (omeprazole, lansopprazole, esomeprazole) and/or antibiotics (clarithromycin, amoxicillin and metronidazole), and variation of the duration of treatment from 7 days to more than 3 weeks. However, there is no significant difference in the overall cure rates among the different studies listed. In multivariate analysis for eradication failure (age, gender, endoscopic findings, dialysis therapy, and previous eradication treatment), only history of previous treatment remained (38). This suggests that antibiotic resistance influences eradication success/failure, as observed in healthy non-dialysis patients. However, there are currently no data on antibiotic-resistant strains in eradication studies with dialysis patients (Table 4).

TABLE 4.

Helicobacter pylori eradication therapy for chronic renal failure patients

Year Author Country Number Regimen Eradication rate Determine methods Resistance
1997 Tamura H (70) Japan 14 LPZ (30) oid/ 8 weeks, AMPC (500) oid/ 3 weeks, plaunotol (80) tid/ 24 weeks 78.6% RUT, Culture, Histology No data
1998 Munos de Bustillo E (28) Spain 23 OPZ (20) bid, AMPC (500) tid/ 14 days 60.8% UBT No data
23 Plus OPZ (20) bid, CAM (500) bid/ 14 days 82.6%
1998 Tokushima H (71) Japan 17 LPZ (30) oid/ 8 weeks, AMPC (500)/3 weeks 76.5% RUT, Culture, Histology No data
10 LPZ (30) oid, AMPC (250), MNZ (250) bid/ 7 days 90.0%
1999 Araki H (31) Japan 17 OPZ (20) oid/ 8 weeks, AMPC (250) oid, CAM (200) oid/ 3 weeks, polaprizinc (0.5) bid/ 24 weeks 88.2% IgG, Histology No data
1999 Gur G (32) Turkey 25 FAM (40) oid, CAM (500) bid, MNZ (250) bid/ 15 days 80.0% Histology, RUT No data
2001 Wang YL (35) China 38 OPZ (20), AMPC (1000), CAM (500) bid/ 7 days 86.8% Stool No data
2002 Mak SK (72) China 21 (CRF) OPZ (20), AMPC (1000), CAM (500) bid/ 7 days 90.5% RUT No data
2002 Tsukada K (38) Japan 39 OPZ (30) bid, AMPC (500) tid, CAM (400) bid/ 7 days 82.1% UBT No data
2003 Mak SK (73) China 25 (CRF) OPZ (20) or LPZ (30), AMPC (1000), CAM (5O0) bid/ 7 days 96.0% Histology No data
2003 Sheu BS (74) China 38 (CRF) LPZ (30), AMPC (750), CAM (500) bid/ 7 days 76.3%
40 (CRF) LPZ (30), CAM (500), MNZ (500) bid/ 7 days 92.5% Stool No data
2004 Sezer S (4) Turkey 17 OPZ (20), AMPC (1000), CAM (500) bid/ 14 days 94.1% Endoscopy No data
2007 Tseng GY (75) China 34 (CRF) ESO (40) or OPZ (20) bid, AMPC (1000) bid, CAM (500) bid/ 7 days 94.1% UBT No data
2007 Itatsu T (46) Japan 11 LPZ (60), AMPC (750), CAM (400)/ 7 days 72.7% RUT No data
9 LPZ (60), CAM (400)/ 7 days 33.3%
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AMPC, amoxicillin; CAM, clarithromycin; Eso, Esomeprazole; FAM, famotidine; LPZ, lansoprazole; MNZ, metronidazole; OPZ, omeprazole; RUT, rapid urease test; UBT, urea breath test.

Antibiotics are known to have the possibility to progress renal dysfunction. Sheu et al. (74) reported that among chronic renal failure non-dialysis patients, those in the lansoprazole–clarithromycin–metronidazole regimen had a lower risk of acute renal failure than those in the lansoprazole–clarithromycin–amoxicillin regimen (2% vs. 18%, P < 0.05; relative risk, 0.128, 95%CI, 0.016–0.979). Because amoxicillin is mainly excreted from the kidney, toxic effects of amoxicillin on renal function in patients with chronic renal failure have been reported in various studies (76,77). However, most previous reports showed no severe adverse effects of amoxicillin in hemodialysis patients who received eradication therapy containing amoxicillin (4,28,31,32,35,38,70,71). Moreover, since PPI and antibiotics are removed by hemodialysis, plasma concentration of PPI and antibiotics is expected to decrease to a concentration that is less than effective. Therefore, it is necessary to set an optimal dosing plan in hemodialysis patients to increase cure rate and to use antibiotics more safely by using established pharmacological methods, such as monitored concentration.

Most patients who received eradication therapy were prevented from recurrence of peptic ulcer and had decreased risk of gastric cancer development (78–80). With eradication therapy in patients treated for early gastric cancer by endoscopic mucosal resection, the odds ratio for metachronous gastric cancer decreased significantly [0.353 (95% CI 0.161–0.775; P = 0.009)] (79). Patients who received hemodialysis often encountered gastric mucosal injuries, such as gastric erosion and gastric ulcer, irrespective to H. pylori infection due to NSAID intake and arteriosclerosis. Therefore, for patients receiving hemodialysis and CAPD, the most important benefit is the prevention of gastric cancer development.

CONCLUSION

Chronic renal failure patients receiving hemodialysis and CAPD have a low prevalence of H. pylori infection. More than one-third (36.2%) of patients receiving less than four years' dialysis had naturally cured H. pylori infection within the four-year observation period. However, because chronic renal failure patients have a higher risk of gastroduodenal disorders, it is recommended that all hemodialysis and CAPD patients receive endoscopic check-ups to reduce the chance of developing peptic ulcers. Moreover, patients with H. pylori infection should receive eradication therapy to prevent peptic ulcer and hemorrhage. The clinical protocol for a detailed endoscopic check-up and eradication therapy for dialysis patients should be evaluated in future studies.

Acknowledgments

The project described was supported by Grant Number R01 DK62813 from the National Institutes of Health (NIH). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the NIH.

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