Gastrointestinal system endoscopy and pathological findings in non-dialysis chronic kidney disease: A single-centre study

doi:10.21203/rs.3.rs-4293560/v1

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Gastrointestinal system endoscopy and pathological findings in non-dialysis chronic kidney disease: A single-centre study

https://doi.org/10.21203/rs.3.rs-4293560/v1

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Different gastrointestinal complications may occur as a result of moderate and severe loss of kidney function in chronic kidney disease (CKD). This study examined upper gastrointestinal tract endoscopy and pathology findings in CKD patients with renal failure who were not receiving dialysis treatment.

Method This study included 60 pre-dialysis CKD patients who underwent endoscopic examination due to dyspeptic complaints (CKD group. Endoscopic and pathological findings were compared with those of non-uremic patients (non-CKD group) with similar complaints.

Results There was no difference in the frequency of gastroesophageal reflux in both groups. The rates of non-ulcerative lesions, esophagitis, antral gastritis, erythematous gastritis and active chronic gastritis were significantly higher in the CKD group than in the non-CKD group (p < 0.001). Erosive pangastritis was significantly higher in the non-CKD group. The frequency of ulcerative lesions was similar in both groups. There was no significant difference in the rates of intestinal metaplasia, atrophy and metaplastic gastritis. The frequency of Helicobacter pylori was significantly higher in the non-CKD group (p < 0.001).

Conclusion Our findings show that some upper gastrointestinal system disorders are more common in non-dialysis CKD patients than non-uremic individuals, but Helicobacter pylori frequency is lower.

Chronic kidney disease

complication

gastrointestinal

dyspepsia

Helicobacter pylori

endoscopy

histopathology

Complications occur due to decreased kidney function in chronic kidney disease (CKD).¹ In patients with CKD, hypergastrinemia due to uremic toxins is associated with decreased gastrointestinal motility, hypo- and hypersecretion of stomach acid, polypharmacy, and the risk of gastrointestinal disturbances due to Helicobacter pylori (HP) infection.^2,3 Psychological problems are also an additional risk factor. Therefore, in patients with CKD, dyspeptic symptoms such as nausea, vomiting, abdominal pain, anorexia, indigestion and regurgitation may occur and the risk of malignancy increases.^1,2 HP that can cause serious diseases such as peptic ulcer, gastritis, stomach cancer and lymphoma.^2,4 While it is seen between 15-74.4% in the normal population, this rate varies between 20–64% in patients with CKD.⁴ It is also important to recognise and treat gastrointestinal system diseases in the pre-transplant period in these patients who are potential kidney transplant recipient candidates. The procedure with the highest diagnostic value in patients with CKD with complaints is endoscopy. In this study, endoscopic and pathological findings were investigated in patients with severe CKD who underwent upper gastrointestinal system endoscopy due to dyspeptic complaints.

Patients with CKD who underwent endoscopy due to upper gastrointestinal symptoms (serum creatinine value ≥ 1.5 mg/dL and estimated glomerular filtration rate (eGFR) according to The Kidney Disease: Improving Global Outcomes KDIGO with stage 3a (45–60), 3b (45 − 30) and 4 (15–30) were included in the study included in this retrospective study. A total of 60 CKD patients (32 men, 28 women) who were not receiving dialysis treatment were participants in the CKD group. Their median age was 59.5 (min: 25, max: 89) years. Thirty-four males and 34 females with normal kidney function and no kidney disease history were included as the control group (non-CKD group). Their median age was 53.8 (min: 25, max: 85) years. The study was conducted by Good Clinical Practice guidelines oath current legislations, and permission was obtained from the local institutional ethics committee to use patient data for publication (Approval Date: xx/xx/20xx; Reference number / Protocol Number: 20xx). –xx/xx). Clinical features, esophagogastroduodenoscopy findings and biopsy (histological evaluation and identification of HP staining) results were obtained from the medical records.

Statistical Analysis

We used the Shapiro-Wilk test to assess the normal distribution of continuous variables. We presented descriptive statistics for group comparisons, including mean ± standard deviation or median (minimum: maximum) values. We made comparisons of numerical variables in both groups using the Mann- Whitney U test and independent paired sample t-test. We used a χ2 test (or Fisher’s exact test if any expected cell count was < 5) and presented descriptive statistics as numbers and percentages to analyse categorical data. Binary logistic regression analysis was performed to determine independent risk factors affecting the presence of endoscopic gastritis and duodenitis, pathological chronic gastritis, and HP. The backward elimination method was used in multivariate logistic regression analysis to find the best final model. Furthermore, we used the ROC curve to determine the cut-off points for the best accuracy (sensitivity and specificity) and the area under the curve (AUC) of haemoglobin, urea and total cholesterol for the presence of relevant events (duodenitis, chronic gastritis and HP). The data was analysed using the SPSS Software (IBM Corp. Released 2015. IBM SPSS Statistics for Windows, Version 23.0. Armonk, NY: IBM Corp). A p-value of < 0.05 was considered statistically significant.

The mean ages and gender distributions of both groups were similar. When comorbid diseases were evaluated, the rates of coronary artery disease (40% vs 8.8%), diabetes mellitus (73.3% vs 10.3%) and hypertension (78.3% vs 17.6%) were significantly higher in the CKD group compared to the non-CKD group (p < 0.001). Laboratory values of both groups were given in Table 1. Compared to the other group, serum urea, creatinine, potassium, phosphorus, CRP, and ferritin values were significantly higher in the CKD group, and eGFR, calcium, total protein, total and HDL cholesterol, erythrocyte, haemoglobin and hematocrit values were significantly higher in the non-CKD group.

Table 1

Comparison of laboratory parameters of both groups
Variables	Total (n: 128)	non-CKD group (n: 68)	CKD group (n: 60)	P-value
Glucose (mg/dL) (n: 98)	102 (66:323)	96 (67:214)	115 (66:323)	0.170^a
Urea (mg/dL) (n: 96)	54.5 (8:165)	27 (8:56.5)	80 (42:165)	< 0.001^a
Creatinin (mg/dL) (n: 110)	1.4 (0.5:4,1)	0.7 (0.5:1.2)	2.4 (1.5:4.1)	< 0.001^a
eGFR ml/dk/1.73m² (n: 110)	44.6 (14:132)	98 (62:132)	28 (14:45)	< 0.001^a
Uric acid (mg/ dL) (n: 45)	5.8 (2.1:14.9)	5.2 (2.1:8.2)	6.2 (2.6:14.9)	0.069^a
Sodium (mmol /L) (n: 82)	139.1 ± 4	139.8 ± 1.8	138.7 ± 4.6	0.124^b
Potassium (mmol /L) (n: 82)	4.5 ± 0.7	4.3 ± 0.3	4.6 ± 0.8	0.007^b
Calcium (mg/dL) (n: 76)	8.9 ± 0.9	9.5 ± 0.5	8.9 ± 0.9	< 0.001^b
Phosporus (mg/dL) (n: 28)	4.1 (2.5:8.2)	3.3 (3.1:3.5)	4.2 (2.5:8.2)	0.029^a
Total protein (g/dL) (n: 51)	62.9 (0.7:84.5)	71.4 (67.7:73.5)	59.8 (0.7:84.5)	< 0.001^a
Total Cholesterol (mg/dL) (n: 33)	174 ± 65.2	207.7 ± 47.8	145.9 ± 65.5	0.005^b
HDL (mg/dL) (n: 31)	48 (23:95)	56 (42:95)	38 (23:65)	< 0.001^a
Triglyceride (mg/dL) (n: 29)	135 (62.4:425)	108.7 (62.4:259)	164 (69:425)	0.444^a
LDL (mg/dL) (n: 93)	113 (1.6:304)	117 (16:304)	105 (1.6:170)	0.270^a
AST (IU/L) (n: 102)	16.5 (5:16503)	17 (7:59)	16 (5:16503)	0.981^b
ALT (IU/L) (n: 115)	15 (5:1161)	18.5 (6:142)	12 (5:1161)	0.012^a
CRP (mg/L) (n: 52)	3.4 (0:314.7)	0.6 (0:6.3)	12 (1:314.7)	< 0.001^a
Iron (µg/dl) (n: 26)	63.2 ± 33.4	67.9 ± 36.8	59.2 ± 30.9	0.519^b
TIBC (µg/dl) (n: 26)	253.8 ± 72.3	266.4 ± 70	243 ± 75	0.421^b
Ferritin (µg/L) (n: 55)	77 (5.2:4250)	40.5 (5.2:548)	215 (11:4250)	< 0.001^a
Eritrosit (10⁶µL) (n: 116)	4.2 (0.1:6.3)	4.7 (3.4:6.3)	3.5 (0.1:4.9)	< 0.001^a
Haemoglobin (g/dL) (n: 116)	11.8 (5.1:18.6)	13.3 (8.8:18.6)	10.1 (5.1:15.8)	< 0.001^a
Hematocrit (%) (n: 116)	36.1 (15.4:50.9)	40.2 (28.7:50.9)	30.5 (15.4:45)	< 0.001^a
RDW (fL) (n: 116)	14.6 (11.8:123.2)	13.6 (11.8:123.2)	15.9 (11.8:30)	< 0.001^a
Platelet (10³µ/L) (n: 116)	234 (18:327)	249.5 (126:327)	195.5 (18:472)	< 0.001^a
MPV (fL) (n: 113)	10 (0:13.2)	9.8 (8.3:11.4)	10.6 (0:13.2)	0.003^a

Data were expressed as median (minimum:maximum) and mean ± standard deviation.

eGFR estimated glomerular filtration rate, HDL high-density lipoprotein, LDL low-density lipoprotein, AST aspartate aminotransferase, ALT alanine aminotransferase, CRP C-reactive protein, TIBC total iron binding capacity, RDW red cell distribution, MPV mean platelet volume.

^a: Mann-Whitney U test, ^b: Independent paired sample t-test.

Endoscopic findings were given in Table 2. In both groups, no significant difference was observed between the rates of non-ulcerous and ulcerous lesions, such as gastroesophageal reflux, antral erosive gastritis, duodenitis and fundus polyp. Compared to the other group, the rates of antral gastritis, erythematous gastritis, erosive pangastritis, active chronic gastritis, and oesophagal varicose veins were significantly higher in the CKD group, and the rates of esophagitis LA and bulbitis were significantly higher in the non-CKD group (Fig. 4). Pyloric diverticulum was not detected in both groups.

Table 2

Comparison of endoscopic findings of both groups
Variables n (%)	Total (n: 128)	non-CKD group (n: 68)	CKD group (n: 60)	P value
Gastroesofageal reflüx	13 (10.2%)	4 (6%)	9 (15%)	0.094^a
Non-ulcerous lesion
Esophagitis LA Antral gastritis Antral erosive gastritis Erythematous gastritis Duodenitis Bulbitis Erosive pangastritis Fundus polyp Active chronic gastritis Esophageal varices	44 (34.6%) 59 (46.5%) 14 (10.9%) 4 (3.1%) 5 (3.9%) 20 (15.6%) 8 (6.3%) 5 (3.9%) 16 (12.5%) 4 (3.1%)	36 (53.7%) 25 (37.3%) 19 (14.7%) 0 4 (5.9%) 16 (23.5%) 0 3 (4.4%) 1 (1.5%) 0	8 (13.3%) 34 (56.7%) 4 (6.7%) 4 (6.7%) 1 (1.7%) 4 (6.7%) 8 (13.3%) 2 (3.3%) 15 (25%) 4 (6.7%)	< 0.001^a 0.029^a 0.146^a 0.046^b 0.370^b 0.009^a 0.002^b > 0.99^b < 0.001^a 0.046^b
Ulcerous lesion
Antral ulcer Duodenal aphthous ulcer	10 (7.8%) 1 (0.8%)	7 (10.3%) 0	3 (5%) 1 (1.7%)	0.334 ^b 0.469 ^b
Pyloric diverticulum	0	0	0	-

Data were expressed as n%.

^a: Chi-Square test, ^b: Fisher's Exact Chi-Square test.

Histopathological findings obtained from biopsy samples were shown in Table 3. The groups had similar rates of intestinal metaplasia and oedema-congestion, atrophic metaplastic gastritis, fundic and hyperplastic polyps and chronic gastritis. The incidence of inflammation in the CKD group was significantly higher than in the non-CKD group (48.3% vs 20.6%, p = 0.008). The incidence of HP in the CKD group was significantly lower than in the non-CKD group (23.5% vs 59.1%, p < 0.001). Dysplasia was not detected.

Table 3

Comparison of pathological findings in groups
Variables n (%)	Total (n: 128)	non-CKD group (n: 68)	CKD group (n: 60)	P-value
İntestinal metaplazi	10 (10.6%)	5 (14.7%)	5 (8.3%)	0.488^a
Edema- congestion	7 (7.4%)	1 (2.9%)	6 (10%)	0.416^a
Inflammation	36 (38.3%)	7 (20.6%)	29 (48.3%)	0.008^b
Helicobacter pylori	51 (43.6%)	39 (59.1%)	12 (23.5%)	< 0.001^b
Atrophy metaplastic gastritis	2 (2.1%)	0	2 (3.3%)	0.533^a
Fundic polyp	3 (3.2%)	1 (2.9%)	2 (3.3%)	> 0.99^a
Hyperplastic polyp	5 (5.3%)	1 (2.9%)	4 (6.7%)	0.650^a
Chronic gastritis	54 (42.2%)	28 (41.2%)	26 (43.3%)	0.805^b
Dysplasia	0	0	0	-

Data were expressed as n%.

^a: Fisher's Exact Chi-Square test, ^b: Chi-Square test.

Multivariate logistic regression analysis determined independent risk factors affecting the development of endoscopic gastritis, duodenitis, pathological chronic gastritis, and HP. The logistic regression models obtained in the last stage of the analysis were found to be significant, and the data set was found to be compatible with the models. The variables included in the regression analysis models were determined for each dependent variable. For the presence of endoscopic gastritis: pathological chronic gastritis, HP positivity, hypertension, triglyceride, LDL and HDL cholesterol (Model χ2 = 11.5, p = 0.009; Hosmer-Lemeshow test p = 0.903). For the presence of endoscopic duodenitis: age, sodium, haemoglobin, calcium and lipase (Model χ2 = 5.31, p = 0.049; Hosmer-Lemeshow test p = 0.724). For the presence of pathological chronic gastritis: gender, antral ulcer, bulbar ulcer, duodenal aphthous ulcer, endoscopic gastritis, urea, sodium, total protein, albumin, LDL cholesterol, ferritin, and phosphorus (Model χ2 = 12.22, p = 0.007; Hosmer-Lemeshow test p > 0.99). For HP positivity: endoscopic gastritis, erosive gastritis, urea, total and LDL cholesterol, ferritin, calcium, and gamma-glutamyl transferase (GGT) (Model χ2 = 12.51, p = 0.002; Hosmer-Lemeshow test p = 0.632). In multivariate analysis, only gastritis (p = 0.028) and calcium (p = 0.008) affected HP positivity. The variables included in the models created in the last step of the multivariate logistic regression analysis were shown in Table 4.

Table 4

Multivariable logistic regression analysis of independent risk factors affecting the development of endoscopic gastritis and duedonitis and pathological chronic gastritis and HP positivity
	Wald	P value	Odds ratio	%95 CI lower-upper
Gastritis
Triglyceride	2.54	0.111	1.03	0.99–1.07
Duodenitis
Calcium	3.47	0.063	0.58	0.33–1.03
Chronic gastritis
Gastritis (presence)	0	0.998	7.181E + 142	0
HP positivity
Gastritis (presence)	4.83	0.028	4.19	1.17–15.05
Calcium	7.08	0.008	3.54	1.39–8.98

HP: Helicobacter pylori, CI: confidence interval.

In ROC curve analysis, the haemoglobin cutoff point for the sensitivity and specificity of haemoglobin in predicting the presence of duodenitis was determined as > 13.3 g/dL (AUC, 0.67; sensitivity 80%, specificity 75%, p = 0.197) (Fig. 1). The cut-off point of urea for predicting the presence of chronic gastritis was determined as > 50.9 mg/dL (AUC, 0.49; sensitivity 58%, specificity 50%, p = 0.94) (Fig. 2). The total cholesterol cut-off point for predicting the presence of HP positivity was determined as > 224 mg/dL (AUC, 0.60; sensitivity 44%, specificity 90%, p = 0.38) (Fig. 3).

Upper gastrointestinal system disorders are common in CKD patients due to high ammonium levels, systemic and local circulatory disorders, frequent drug use, and hypergastrinemia.⁵ However, most patients do not correlate with their complaints and endoscopic gastroduodenal lesions. The patient's symptoms appear to be fainter or milder.⁶ In our previous study of patients receiving hemodialysis (HD) or peritoneal dialysis (PD) maintenance therapy for end-stage renal disease, most of the patients did not have any significant upper gastrointestinal symptoms despite the high rate of gastritis in HD (63.6%) and PD (61.3%) patients.⁷ In the current study, antral gastritis, erythematous gastritis, erosive pangastritis and active chronic gastritis were found to be significantly higher in our non-dialysis uremic patients with Stage 3b and Stage 4 CKD, while the rates of oesophagal varicose veins, esophagitis and bulbitis were higher in the non-uremic control group. Lower albumin, total cholesterol, LDL and HDL levels may be seen in addition to anaemia in many patients, often due to infection, inflammation, nutritional deficiency and erythropoietin deficiency.

In different studies conducted in chronic HD patients, erosive esophagitis 30.2%, gastroesophageal reflux 10%, esophagitis 5.8%, enanthematous pangastritis 57.3%, diffuse antral erythema 27.8%, gastric erosion 5.8%, gastric antral erosion 22.8%, gastric intestinal metaplasia 8.3%, gastritis and doudenitis 42%, doudenal erosion 18–32%, peptic ulcer 7.3%, gastric ulcer 7–14%, doudenal ulcer 7.3–18%, angiodysplasia 4.4%, and gastric polyp were observed at rates of 1.5%.^5,8–11 In our previous study, gastroesophageal reflux was observed in 41.5%, chronic gastritis at 75.5%, non-specific gastritis at 24.5%, intestinal metaplasia at 17%, atrophy at 15.1%, HP at 28.3% and hyperplastic polyp at 3.8% of our dialysis patients.⁷ Gastric dysplasia was not detected in both of our studies. While rates of antral gastritis, erythematous gastritis, erosive pangastritis, active chronic gastritis and oesophagal varicose veins were detected at a lower rate in the CKD group, esophagitis and bulbitis rates were significantly higher in the non-CKD-group-according to CKD group.

The frequency of ulcerous lesions was similar in both groups. The frequency of ulcerative lesions in the normal population varies between 10–20%.¹² In a retrospective study conducted on dialysis patients, the peptic ulcer rate was found to be 31.8% and age, low albumin, high GGT, peritoneal dialysis and diabetes were reported as risk factors.¹³ In our study, intestinal metaplasia was detected in 8.3%, edema-congestion in 10%, inflammation in 48.3%, presence of HP in 23.5%, atrophy metaplastic gastritis in 3.3%, fundus polyp in 3.3%, hyperplastic polyp in 6.7% and chronic gastritis in 43.3%. The rates in the control group were determined as 14.7% for intestinal metaplasia, 2.9% for oedema-congestion, 20.6% for inflammation, 59.1% for the presence of HP, 2.9% for fundus polyp, 2.9% for hyperplastic polyp and 41.2% for chronic gastritis, respectively. Inflammation was significantly higher in the CKD group than in the control group. However, although this rate in dialysis patients is reported to be as high as 75.5% in the literature, the frequency of chronic gastritis that we found to be higher in the CKD group in our study did not reach statistical significance.⁷

HP was more common in the control group than in the CKD group (59.1% vs 23.5%). While the prevalence of HP is 24–32% in the general population, it was found to be 28.3% in dialysis patients.^7,12 Chronic gastritis was 41.2% in the non-uremic patient group with high HP and 43.3% in the CKD group. In a previous study on hemodialysis patients, the prevalence of H. pylori infection decreased as dialysis periods progressed within the first 4-year follow-up after the start of HD.¹⁴ Possible protective mechanisms include antibiotic use or antiacid drugs causing hypochlorhydria, which could contribute to the decreased frequency of HP. Our study's HP prevalence was 23.5%, less than in the non-CKD population. Also, uremia has a deteriorating effect on glycolipids and external membrane proteins resistant to the external environment, including the lipopolysaccharide cell wall structure of HP colonising in the gastric mucosa. Our patients with CKD had a higher rate of chronic gastritis despite a lower HP rate, but we did not detect a relationship between HP and chronic gastritis. In multivariate regression analysis, only the presence of gastritis and serum calcium level were associated with HP positivity.

The rates of esophagitis (13.2%) and duodenitis (18.9%) in chronic dialysis patients in our previous study were close to the rates in the current study (13.3%).⁷ In the non-uremic patient group, the rate of esophagitis was higher (53.7%). In studies conducted in HD patients, gastroesophageal reflux was found to be 10%, 15% in our patients and 6% in the control group^5,9–10, while pangastritis was high in HD patients (57.3%), this rate was lower in our patients (13.3%). Pangastritis is very common in HD patients. While antral erosive gastritis was 27.8% in HD patients, this rate was lower at 6.7% in our non-dialysis CKD patients. Antral gastritis, erythematous gastritis, erosive pangastritis, active chronic gastritis and inflammation were significantly higher in our patients with non-dialysis CKD than in the control group. Many drugs used for complications such as high serum urea level, inflammation, stress, mineral bone disorder, anaemia, and hypertension in patients with CKD may be effective in this condition, together with uremic toxins.^13,15

A recent study found that gastrointestinal symptoms and signs were common in CKD. Some symptoms and diseases also varied according to whether the renal replacement was peritoneal or hemodialysis type. The prevalence of esophagitis and gastritis diagnosed by symptomatic evaluation varied depending on the type of dialysis and whether it occurred in the pre-dialysis period. Although our study differs from this one in that it includes endoscopic diagnostic classification of symptomatic pre-dialysis patients compared to non-uremic patients, the significant difference in the frequency of esophagitis and gastritis histologic subtypes between the groups is compatible with the above study.¹⁶

In our study, no statistically significant independent relationships were detected between haemoglobin, urea and total cholesterol and the presence of duodenitis, chronic gastritis and HP in multivariate logistic regression analysis. Our previous study on our dialysis patients showed the independent effect of HP and total cholesterol.⁷

In uremic patients, risk factors like urea-related toxins, impairment of local and systemic circulations and hypergastrinemia cause damage to the gastric mucosa. In addition, in chronic uremic patients’ cardiovascular damage, anaemia and mineral bone disease are frequently seen. These complications and the medication that is entailed by these complications adversely affect the upper gastrointestinal system. In the normal population, chronic gastritis, inflammation, and gastric and duodenal ulcers are seen frequently. These diseases generally cause symptoms such as vomiting, anorexia, abdominal pain, heartburn and bleeding. Although most chronic uremic patients have these lesions, they remain asymptomatic.

Even though most chronic uremic patients have these lesions since they remain asymptomatic so, their diagnosis and treatment are often delayed; for this reason, the lesions that arise in the gastrointestinal system among the pre-dialysis uremic patients should be treated early, bearing in mind that they are potential candidates for kidney transplantation. Side effects of the drugs used, especially in uremic patients, on the gastrointestinal system should be minimised.

Author Contribution

M.U. and AE. designed the study and drafted the article. M.Ö. made endoscopic procedures. N.O.Ş and O.B.K. obtained the patients' data and documented it. H.O analysed the data. A.E. reviewed the article and made critical revisions, contributions and comments for important intellectual content. All authors gave final approval for the version to be submitted.

Conflict of Interest Statement

None declared.

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No competing interests reported.

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Gastrointestinal system endoscopy and pathological findings in non-dialysis chronic kidney disease: A single-centre study

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