gastrins and Kidney-Failure--Chronic

Today, calcitonin assay is used for the diagnosis of thyroid medullary cancer in the context of nodular thyroid disease. Calcitonin is an excellent marker of thyroid medullary cancer but some hypercalcitoninemia can also be related to other diseases, such as renal failure, endocrine tumors other than thyroid medullary cancer and sometimes to C cell hyperplasia, which is a not well-defined situation. Recent studies contributed to define calcitoninemia thresholds, which guide decision and avoid excessive invasive treatment.. After a brief reminder of physiological role of calcitonin and assays, the difficulties encountered in interpreting hypercalcitoninemia and its potential causes other than thyroid medullary cancer are addressed. Recent studies, on large series, now allow a better knowledge of specificity and sensitivity of calcitonin measurement in patients with nodular thyroid disease and a well-argued management.. In the future, calcitonin dosage will be ordered even more frequently, as some authors recommend it for the diagnosis of thyroid nodule. It is up to us to know how to use this remarkable marker, by considering all possible situations of benign hypercalcitoninemia and reserving aggressive treatments for patients who really need them.

Topics: Adult; Biomarkers; Calcitonin; Carcinoma, Medullary; Diagnosis, Differential; Endocrine Gland Neoplasms; Gastrins; Humans; Hypercalcemia; Hyperplasia; Kidney Failure, Chronic; Sensitivity and Specificity; Sepsis; Thyroid Diseases; Thyroid Gland; Thyroid Neoplasms; Thyroid Nodule

Topics: Anemia; Anti-Bacterial Agents; Anti-Ulcer Agents; Comorbidity; Disease Susceptibility; Drug Therapy, Combination; Duodenal Diseases; Duodenal Ulcer; Enzyme Inhibitors; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Malabsorption Syndromes; Prevalence; Proton Pump Inhibitors; Renal Dialysis; Stomach Diseases; Stomach Ulcer; Urea

On the basis of the existing experimental and clinical studies about the factors affecting the appearance of hypergastrinemia in renal failure, it can be concluded that the kidney plays an important, but not the only, role in the degradation of endogenous gastrin in humans. In this process the key role is played by the blood flow through the kidney, the preservation of the peritubular capillary system, and the functional kidney mass. Glomerular filtration has no particular importance in the extraction of gastrin from the circulation, while through the urine only a small amount of gastrin is excreted. In the decomposition of a part or at least some molecular gastrin forms, an important role is played by the capillary systems of extra-renal tissue. One further conclusion is that hypergastrinemia in patients with renal failure is the result of the combined effects of the reduced catabolism of gastrin in the kidney and its increased synthesis which is for the most part connected with hypochlohydria and secondary hyperparathyroidism. In patients with renal failure there exists the inhibition of the gastrin acid secretion which is the cause of the weakening of the mechanism of the feedback connection between HCl and gastrin, while because of a permanent stimulation of G-cells, the hyperplasia of these cells develops, as well as the increased secretory activity, and hypergastrinemia. Parietal cells become less sensitive to a permanently increased serum gastrin concentration but still capable of reacting to the maximal stimulus. In patients with renal failure, especially those with extreme hypergastrinemia, there develops the increased concentration of large, mainly biologically inactive (big big gastrin, component I) molecular forms of gastrin.

Topics: Animals; Gastric Acid; Gastrins; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic

Topics: Acute Kidney Injury; Duodenal Ulcer; Gastrinoma; Gastrins; Humans; Kidney Failure, Chronic; Pancreatic Neoplasms; Pyloric Antrum; Zollinger-Ellison Syndrome

Topics: Acute Kidney Injury; Bile; Digestive System Diseases; Gastrins; Gastritis; Humans; Kidney; Kidney Failure, Chronic; Peptic Ulcer

Topics: Bombesin; Calcium; Eating; Gastric Emptying; Gastrins; Gastrointestinal Hormones; Histamine H2 Antagonists; Humans; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Stenosis; Secretin; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastrins; Gastrointestinal Hormones; Humans; Intestine, Small; Kidney Failure, Chronic; Liver Cirrhosis; Malabsorption Syndromes; Peptic Ulcer; Postoperative Complications; Short Bowel Syndrome

Much epidemiological, clinical, and pathophysiological evidence has accumulated to indicate that the aetiology of duodenal ulcer is heterogeneous (Table 8). Recent advances in the medical therapy of duodenal ulcer support the long held concept that hyperacidity is an important physiological abnormality in the majority of patients with duodenal ulcer. It can also be shown that the origin of hyperacidity is heterogeneous. Certain specific physiological abnormalities that lead to hyperacidity may have a genetic basis. The various physiological abnormalities, alone or in combination, may lead to two final common pathways: abnormally large meal-stimulated acid secretion, and nocturnal acid hypersecretion. Indeed, success of medical therapy aiming at the control of postprandial acid secretion or of nocturnal acid secretion strongly supports their significance. It is possible that hyperacidity occurs as a temporary phenomenon and is associated with stressful life events. However, it is also possible that it occurs as a constant abnormality, bestowed perhaps genetically on the duodenal ulcer patient. In the presence of hyperacidity, mucosal repair may be affected adversely. In either situation, an acute ulcer, such as that associated with stress, is allowed to develop into a full-blown ulcer. Healing takes place if the hyperacidity recedes or is reduced therapeutically, allowing normal mucosal repair to take place.

Topics: Age Factors; Analgesics; Cell Count; Duodenal Ulcer; Eating; Gastric Acid; Gastrins; HLA Antigens; Humans; Intestinal Mucosa; Kidney Failure, Chronic; Lung Diseases; Parietal Cells, Gastric; Sleep; Smoking; Stress, Psychological

The past 20 years have seen gastrin attain true hormonal status. Its structure has been characterized, it has been synthesized, radioimmunoassays for its measurement in blood and tissues have been developed and its physiology and metabolism elucidated. Of much interest to clinicians has been the association between gastrin and tumours of the pancreas (gastrinomas) and atrophic gastritis. The advent of gastrin measurement has facilitated the diagnosis of gastrinoma and the availability of powerful acid suppressants has altered the therapy of gastrinoma.

Topics: Duodenal Ulcer; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Acute Kidney Injury; Animals; Dogs; Gastric Mucosa; Gastrins; Graft Rejection; Humans; Insulin; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Metabolic Clearance Rate; Proteinuria; Rats; Zollinger-Ellison Syndrome

Topics: Aldosterone; Angiotensin II; Calcium; Gastrins; Growth Hormone; Humans; Kidney Failure, Chronic; Parathyroid Hormone; Renin; Testosterone; Thyroid Gland; Vitamin D

Topics: Digestion; Esophageal Achalasia; Esophagitis, Peptic; Gastric Inhibitory Polypeptide; Gastric Mucosa; Gastrins; Gastritis; Glucagon; Humans; Ileum; Islets of Langerhans; Jejunum; Kidney Failure, Chronic; Liver; Protein Hydrolysates; Pyloric Antrum; Somatostatin; Vagotomy; Vasoactive Intestinal Peptide; Zollinger-Ellison Syndrome

Topics: Adult; Animals; Bone and Bones; Calcitonin; Calcium; Gastrins; Humans; Kidney; Kidney Failure, Chronic; Liver; Middle Aged; Phosphorus; Renal Dialysis

Topics: Anemia, Pernicious; Calcium; Dietary Proteins; Duodenal Ulcer; Gastric Juice; Gastrins; Gastritis; Glucagon; Humans; Hyperplasia; Intestine, Small; Kidney Failure, Chronic; Pyloric Antrum; Pyloric Stenosis; Secretin; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Acute Kidney Injury; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Kidney; Kidney Diseases; Kidney Failure, Chronic; Renal Dialysis; Uremia

There is evidence that under various physiological circumstances long-term adaptation of structure and function of the gut occurs. The mechanisms of these changes are not clear but gastro-intestinal hormones may be involved. In particular, gastrin which has been shown experimentally to stimulate growth and development of parts of the gut, probably has a role in maintaining the structure of the normal upper alimentary tract. Cholecystokinin may be of major importance in producing adaptive changes in the pancreas in response to dietary modifications and enteroglucagon is possibly concerned with maintaining a normal small intestinal structure. The importance of the 'trophic' action of gatrointestinal hormones is becoming more widely recognised and as new gastro-intestinal hormones become established, this aspect of their physiological importance as well as their acute effects, will deserve attention.

Topics: Animals; Cholecystokinin; DNA; Duodenum; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Intestinal Diseases; Intestine, Small; Kidney Failure, Chronic; Lactation; Pancreas; Pregnancy; Rats; Secretin; Starvation; Weaning; Zollinger-Ellison Syndrome

Topics: Animals; Cats; Chronic Disease; Creatinine; Dogs; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Antrum; Rats; Scleroderma, Localized; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

The study aimed to assess the influence of long-term rhu-EPO treatment on secretion of pancreatic polypeptide (PP) and gastrin. A total of 27 haemodialysed patients and nine healthy subjects were examined. Nine patients with uraemic anaemia were treated with rhu-EPO for 12 months (EPO group), while another nine patients did not receive rhu-EPO (non-EPO group), but were monitored biochemically and clinically as patients of the EPO group. The third group (HD) comparised nine haemodialysed patients with a haematocrit value > or = 30% without rhu-EPO therapy. In all subjects plasma levels of PP and gastrin were estimated before and after administration of a test meal. Patients of the EPO and non-EPO group were examined before and after 6 and 12 months of rhu-EPO therapy (EPO group) or clinical monitoring (non-EPO group) respectively, while only one test was performed in patients of the HD group and healthy subjects. Six months rhu-EPO therapy was followed by an decrease of basal plasma level of PP and increased response of gastrin to the test meal. After 12 months of rhu-EPO therapy basal plasma level of PP was still lower, the response of PP secretion to a test meal was higher, while that of gastrin secretion lower that the pretreatment ones. Our results suggest, that rhu-EPO treatment exerts effect on secretion of PP and gastrin. These alterations seem not to be related to improvement of the haematological status.

Topics: Adult; Erythropoietin; Gastrins; Humans; Kidney Failure, Chronic; Middle Aged; Pancreatic Polypeptide; Recombinant Proteins; Renal Dialysis

The aim of this study was to determine serum gastrin levels and gastroduodenal lesions in children with chronic renal failure (CRF) on continuous ambulatory peritoneal dialysis (CAPD).. A total of 19 patients (mean age: 11.7±3.9 years, M/F: 1.37) with CRF on CAPD and 20 age-matched and sex-matched patients (mean age: 10.2±1.4 years, M/F: 1.5) with peptic ulcers were included in the study. Serum gastrin, creatinine, phosphate, and parathormone levels were determined. Upper gastrointestinal endoscopy was performed in all patients.. The basal gastrin concentrations of CAPD patients were significantly higher than those of patients with peptic ulcer disease without CRF (124.2±59.1 and 53.0±9.4 pg/ml, respectively) (P<0.001). A significant correlation was found between age, duration of uremia, and serum gastrin levels (r=0.59, P<0.01; r=0.60, P<0.01, respectively). No correlation was found between the duration of CAPD and serum gastrin levels in the patient group. Of the patients, 73.6% had abnormal upper gastrointestinal endoscopic findings. The gastroduodenal lesion observed was hemorrhagic gastritis (31.5%), followed by hemorrhagic gastroduodenitis (26.3%), gastric nodular gastritis (10.5%), and polyps (10.5%).. On the basis of our findings, such as higher serum gastrin levels in patients with CRF than those of the control group and the frequent endoscopic findings of gastroduodenal lesions in most of the patients, we recommend that an endoscopic examination should be considered for all the children with CRF on CAPD awaiting renal transplantation even if they are asymptomatic.

Topics: Adolescent; Case-Control Studies; Child; Child, Preschool; Creatinine; Duodenitis; Endoscopy, Gastrointestinal; Female; Gastrins; Gastritis; Humans; Incidence; Intestinal Polyps; Kidney Failure, Chronic; Male; Parathyroid Hormone; Peritoneal Dialysis, Continuous Ambulatory; Phosphates

Our aim was to determine the frequency of peptic ulcer and Helicobacter pylori infection by gastrointestinal evaluations in pretransplantation phase in children with end-stage renal disease (ESRD).. Twenty-four children with ESRD (13 girls and 11 boys) with a mean age of 14.7 +/- 3.4 years on maintenance hemodialysis were included in this study. Upper gastrointestinal endoscopies were performed and 4 gastric, antral, and duodenal biopsy specimens were obtained for urease test and histological study. Serum gastrin levels were measured in all patients, too. A control group was chosen to compare the rate of H pylori infection between children with ESRD and healthy children.. Gastrointestinal symptoms were present in 16 (66.7%) of 24 patients. Seventeen (70.8%) patients had abnormal upper gastrointestinal endoscopic findings. Infection with Helicobacter pylori was detected in 16 patients and 5 healthy children (66.7% versus 20.0%, P < .001). The frequency of dyspeptic symptoms was not different significantly between uremic patients with and without H pylori infection (P = .67). The same results were found regarding the upper gastrointestinal abnormalities found by endoscopy (P = .65). Oral alkalizing supplement was received by 63% of symptomatic and 80% of asymptomatic patients. Serum gastrin levels were significantly higher in infected patients than in noninfected patients with H pylori (P < .001).. We found a significant number of patients with peptic ulcer diseases, H pylori infection, and secondary hypergastrinemia. This study showed that clinical symptoms are not a reliable predictor of gastrointestinal problems and this is more confusing in patients who received alkalizing solutions.

Topics: Adolescent; Biopsy; Case-Control Studies; Child; Dyspepsia; Endoscopy, Gastrointestinal; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Male; Peptic Ulcer; Renal Dialysis; Young Adult

Topics: Carcinoid Tumor; Female; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Remission Induction; Stomach; Stomach Neoplasms

The incidence of gastroduodenal diseases is high in patients with chronic renal failure (CRF). However, gastric acidity in CRF has been reported to range in level from low to high. Moreover, it remains unknown whether Helicobacter pylori infection influences gastric acidity in such patients. Thus, we aimed to clarify the pathophysiological perturbation in gastric acidity and to determine the influence of H. pylori infection in CRF.. Case-control study.. A university hospital.. Twenty-seven patients with CRF and 24 control patients, presenting with either gastrointestinal symptoms, positive faecal occult blood, or anaemia (haemoglobin <10 g dL(-1)).. The patients underwent gastroduodenal endoscopy with simultaneous determination of H. pylori infection. Gastric ammonium concentration, serum pepsinogen I and II, and basal gastrin level were measured. Thereafter, gastric acid secretion was monitored by 24-h intragastric acidity measurement with calculation of pH-3 holding time (%) (hours showing pH>3/24 h).. In the CRF group, pH-3 holding time of H. pylori (+) subgroup was significantly greater than that of H. pylori (-) subgroup (71.2 +/- 32.4% vs. 32.8 +/- 30.0%, mean +/- SD; P=0.03). Pepsinogen I/II ratio was inversely correlated with pH-3 holding time in the control and CRF groups. Gastric ammonium concentration in CRF/H. pylori (+) subgroup (14.1 +/- 9.2 mmol L(-1)) was significantly higher than in CRF/H. pylori (-) (2.5 +/- 2.7 mmol L(-1); P=0.002) and control/H. pylori (+) subgroups (6.1 +/- 4.2 mmol L(-1); P=0.01). Serum gastrin level was significantly higher in the CRF group than in the control group (297 +/-343 pg mL(-1) vs. 116 +/- 69 pg mL(-1); P=0.02) as a whole. However, there was no significant correlation between serum creatinine and gastrin levels in the CRF group. Gastrin level in CRF/H. pylori (+) subgroup was significantly higher than in CRF/H. pylori (-), control/H. pylori (+), and control/H. pylori (-) subgroups (423 +/-398 pg mL(-1) vs. 113 +/- 79, 124 +/- 78, and 96 +/-43 pg mL(-1), respectively; P=0.01-0.03). Significant positive correlations amongst pH-3 holding time, ammonium and gastrin concentrations were found in the CRF group, but not in the control group.. CRF without H. pylori infection primarily shows a tendency for high gastric acidity, but without hypergastrinaemia. Persistent H. pylori infection in CRF leads to decreased acidity and, consequently, to fasting hypergastrinaemia via a feedback mechanism. The hypoacidity in CRF with H. pylori infection appears to result from neutralization of acid by ammonia as well as from gastric atrophy. Thus, H. pylori infection status critically determines perturbation in gastric acidity and fasting gastrin level in CRF.

Topics: Adult; Aged; Case-Control Studies; Fasting; Female; Gastric Acid; Gastric Acidity Determination; Gastric Juice; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Quaternary Ammonium Compounds

Helicobacter pylori (H. pylori) infection in patients with chronic renal failure plays an important role in the pathogenesis of upper gastrointestinal tract diseases. In our earlier study we did not find significant relationship between parathormone (PTH) concentration abnormalities and H. pylori infection in hemodialysis patients (HD pts). The aim of our present study was to examine other parameters and interrelationships between them, connected with H. pylori infection in HD pts. The serum concentration of the following substances were measured: gastrin (G), parathormone (PTH), and IgG antibodies against H. pylori. The study was conducted in 65 (36 M, 29 F) stable HD pts: age 49 +/- 12 years, dialysed from 6 to 288 months. The control group (CG) consisted of 15 healthy people, mean age 38 +/- 8 years. The mean concentration of serum PTH serum was significantly higher in HD pts than in CG (538 +/- 520 vs 35 +/- 9.3 pg/ml, p < 0.001). The mean concentration of gastrin in serum was significantly higher in HD pts than in CG (155.37 +/- 235.4 vs 87.97 +/- 9.5 pg/ml, p < 0.01). The mean concentrations of IgG antibodies against IgG H. pylori was similar in HD pts and CG (88.1 +/- 80.0 vs 91.34 +/- 66.8 U/ml). We found significant positive correlation between IgG antibodies against H. pylori infection and gastrin level in serum of HD pts (r = 0.315, p < 0.001). We did not find significant correlation between concentrations: PTH vs G and PTH vs IgG against H. pylori.. Helicobacter pylori infection contributes to hypergastrinaemia in hemodialysed patients. There is no relationships between PTH abnormalities and H. pylori infection.

Topics: Adult; Case-Control Studies; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Immunoglobulin G; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis; Risk Factors

The association between gastroesophageal reflux disease and end-stage renal disease remains unclear. We aimed to assess the prevalence of gastroesophageal reflux disease and also to identify possible pathogenetic factors in the development of reflux in symptomatic end-stage renal disease patients.. The study involved 42 end-stage renal disease patients with upper GI symptoms (group I) and 46 age- and sex-matched controls who did not have renal disease but had the same symptoms (group II). Endoscopy, endoscopic biopsies, and 24-h esophageal pH studies were used to diagnose gastroesophageal reflux disease. Subjects were also investigated for Helicobacter pylori gastritis and GI amyloidosis.. The prevalences of gastroesophageal reflux disease in the two groups were similar (81% vs 84.8%, p = 0.423). The prevalence of H. pylori infection was significantly lower in group I than in group II (38.1% vs 67.4%, p = 0.01). There were II cases of GI amyloidosis in group I. Multivariate logistic regression analysis in group I showed that GI amyloidosis (OR = 7.28, 95% CI = 1.13-46.93), chronic ambulatory peritoneal dialysis treatment (OR = 5.54, 95% CI = 1.01-30.43), and absence of H. pylori infection (OR = 3.75, 95% CI = 1.01-13.9) were significantly associated with reflux esophagitis.. Upper GI symptoms are important in predicting gastroesophageal reflux disease in end-stage renal disease patients. Chronic ambulatory peritoneal dialysis, GI amyloidosis, and absence of H. pylori infection seem to be risk factors for the development of gastroesophageal reflux disease in end-stage renal disease patients.

Topics: Adult; Amyloidosis; Esophagitis; Esophagus; Female; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Diseases; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Middle Aged; Monitoring, Physiologic; Multivariate Analysis; Prevalence; Risk Factors

Helicobacter pylori infection is associated with increased gastrin release in patients with normal renal function. Hypergastrinaemia is a common finding in haemodialysis patients and, in many cases, may be linked to H. pylori infection. The aim of this study was to examine the effect of H. pylori infection, and its eradication, on elevated gastrin levels in haemodialysis patients.. Eighty-nine dyspeptic patients were included in the study. While 44 patients had normal renal function, the remaining 45 were end-stage renal failure patients. Patients were assigned to one of four groups according to their H. pylori and renal function status. Infected patients were re-evaluated after 2 months following eradication treatment. Serum gastrin levels were measured in these groups both before and after eradication treatment.. Haemodialysis patients with H. pylori infection had higher serum gastrin levels than did H. pylori negative haemodialysis patients (321+/-131 pg/ml vs 154+/-25 pg/ml) (P<0.05). Mean serum gastrin concentration was 152+/-21 pg/ml in the non-uraemic H. pylori-positive group. This value was 58+/-17 pg/ml in the non-uraemic H. pylori-negative group (P<0.05). There were significant decreases in serum gastrin levels from pre- to post-eradication of H. pylori in the infected haemodialysis and non-uraemic patient groups (312+/-131 pg/ml to 179+/-85 pg/ml and 152+/-21 pg/ml to 72+/-2.4 pg/ml respectively, P<0.05). Four patients in group Ib and 5 patients in group IIb who had persistent infection did not have a decrease in serum gastrin level. All patients with successful eradication had a decrease in serum gastrin concentration.. Our findings suggest that H. pylori infection contributes to hypergastrinaemia in haemodialysis patients. More research is needed regarding the clinical consequences of hypergastrinaemia in these individuals.

Topics: Adult; Anti-Bacterial Agents; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Male; Renal Dialysis

In order to explore the role of Helicobacter pylori (H. pylori) infection in hypergastrinemia in patients on dialysis, the changes in serum gastrin concentration were examined before and after eradication treatment for H. pylori. Twenty-seven patients on dialysis were treated for the eradication of H. pylori. Fasting serum gastrin concentrations were measured by a radioimmunoassay which detects gastrin 17. Ammonia and pH levels of the gastric juice were also measured. The serum gastrin concentrations were significantly decreased following eradication of H. pylori, and the mean value reached the normal range. The restoration of hypergastrinemia was associated with marked reductions of gastric juice ammonia and pH levels. In contrast, patients in whom H. pylori was not eradicated showed no changes in these parameters. In conclusion, the elevation of the fasting serum gastrin 17 concentration seen in dialysis patients appeared to be attributable to H. pylori infection in the stomach.

Topics: Ammonia; Anti-Bacterial Agents; Anti-Ulcer Agents; Drug Therapy, Combination; Female; Gastric Juice; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Metronidazole; Middle Aged; Peptic Ulcer; Renal Dialysis

To determine the prevalence of hypergastrinemia in cats with naturally developing chronic renal failure (CRF) and the correlation between gastrin concentration in plasma and severity of CRF.. Cohort study.. 30 cats with naturally developing CRF and 12 clinically normal control cats.. Gastrin concentrations in plasma were determined by double-antibody radioimmunoassay of blood samples obtained from cats after food was withheld 8 hours. Concentrations were compared, using a nonparametric Kruskal-Wallis ANOVA.. 18 cats with CRF had high gastrin concentrations (median, 45 pg/ml; range, < 18 to > 1,333 pg/ml), compared with those for control cats (< 18 pg/ml). Prevalence of hypergastrinemia increased with severity of renal insufficiency. Three of 9 cats with mild CRF, 6 of 11 cats with moderate CRF, and 9 of 10 cats with severe CRF had high gastrin concentrations. Gastrin concentrations were significantly different between control cats and cats with CRF, regardless of disease severity.. The potential role of high concentrations of gastrin on gastric hyperacidity, uremic gastritis, bleeding from the gastrointestinal tract, and associated clinical signs of hypergastrinemia (e.g., anorexia and vomiting) may justify use of histamine2-receptor antagonists or proton pump inhibitors to suppress gastric acid secretion in cats with CRF that have these clinical signs.

Topics: Animals; Cat Diseases; Cats; Cohort Studies; Female; Gastrins; Kidney Failure, Chronic; Male; Prevalence; Prospective Studies; Radioimmunoassay; Severity of Illness Index

From March 1992 to July 1992, 30 uremic patients (15 dialysed, 15 non-dialysed) and 15 non-uremic patients who had dyspeptic complaints were compared in terms of gastric and duodenal diseases. Gastritis and duodenitis graded as I, II and III were not found different in three groups (p > 0.05). Although the incidence of peptic ulcer disease is very high in both groups of uremic patients in comparison with the controls, there was no significant difference between two uremic groups (p > 0.05). Also the prevalence of gastritis determined histologically was not different in dialysed and non-dialysed uremic patients (p > 0.05). The incidence of the histologically proven gastritis was found higher in uremic patients than in non-uremic patients (p < 0.05). But, there were no significant differences among the three groups with regard to the rate of histologically proved duodenitis (p > 0.05). Gastrin levels, urea positivity, the incidence of gastritis and duodenitis and peptic ulcers did not differ in both uremic groups. However, these values were found significantly high in the uremic patients when compared to non-uremics. These findings showed serum gastrin levels, H.-pylori-infection, gastritis and duodenal disease in the uremic patients to be higher than those of the control group. Moreover, no effect of hemodialysis treatment on these results was observed.

Topics: Adult; Aged; Aged, 80 and over; Endoscopy, Digestive System; Female; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Humans; Incidence; Intestinal Mucosa; Kidney Failure, Chronic; Male; Middle Aged; Prevalence; Renal Dialysis; Retrospective Studies; Uremia

Gastrin circulates at higher than normal concentrations in patients with end-stage renal failure (ESRF). However, it remains unclear which forms of gastrin are elevated and whether there is also an alteration in the secretory profile after stimulation. In the present study all processed and partially processed forms of circulating gastrin were measured in plasma before and after meal stimulation in ESRF patients and control subjects. Since Helicobacter pylori (HP) infection affects gastrin secretion, HP status was determined. Fasting gastrin-amide (36 +/- 8 pmol/L), gastrin-Gly (55 +/- 16 pmol/L), and total gastrin (218 +/- 32 pmol/L) measured in ESRF/HP-patients were all significantly greater than those in the control group (10 +/- 1, 15 +/- 3, and 17 +/- 2 pmol/L, respectively; P < 0.01). Plasma gastrin-amide (126 +/- 67 pmol/L) and total gastrin (397 +/- 164 pmol/L) were highest in the ESRF/HP+ patients. The proportion of nonamidated gastrin products was 4-fold higher in ESRF patients than in control subjects, suggesting structure-specific changes in gastrin secretion and metabolism, and this was confirmed by chromatography. The meal-stimulated increments in control/HP- and ESRF/HP-groups were similar. However, the ESRF/HP+ group had a markedly potentiated gastrin response. Fasting plasma somatostatin, an inhibitor of gastrin secretion, was also measured and was significantly lower in the ESRF patients than that in the control group. These studies show that the hypergastrinemia associated with renal failure has been underestimated. This is because only amidated products were measured. The potentiated gastrin meal response in ESRF attributed previously to changes in gastrin metabolism are in part explained by the effect of HP infection. The observed diminished somatostatin response suggests that the increase in circulating gastrin in ESRF is the result of loss of inhibition of secretion as well as decreased metabolism. As both amidated and nonamidated gastrin are now considered to have trophic and secretory effects, these findings may explain the gastrointestinal tract hypertrophy often associated with ESRF.

Topics: Adult; Aged; Antibodies, Bacterial; Fasting; Food; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Middle Aged

It has been shown previously that antisecretory response of famotidine is altered in patients with renal failure. To evaluate the underlying mechanism(s) of this clinical observation we obtained biopsy specimens of fundic mucosa from 3 groups of patients with variable renal function (group 1 normal renal function (n = 16); group 2 chronic renal failure (n = 16), CLCR > or = 5 < 90 ml/min; group 3 hemodialysis therapy (n = 16)) (matched for age, sex, and Helicobacter pylori (Hp) status. In the homogenized samples adenylate cyclase (AC) activity was assessed and the influence of uremia on this second messenger system involved in gastric acid secretion was tested. AC activity was measured as the formation of cAMP, which was determined by RIA. The mean basal AC activity was 150 in group 1, 190 in group 2, and 120 pmol cAMP/mg protein/20 min in group 3. There was a dose-dependent stimulation by histamine (1 microM-1 mM). Emax of cAMP formation ranged between 230 and 403 pmol cAMP/mg protein/20 min and EC50 between 5.9 and 20.1 microM histamine, dependent on Hp status. Histamine-stimulated AC activation was reduced to about 50% by 0.1 mM famotidine. The sensitivity of AC to histamine seems to decrease in patients undergoing hemodialysis. Similarly, the colonization with Hp may result in decreased maximal response of the AC system towards histamine.

Topics: Adenylyl Cyclases; Anti-Ulcer Agents; Cyclic AMP; Famotidine; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Male; Middle Aged; Sodium Fluoride; Uremia

1. Roxatidine acetate, a new histamine H2-receptor antagonist, was administered in the evening (75 mg p.o.) to eight patients with renal insufficiency (CLCR 8-17 ml min-1) for 12 days and plasma drug concentrations were measured. 2. Ambulatory intragastric pH was monitored following the last dose and values were compared with those on day 1 when all patients received a placebo. 3. The terminal elimination half-life (mean +/- s.d.) of roxatidine was 10.8 +/- 2.4 h and its oral clearance was 178 +/- 43 ml min-1. 4. During roxatidine treatment gastrin levels increased slightly (median 189 vs 289 ng l-1) and the hyperparathyroid status of the patients was almost normalized (parathyroid hormone levels: median 199 vs 132 ng l-1). 5. The mean latency to a gastric pH of at least 4 was 4.3 +/- 1.4 h. The duration of action (intragastric pH > 4) was 10.6 +/- 3.9 h. 6. As in a pilot study with six patients (CLCR < or = 17 ml min-1) the recommended dosage regimen (75 mg 48 h-1) was unable to maintain gastric pH > 4 for more than 6 h, daily nocturnal intake of 75 mg roxatidine acetate appears appropriate to elevate gastric pH > 4 for a sufficient period of time.

Topics: Adult; Drug Administration Schedule; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Histamine H2 Antagonists; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Piperidines

Hypercalcitoninemia has been reported in renal failure. Using a specific monomeric calcitonin (CT) immunoassay, we measured CT levels in 154 hemodialyzed patients. The relationship between CT and serum intact parathyroid hormone (PTH), gastrin, alkaline phosphatases, phosphate and calcium was studied. The pentagastrin test was performed in 26 patients exhibiting basal hypercalcitoninemia. Basal CT levels over 5.7 pmol/l (20 ng/l) were found in 25.3% of the patients and values higher than 26 pmol/l (90 ng/l) in 7.8%. Although CT is cleared by hemodialysis, post-dialysis CT levels either were unchanged or increased as compared with pre-dialysis values. This suggests that hypercalcitoninemia is not related to a decreased renal clearance, and that hemodialysis induces a specific regulatory pathway. None of the parameters studied were found to explain high CT levels. Of the patients with hypercalcitoninemia, 11.5% exhibited abnormal CT response to pentagastrin but no relationship between CT and phosphate, calcium and PTH levels was evidenced. Our findings confirm high CT monomer levels in renal failure. As there was no correlation with parameters classically involved in CT regulation, its physiological significance remains unclear. Abnormal CT response to pentagastrin raises the problem of its specificity as a tumoral marker with regard to medullary thyroid carcinoma.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Calcitonin; Calcium; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Pentagastrin; Phosphates; Renal Dialysis

The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.

Topics: Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Peptic Ulcer; Peptic Ulcer Hemorrhage; Uremia

Topics: Carcinoid Tumor; Dyspepsia; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Ranitidine; Self Administration; Stomach Neoplasms

The prevalence of Helicobacter pylori (H. pylori) was investigated in 164 consecutive patients with different degrees of renal function; group I (normal renal function) n = 84, group II (chronic renal failure, CLCR > or = 5 < 90 ml/min) n = 45, group III (haemodialysis therapy) n = 35, to test the hypothesis that the resulting different concentrations of urea in the gastric juice would have an influence on the colonization of the gastric mucosa by these urea-splitting bacteria. As every individual method for the detection of H. pylori shows disadvantages, the results of the detection methods used (urease test, Warthin-Starry stain, bacterial cultivation, direct examination of the processed sample by phase-contrast microscopy) were combined in a cumulative evaluation. These calculated cumulative indices for the antrum and corpus showed no statistically significant differences between the studied groups. The prevalence of H. pylori ranged from 34 to 54%. The histopathological findings were similar in all groups. In spite of the fact that patients with renal dysfunction had significantly higher levels of serum gastrin (P < 0.05), there was no influence on the gastric juice pH value. The relationship between the cumulative index and ammonia concentration in gastric juice was found to be linear (P < 0.05). The higher urea levels in the blood and gastric juice of patients with renal failure do not seem to be a risk factor for infection with H. pylori.

Topics: Ammonia; Gastric Juice; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Stomach Ulcer

Thirty nine patients with end-stage renal disease on haemodialysis therapy with upper gastrointestinal symptoms were investigated for gallbladder motor function as the cause of their symptoms using cholecystosonography in fasting state, after a cholecystokinetic agent (BILOPTIN fatty meal) and after a smooth muscle relaxant (BUSCOPAN). Forty healthy individuals served as a control group. No significant difference was found between dialysis patients and healthy controls regarding the gallbladder area during fasting state, or the variation in the area of gallbladder during maximal contraction and dilatation. However, the patients on dialysis therapy of longer duration had stronger gallbladder contraction in response to a cholecystokinetic agent. Serum gastrin concentrations were increased in haemodialysis patients, but there was no consistent relationship between serum gastrin and gallbladder motility. The upper gastrointestinal symptoms of dialysis patients are unlikely to be due to disturbed gallbladder motility.

Topics: Adult; Aged; Female; Gallbladder; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Muscle Contraction; Renal Dialysis; Ultrasonography

We report our experience of gastrocystoplasty in 8 children (mean age 10.1 years) with compromised renal function (mean creatinine 186 mmol/l, mean glomerular filtration rate 39 ml/min/1.73 m2). Current follow-up ranges from 11 to 35 months (mean 21). The physiological outcome of the procedure has been excellent, with improved biochemical and urodynamic parameters in all cases. Six patients are off H2-receptor blockers and are asymptomatic. In 2 children we have encountered significant symptoms related to acid secretion in the bladder. Detailed investigations suggest that the excess aciduria is related to the size of the gastric patch in 1 patient. The second child underwent renal transplantation 5 months after gastrocystoplasty and it is postulated that his immunosuppressive regimen (which includes prednisolone) may be responsible for the increased acid secretion. It is concluded that gastrocystoplasty is a very satisfactory alternative to intestinal segment bladder enhancement in children with compromised renal function, but the size of the gastric patch is critical in determining the resultant acid secretion. Post-transplantation immunosuppressive therapy may increase acid production from the gastric patch; since the children most suitable for gastrocystoplasty are also those likley to require transplantation, this aspect requires further study.

Topics: Adolescent; Child; Child, Preschool; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Infant; Kidney Failure, Chronic; Male; Stomach; Urinary Bladder; Urodynamics

The fasting plasma levels of 9 gastrointestinal regulatory peptides were measured by radioimmunoassay in 13 stable patients with chronic renal failure receiving hemodialysis treatment regularly and compared with those of 10 healthy controls. The plasma concentrations of gastrin-releasing peptide, motilin, neurotensin, pancreatic polypeptide, peptide YY, somatostatin, substance P, and vasoactive intestinal peptide were increased. The plasma level of gastrin was not statistically different from that of the controls (p = 0.077). We conclude that patients with chronic renal failure receiving hemodialysis treatment regularly have increased concentrations of eight of nine measured gastrointestinal regulatory peptides. The elevated levels of gastrointestinal peptides in patients with chronic renal failure may contribute to uremic gastrointestinal symptoms and dysfunctions. It is necessary to make a renal function evaluation before interpreting measured plasma levels of gastrointestinal regulatory peptides.

Topics: Adult; Aged; Aged, 80 and over; Gastrin-Releasing Peptide; Gastrins; Gastrointestinal Hormones; Humans; Kidney Failure, Chronic; Middle Aged; Motilin; Neuropeptides; Neurotensin; Pancreatic Polypeptide; Peptide YY; Peptides; Radioimmunoassay; Renal Dialysis; Somatostatin; Substance P; Vasoactive Intestinal Peptide

We calculated morphometrically the amount of antral gastrin-producing (G) cells and body parietal and chief cells in gastric biopsy specimens from 30 undialysed patients with chronic renal failure (CRF) and from sex- and age-matched controls. The CRF patients had raised fasting serum gastrin levels, whereas these were normal in the controls (mean, 290 +/- 283 (+/- SD) ng/l (n = 27) versus 33 +/- 36 (n = 30)). Serum gastrin values of the patients and controls correlated positively with G-cell density (r = 0.501, n = 36, p = 0.002), as did the maximal acid output of the CRF patients with parietal cell density (r = 0.617, n = 14, p = 0.019). In CRF patients the densities of G, parietal, and chief cells were higher than those in the controls (G cells, 351 +/- 151 (+/- SD) cells/mm2, n = 21 versus 211 +/- 90, n = 16, p = 0.002; parietal cells, 299 +/- 94, n = 15 versus 224 +/- 72, n = 14, p = 0.025; chief cells, 886 +/- 346, n = 15 versus 743 +/- 182, n = 14, p = 0.181). The results agree with previous findings indicating that hyposecretion of gastric acid in CRF does not derive from decreased capacity for acid secretion but rather from the inhibition of acid output. Increased parietal cell density in CRF patients gives cause to suspect that the maximum acid output might even in raised, possibly depending on the permanent hypergastrinaemic state with its trophic influence on the gastric body mucosa.

Topics: Adult; Biopsy; Cell Count; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parietal Cells, Gastric

We studied histologically antral biopsies from 89 consecutive patients with chronic renal failure for Helicobacter pylori (previously Campylobacter pylori). A dose-response gastric secretion test was also performed. The frequency of Helicobacter-positive subjects was low (15/89, 17%), corresponding to figures reported in the literature for young symptomless volunteers. Helicobacter-positive patients had significantly more frequently upper gastrointestinal symptoms than Helicobacter-negative individuals (P less than 0.05). Antral gastritis was more common in the Helicobacter-positive than in the Helicobacter-negative renal patients (P less than 0.01), but the incidence of body gastritis did not differ between them. The Helicobacter-positive patients had lower serum urea levels (P less than 0.01) and higher acid outputs (P less than 0.001) than Helicobacter-negative subjects. All patients had raised fasting serum gastrin levels, which possibly obscured the difference between Helicobacter-positive (283 pg/ml) and -negative (331 pg/ml) patients. We conclude that in chronic renal failure gastric colonization of Helicobacter pylori is not more frequent than usual. It correlates positively with antral gastritis, gastric acid output and upper gastrointestinal symptoms, but negatively with serum urea levels.

Topics: Biopsy; Female; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Incidence; Kidney Failure, Chronic; Male; Middle Aged; Pyloric Antrum

The physiological release mechanism for gastrin is complex, including both mechanical and chemical stimuli. Distention of the antrum is the main mechanical stimulus, and proteins and their degradation products constitute the most potent chemical stimuli. The aim of the present study was to examine the little gastrin (G-17) response to a test meal and to study the relationship between the G-17 concentration and gastric acid secretion in patients with various degrees of chronic renal failure (CRF). In 14 CRF patients under conservative treatment and 12 healthy control subjects, fasting and stimulated G-17 concentrations, as well as basal (BAO), maximal (MAO) and peak acid secretion (PAO) were measured. Mean fasting serum G-17 in CRF patients was 7.8 +/- 0.8 pmol/L, significantly higher (p less than 0.001) than in control subjects (5.9 +/- 1 pmol/L). However, the range of basal G-17 concentrations in both groups of subjects was not different from the normal values (4.2 +/- 11.3 pmol/L). The serum G-17 response to the food stimulation was significantly higher (p less than 0.001) in the control subjects than in the CRF patients. In normal subjects, the increment in the serum G-17 concentration rose to a peak at 30 min, but in the CRF patients the peak increment occurred at 60 min, and the response was more prolonged. There was a little difference in meal-stimulated serum G-17 concentrations in patients with various degrees of renal functional impairment. Basal acid output (BAO) was significantly higher (p less than 0.001) in the control subjects (2.62 +/- 0.51 mmol/h) than in the CRF patients (1.68 +/- 0.4 mmol/h). No significant difference in both the maximal acid output (MAO) and peak acid output (PAO) was found between the groups of CRF patients and control subjects. There was no relationship between G-17 concentrations and the gastric acid output in the CRF patients. From the results of the present study it is concluded that the human kidney is unimportant in the catabolism of G-17 but that the renal failure seems to decrease the rate of the peripheral extraction of gastrin by other tissues. The raised basal and meal-stimulated G-17 concentrations sometimes seen in CRF patients are associated with decreased rather than increased gastric acid secretions.

Topics: Adult; Aged; Eating; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

Topics: Adult; Blood Glucose; Erythropoietin; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Insulin Secretion; Kidney Failure, Chronic; Middle Aged; Pancreatic Polypeptide; Renal Dialysis

The interrelations among fasting serum gastrin, serum creatinine, gastric acid secretion variables, and G-cell densities were analyzed in 47 patients with chronic renal failure (CRF). The patients also underwent gastroscopy and radiologic upper gastrointestinal barium examination. It is suggested that the hypergastrinemia seen in CRF is related to several factors: gastric acidity, grade of renal failure, G-cell density, and basal gastrin secretion rate. With regard to serum gastrin two different populations can be found, the cutting-off point being 300 ng/l. Although the group with high gastrin levels included significantly more patients with gastric body atrophy than the other group (4 of 11 versus of 1 of 36), most of them had no atrophy, which indicates that (an)other mechanism(s) is responsible for the hypergastrinemia. In the relation between serum gastrin and gastric acidity also, two differently behaving subgroups emerged. In the first, strong acidity change corresponded to minor gastrin change, whereas in the other, minor acidity change corresponded to marked gastrin change. The correlation coefficients between gastrin and acidity were high within both subgroups. During regular dialysis patients preserve the characteristics delineated from non-dialyzed values. Patients with signs of duodenal ulcer disease had high maximal acid output and low serum gastrin. Otherwise no associations were found between GI findings and the variables studied.

Topics: Cell Division; Creatinine; Gastric Acid; Gastrins; Gastroscopy; Humans; Kidney Failure, Chronic; Parietal Cells, Gastric

In 40 young patients with chronic renal failure (CRF) on maintenance hemodialysis and 22 control subjects, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Age-matched CRF patients with control subjects had higher circulating gastrin levels both in the fasting and the test meal-stimulated state and they also had hypochlorhydria. After a test meal, the peak increment of serum gastrin in the CRF patients was more prolonged and greater than in controls. Endoscopic findings showed that the most predominant lesion in the CRF patients was hemorrhagic gastritis. Nine (64.2%) out of 14 patients were hyposecretors and none were hypersecretors. Patients with hyposecretion had higher gastrin levels as well as the same incidence of abnormal endoscopic findings as patients with normosecretion. It is concluded that hypergastrinemia in young CRF patients might be due to a combined effect of impaired renal clearance capacity and overproduction of gastrin associated with hypochlorhydria and also that the cause of gastritis in the young CRF patients might partly be due to a relative impairment of the mucosal defensive mechanism to acid. Our data suggest that the parietal cell response to gastrin in CRF patient may be impaired.

Topics: Adult; Eating; Female; Gastric Juice; Gastrins; Gastritis; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Pentagastrin

Topics: Adult; Eating; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

In 15 undialyzed (UD) patients and 26 hemodialyzed (HD) patients, (1) basal and test meal-stimulated gastrin concentrations, (2) basal and pentagastrin-stimulated gastric acid outputs, and (3) endoscopic examinations were studied. Also studied were the morphological and functional differences of the gastrointestinal tract between UD and HD patients. HD patients had lower gastric acid outputs and higher circulating gastrin levels in the fasting state. After a test meal, the peak increment of serum gastrin in UD and HD patients occurred 30 and 60 min later, respectively, and the response was prolonged in each group. Endoscopic findings showed that the incidence of abnormalities in each group was very similar, that is, the most predominant lesions in each group were hemorrhagic and atrophic gastritis. The data suggested that the response to gastrin of parietal cell and the defensive mechanism of gastrointestinal mucosa in HD patients may be impaired.

Topics: Adult; Eating; Female; Gastric Juice; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Our previous secretin provocation studies in normal volunteers and unoperated duodenal ulcer patients suggested that the gastrin rise in gastrinoma may be an exaggeration of the normal response rather than paradoxical. We report further studies in various clinical settings having normogastrinemia (normal, n = 17; unoperated duodenal ulcer, n = 13; primary hyperparathyroidism, n = 7) and hypergastrinemia (postvagotomy, n = 5; hypochlorhydria, n = 7; achlorhydria, n = 10; chronic renal failure, n = 10; gastrinoma, n = 5). Under all nongastrinoma conditions, there were similar gastrin rises of 9-19% between 2 and 5 min after bolus intravenous GIH secretin (2 CU/kg), which fell to baseline by 8 min, except for chronic renal failure. In chronic renal failure, gastrin remained elevated from 7 to 30 min and was significantly different (p less than 0.05) at 10-30 min compared to all other nongastrinoma conditions except hyperparathyroidism. Peak rises occurred within 5 min in all entities, but only three gastrinoma patients had positive secretin provocation tests by the predefined criterion of a gastrin rise greater than 200 pg/ml. The results of secretin provocation in various clinical entities with and without hypergastrinemia further support the hypothesis that the gastrin rise in gastrinoma is an exaggeration of the normal response. The prolonged gastrin rise seen in chronic renal failure may be due to altered renal clearance, inasmuch as other hypergastrinemic states had responses similar to normal and duodenal ulcer.

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Male; Middle Aged; Secretin; Vagotomy

Gastrin releasing peptide(GRP)-like immunoreactivity in human plasma was measured using radioimmunoassay of neuromedin C (NMC) in 83 healthy and 58 diseased subjects. In the healthy group, the mean value of fasting GRP-like immunoreactivity was 2.1 +/- 1.4 (mean +/- SD) pmol/L. There was a slight positive correlation between the GRP-like immunoreactivity values and aging. Postprandial serial measurements demonstrated that GRP-like immunoreactivity showed no response to a significant elevation of serum gastrin concentration. The group with chronic renal failure on hemodialysis gave the highest value, 7.1 +/- 2.1 pmol/L (p less than 0.01). There were no statistical differences between the healthy controls and groups with peptic ulcer, liver cirrhosis, diabetes mellitus or carcinomas, although some cancer patients had a marked increase in GRP-like immunoreactivity value.

Topics: Adult; Aged; Bombesin; Diabetes Mellitus; Female; Gastrin-Releasing Peptide; Gastrins; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Neoplasms; Peptic Ulcer; Peptide Fragments; Peptides; Radioimmunoassay

Conflicting results are reported in the literature on the structure and function of gastric mucosa in patients with chronic renal failure (CRF). In the present endoscopic study of 68 CRF patients on conservative treatment (regular dialyses or transplantations had not yet been undertaken), we sought to clarify whether CRF leads to hypertrophic or hypotrophic phenomena in gastric mucosa, as interpreted by the presence and grade of gastritis and by the thickness of the gastric mucosa. We found that the mean progression of gastritis in both antrum and body was significantly slower than expected in CFR patients, and that the thickness of both antral and body mucosa was significantly lower in CFR patients than in non-CRF controls. Furthermore, although the thickness of the oxyntic body mucosa in CRF showed a positive correlation to serum gastrin (SeGa) levels and even though 12 of the patients showed high SeGa levels corresponding to those seen in the Zollinger-Ellison synbdrome (300-1500 ng/l), the thickness of the oxyntic body mucosa in CRF patients did not exceed that seen in control subjects with normal SeGa. We conclude that CRF exerts inhibitory effects on the gastric mucosa resulting in retardation in the progression of chronic gastritis and hypotrophy of the gastric mucous membrane.

Topics: Adult; Age Factors; Aged; Creatinine; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Pyloric Antrum

Topics: Adult; Aged; Calcitonin; Female; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Humans; Hyperparathyroidism, Secondary; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Topics: Acute Kidney Injury; Adult; Aged; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

Topics: Adolescent; Adult; Calcium; Female; Gastric Acid; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Elevated serum gastrin (SG) has been reported in chronic renal failure (CRF). We studied SG levels in relation to various humoral and gastroduodenal histopathologic findings in 20 controls, 12 uremics under conservative therapy (CT), 27 patients on regular dialysis (RDT) and 8 transplanted patients (Tx). SG and parathyroid hormone (PTH) levels were estimated by radioimmunoassay (RIA), in addition serum BUN, creatinine, Ca++PO4---and alkaline phosphatase (predialysis in RDT) were determined. 20 patients (12 on CT and 8 on RDT) underwent pentagastrin (PG) stimulation test and upper gastrointestinal endoscopy with biopsy of gastric and duodenal mucosa. The mucosal samples were stained for mucopolysaccharides (MPS), nucleic acid (NA) and alkaline phosphatase (AP), and divided into intense, normal or faint staining. Mean SG was 688.71 pg/ml (CT cases), 636.2 pg/ml (RDT cases) and 280.6 pg/ml (Tx cases), all values being significantly higher than controls (118.46 pg/ml). SG level had a linear correlation with serum creatinine in CT patients and predialysis creatinine in RDT patients, but not with other parameters studied (BUN, Ca++,PTH,PO4---AP). The incidence of gastroduodenal erosions (40%) had a significant negative correlation with SG. They were more frequent with normal MPS stain (p = 0.01) and NA staining (p less than 0.001) than faint staining of gastric mucosa biopsy. The acid response to PG stimulation was inversely correlated with SG. We believe that elevated SG is compensatory to a decreased response of the gastroduodenal mucosa to PG. Mere retention of SG does not explain its elevation as its correlation with serum creatinine existed not only in patients on CT, but also in RDT patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Alkaline Phosphatase; Female; Gastric Acid; Gastric Mucosa; Gastrins; Gastroscopy; Glycosaminoglycans; Histocytochemistry; Humans; Kidney Failure, Chronic; Male; Nucleic Acids; Parathyroid Hormone

In 68 patients with chronic renal failure (CRF), 15 patients with duodenal ulcer and 15 normal subjects, basal plasma gastrin levels and basal and stimulated gastric acid secretion were measured. Two antisera were used: antiserum R2702 with specificity for human G34 and its N-terminal fragments [G34] and antiserum 2604 with specificity for the four main components of gastrin (total gastrin). Basal gastrin concentrations of both total gastrin and G34-like immunoreactivity (G34LI) were significantly higher in the CRF patients than in the other two groups, irrespective of dialysis. Total gastrin levels were not correlated with serum creatinine levels. Total gastrin levels were significantly decreased during hemodialysis, but G34LI levels showed no significant change. A small amount of total gastrin was detected in the dialysate by antiserum 2604. As to the postprandial gastrin release, in the first 30 min, the pattern of response in the patients with CRF was similar to that of the normal subjects, but the peak value was attained later, and the response was more rather prolonged. Gastric analysis showed a low basal acid out put and impaired acid secretion in response to secretagogue. It is concluded that (1) one of the predominant circulating forms of gastrin in CRF is G34LI, and (2) the hypergastrinemia in the CRF patients is probably due to reduced removal of gastrin by kidneys, increased gastrin production by impairment of the negative acid feedback mechanism induced by parietal cell dysfunction or reduced parietal cell sensitivity to gastrin by atrophic gastritis.

Topics: Achlorhydria; Adult; Endoscopy; Female; Food; Gastric Acid; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Protein Precursors; Renal Dialysis

Topics: Adolescent; Adult; Aged; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peptic Ulcer; Ranitidine; Renal Dialysis

Fifteen patients with chronic renal failure (serum creatinine level greater than 5 mg/dl) of long duration (more than 2 years) requiring hemodialysis were studied. Blood samples before and after 4 hours of hemodialysis were assayed for creatinine, blood urea nitrogen, potassium, calcium, glucose, insulin, gastrin, gastric inhibitory polypeptide, vasoactive intestinal polypeptide, pancreatic polypeptide, somatostatin, motilin, and neurotensin levels. Before dialysis, serum gastrin was minimally increased whereas gastric inhibitory polypeptide and pancreatic polypeptide were grossly increased compared with normal fasting values. Hemodialysis produced no changes in serum gastric inhibitory polypeptide, vasoactive intestinal polypeptide, pancreatic polypeptide, somatostatin, motilin, and neurotensin. Slight increases in serum insulin and gastrin levels may have occurred secondary to a dialysis-induced increase in the serum calcium level. The kidneys appear to be a major site of inactivation of insulin, gastrin, gastric inhibitory polypeptide, and pancreatic polypeptide. The gastrin level, although elevated in renal failure patients, may be suppressed by very high circulating levels of gastric inhibitory polypeptide.

Topics: Adult; Aged; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Insulin; Kidney Failure, Chronic; Middle Aged; Motilin; Neurotensin; Pancreatic Polypeptide; Renal Dialysis; Somatostatin; Vasoactive Intestinal Peptide

Topics: Gastric Acid; Gastric Mucosa; Gastrins; Glomerulonephritis; Humans; Insulin; Kidney Failure, Chronic; Pentagastrin; Risk; Stomach Ulcer

The serum values of PG I and gastrin have been established in a normal population and in several clinical diseases. The PG I is raised in duodenal, gastric, and pyloric ulcer even though the gastrin is normal. Both PG I and gastrin values are raised in renal insufficiency and the Zollinger-Ellison syndrome. The PG I is lowered in atrophic gastritis and alcoholic cirrhosis, and is at the limit of detection in Biermer anemia and total gastrectomy. Insulin and sham-feeding are stimulants for PG I release by patients with duodenal ulcer, but no correlation is observed between PG I output and PAO in the studied group. The results show that PG I is able to distinguish between associated hypergastrinemia and hypoacidity (Biermer anemia type) or a hyperacidity (Zollinger-Ellison syndrome type), and that PG I is a good indicator for gastric hypoacidity. Overlapping between normal and ulcer subjects is comparable to those obtained in acid output determinations.

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Duodenal Ulcer; Female; Gastrectomy; Gastrins; Gastritis, Atrophic; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Pepsinogens; Reference Values; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Female; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Renal Dialysis

Gastroduodenal disease such as peptic ulcer and duodenitis is increased in patients with end-stage renal disease. Gastric hypersecretion of acid proposed as the underlying mechanism has been disputed because peptic ulcer has occurred even in those with normal or low gastric acid secretion. We studied the pancreatic exocrine secretion of bicarbonate (HCO3) and the concentration of plasma pepsinogens in addition to gastric acid secretion in 15 patients on chronic hemodialysis, 10 patients wih previous renal transplantation and compared them with 10 subjects without gastrointestinal or renal disease. We confirmed hypersecretion of gastric acid in renal disease. We confirmed hypersecretion of gastric acid in renal patients on chronic hemodialysis but not in transplant patients. In addition, we found basal but hyposecretion of HCO3 and hyperpepsinogenemia in both renal groups. These observations suggest that the high incidence of gastroduodenal disease in end-stage renal disease might, in part, be due to the simultaneous occurrence of gastric acid hypersecretion, basal hyposecretion of HCO3 by the pancreas, and hyperpepsinogenemia.

Topics: Adult; Bicarbonates; Female; Gastric Acid; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Pancreas; Pepsinogens; Renal Dialysis; Secretin

Topics: Gastrins; Humans; Kidney Failure, Chronic; L-Lactate Dehydrogenase; Lymphocytes

Topics: Adult; Female; Gastrins; Glucagon; Growth Hormone; Hormones; Humans; Insulin; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Somatostatin; Thyrotropin

Glucagon provocation test was performed in the patients with hypergastrinemia and hyperchlorhydria to investigate its diagnostic value. A paradoxical response of plasma gastrin level in the patients with the Zollinger-Ellison syndrome and a marked decrease of plasma gastrin level in the patients with gastric ulcer, duodenal ulcer, excluded gastric antrum, multiple endocrine adenomatosis, pernicious anemia and chronic renal failure were demonstrated by glucagon infusion. Glucagon provocation test, therefore, was considered to be of great value in the diagnosis of the Zollinger-Ellison syndrome, particularly, in the case of an excluded gastric antrum in which secretin provocation test caused the false positive result because of a marked increase of pancreatic secretion. Glucagon provocation test in combination with secretin provocation test, therefore, is at present the most preferable diagnostic procedure for detecting the Zollinger-Ellison syndrome.U

Topics: Adult; Diagnosis, Differential; Duodenal Ulcer; Female; Gastrectomy; Gastrins; Glucagon; Humans; Kidney Failure, Chronic; Middle Aged; Multiple Endocrine Neoplasia; Pyloric Antrum; Secretin; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Adrenocorticotropic Hormone; Aldosterone; Angiotensins; Carbohydrate Metabolism; Catecholamines; Endocrine System Diseases; Erythropoietin; Female; Gastrins; Gonadal Steroid Hormones; Humans; Hydrocortisone; Kidney Failure, Chronic; Male; Renal Dialysis; Renin; Thyroid Gland; Uremia; Vasopressins

In 10 anephric patients awaiting transplantation, 15 patients with chronic renal failure and 30 patients with acute renal failure, daily basal plasma gastrin levels and basal and stimulated gastric acid secretion were measured. Significant elevated plasma gastrin levels were found in all of the anephric patients and in 50 percent of the patients with acute and 55 percent of those with chronic renal failure. Elevated plasma gastrin levels decreased to normal after kidney transplantation or when kidney function returned to normal in the patients with acute renal failure. Gastric acid secretion studies showed a consistent pattern in all three groups of patients with a low basal acid output, a high basal intragastric pH and a very significant peak acid output, perhaps secondary to elevated plasma gastrin levels due to inadequate renal inactivation of gastrin. This may partly explain the increased incidence of gastrointestinal bleeding and gastritis seen in patients with different degrees of renal failure.

Topics: Acute Kidney Injury; Adult; Gastric Acid; Gastric Acidity Determination; Gastrins; Humans; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Transplantation, Homologous

Topics: Adolescent; Adult; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Terminal Care

In a series of chronic experiments on 30 rats subjected to nephrectomy, use was made of the present-day morphological and quantitative histochemical techniques to study the activity of oxidation-reduction enzymes, hydrolases and PAS-reaction in cellular elements of the mucous membrane of the fundal and antral parts of the stomach. It was found that in the early stages of experimental renal insufficiency, all the main cells of the glands manifested marked hyperplasia. These alterations seem likely to be adaptive in nature and are caused by the stimulatory action of the increased amounts of nitrous residue in the gastric lumen of such animals. The authors discuss the origin of gastric pathology in experimental animals and make clinical and experimental correlations.

Topics: Animals; Female; Gastric Juice; Gastric Mucosa; Gastrins; Hyperplasia; Kidney Failure, Chronic; Male; Oxidoreductases; Periodic Acid-Schiff Reaction; Rats

Endoscopy of the upper gastrointestinal tract was performed on 84 patients with end-stage chronic renal failure undergoing hemodialysis. Gastric acid secretion and fasting plasma gastrin levels were also examined in these patients. Hemorrhagic gastritis was most frequently observed (23 cases) followed by erosive gastritis (18 cases). No patients had gastric ulcers. Duodenal ulcers were observed in only two patients. Gastrointestinal bleeding was observed in 15 cases (17.9%). Thirteen of these 15 cases had hemorrhagic gastritis, one of which had a duodenal ulcer as a complication. Fasting plasma gastrin levels (359.6 +/- 336.5 pg/ml) were significantly higher than those of normal subjects (35.2 +/- 37.1 pg/ml), but no acceleration in gastric acid secretion was observed either in the basal condition (BAO 0.8 +/- 0.7 mEq/h) or following tetragastrin stimulation (MAO 9.0 +/- 6.9 mEq/h). Our results were inconsistent with the previous reports that high frequencies of peptic ulcers and increased gastric acid secretion were observed in patients with chronic renal failure. Our data suggest that the defensive factors rather than the aggressive factors of the gastroduodenal mucosa may be involved in chronic renal failure.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Gastritis; Gastrointestinal Hemorrhage; Gastroscopy; Humans; Kidney Failure, Chronic; Male; Middle Aged

Basal serum gastrin concentration was measured before and every week during the initial 5 weeks after renal transplantation in 9 of 20 patients with chronic renal failure who obtained a well functioning renal transplant. Furthermore, calcium and phosphorus metabolism in relation to serum gastrin was investigated in all 20 patients 5 weeks after transplantation. Before renal transplantation, serum gastrin was markedly elevated as compared with the levels in normal controls. During the first 3-5 weeks after renal transplantation, serum gastrin decreased towards normal values. A slight but significant increase in serum gastrin persisted 5 weeks after transplantation. No significant relation between changes in serum gastrin concentration and in calcium and phosphorus metabolism was observed.

Topics: Adolescent; Adult; Calcium; Creatinine; Female; Gastrins; Humans; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Phosphorus; Transplantation, Homologous

Basal serum gastrin levels have been studied in chronic renal failure (CRF), hemodialysis (MHDT) and renal transplant patients. There was no significant difference between the levels in CRF and controls and between anephric and nephric MHDT patients. However, levels in transplant patients were lower than those in the other groups. There was no relationship between fasting gastrin levels and peptic ulceration in any of the groups studied. It is doubtful whether basal gastrin estimations are of much value in management of these patients.

Topics: Gastrins; Humans; Kidney Failure, Chronic; Kidney Transplantation; Renal Dialysis; Transplantation, Homologous

Previous studies of gastric secretory function and serum gastrin levels in patients with chronic renal failure (CRF) have yielded conflicting results. In a study of 30 patients on regular hemodialysis, serum gastrin levels were higher than normal (p less than 0.05), and the gastric secretory response to pentagastrin was normal for the group as a whole. There were, however, 8 patients who were hypochlorhydric (4 achlorhydric) and 7 who were hyperchlorhydric. The patients with gastric hyposecretion were older, predominantly male and this group was associated with the highest gastrin levels as well as the highest incidence of gastrointestinal hemorrhage. Chronic gastritis is thus more common in CRF than generally believed and may be responsible for much of the morbidity from gastrointestinal complications during hemodialysis.

Topics: Adolescent; Adult; Female; Gastric Juice; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Topics: Adult; Antigens; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

Topics: Adult; Calcium Chloride; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypercalcemia; Kidney Failure, Chronic; Male; Middle Aged

Topics: Fasting; Gastrins; Humans; Kidney Failure, Chronic; Renal Dialysis

Topics: Acute Kidney Injury; Adult; Calcium; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

The realisation that circulating gastrin is heterogeneous necessitates a reappraisal of gastrin's role in the increased incidence of duodenal ulcer disease that occurs in chronic renal failure. Radioimmunoassays employing region-specific antisera have been used to examine renal and extrarenal factors controlling serum gastrin concentration in patients with chronic renal failure. The present study has shown that basal serum gastrin concentrations measured with a carboxyl-terminal specific antibody were significantly higher in eight patients with chronic renal failure treated by dietary restriction (388+/-196 pM) than in 14 patients with chronic renal failure treated by haemodialysis (28.7+/-4.6 pM). However, basal gastrin concentrations in both groups of patients were significantly higher than in 25 normal subjects (12.3+/-1.8 pM) and showed significant negative correlations with maximal gastric acid secretion (p < 0.01). Markedly raised basal gastrin concentrations were observed only in chronic renal failure patients who were also achlorhydric. Although the peak postprandial increment in big gastrin concentration in 11 chronic renal failure patients (34.0+/-7.5 pM) was significantly greater (p < 0.05) than in 25 normal subjects (19.5+/-4.6 pM), the little gastrin responses were not significantly different. In addition, clearance of exogenous little gastrin was similar in four chronic failure patients (clearance half time: 8.1+/-0.7 min) and four normal subjects (clearance half time: 6.5+/-1.2 min). These studies suggest that the human kidney is unimportant in the metabolism of little gastrin. As circulating little gastrin is six times more potent than big gastrin in stimulating acid secretion, these studies suggest that the raised gastrin concentrations observed in patients with chronic renal failure have little significance in terms of their increased incidence of duodenal ulcer disease.

Topics: Food; Gastric Acid; Gastrins; Humans; Kidney Failure, Chronic; Metabolic Clearance Rate; Radioimmunoassay; Renal Dialysis

Gastric function and histology were investigated in 24 patients with untreated chronic renal failure. At endoscopy nine patients had oesophagitis, 12 patients were considered to have gastritis, and the duodenum appeared inflamed in 20 patients. Endoscopic biopsies were taken at standard sites in the stomach and duodenum; gastritis was found in all patients, and 17 patients had duodenitis. Stimulated acid secretion was impaired in seven out of 20 patients and acid hypersecretion was found in a further two patients. Pepsin output correlated well with acid output in these patients. Fasting serum gastrin levels were elevated in 12 of the 19 patients tested. Patients with atrophic gastritis had low acid outputs and hypergastrinaemia, and when extensive gastritis was present, the patients tended to have more severe renal failure and hyposecretion of acid. Three patients were studied again after regular haemodialysis or renal transplantation and were found to show marked endoscopic and histological improvement.

Topics: Adult; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Kidney Failure, Chronic; Male; Middle Aged; Pepsin A; Renal Dialysis

Antral somatostatin- and gastrin-producing cells (D and G cells) were studied in a group of patients with chronic renal failure (CRF) in comparison with a control group. Gastric acid secretion and serum gastrin, phosphate, and parathormone (PTH) levels were also evaluated in every patient. The group with CRF showed a mild increase both in G- and in D-cell denisty. In this group serum phosphate and PTH levels were higher than normal, showing hyperparathyroidism in every patient. A direct correlation was found between G-cell density and parathyroid function in patients with CRF. Hyperparathyroidism, therefore, seems to play a role in the mechanism of increased serum gastrin levels in CRF.

Topics: Adult; Cell Count; Female; Fluorescent Antibody Technique; Gastric Juice; Gastrins; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Glands; Parathyroid Hormone; Pentagastrin; Phosphates; Pyloric Antrum

Whisky (25-50 ml) increased plasma levels of immunoreactive calcitonin (iCT) in seventeen of nineteen patients with chronic renal failure. The effect was greater in patients with high levels of iCT than in those with normal levels. Changes in plasma iCT were not related to changes in calcium, phosphate or immunoreactive gastrin, but were inhibited by the prior administration of propranolol.

Topics: Calcitonin; Calcium; Ethanol; Gastrins; Humans; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Propranolol; Radioimmunoassay

The interrelationship between serum gastrin and serum calcitonin concentrations was studied in 73 patients with chronic renal failure. In both haemodialyzed and non-dialyzed patients increased serum concentrations of these hormones were found compared with normal controls. In non-dialyzed patients with creatinine clearance above 10 ml/min a highly significant correlation between serum gastrin and creatinine clearance was found, whereas no correlation was found in patients with creatinine clearance below 10 ml/min. Between serum gastrin and serum calcitonin, a significant positive correlation was found in non-dialyzed patients. These findings may be explained by a relationship between the two hormones or be secondary to a decreased elimination due to the reduced renal function.

Topics: Adolescent; Adult; Aged; Calcitonin; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Radioimmunoassay; Renal Dialysis

Plasma levels of somatostatin-like immunoreactivity (SLI) and gastrin were determined by radioimmunoassay in patients with varying degrees of renal dysfunction. The plasma SLI was not increased in patients with end-stage renal failure as compared to healthy controls. In patients with varying degrees of renal insufficiency no significant correlation was found between the plasma SLI and kidney function as estimated by the 51Cr-EDTA-clearance rate. In uraemic patients a significant inverse correlation was found between plasma SLI and plasma gastrin.

Topics: Adolescent; Adult; Aged; Child; Female; Gastrins; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Somatostatin; Uremia

Fasting serum gastrin, cholecystokinin, glucagon, and gastric inhibitory polypeptide concentrations were simultaneously measured in normal subjects and in patients with different degrees of renal failure. Values of gastrin, cholecystokinin, gastric inhibitory polypeptide, and glucagon were significantly higher in all patients with serum creatinine concentrations greater than 3 mg/dl than in controls (P less than 0.01). The degree of renal insufficiency was significantly correlated (P less than 0.05) with serum concentrations of each hormone, but no significant linear correlation existed among the serum concentrations of different gastrointestinal hormones in individuals. Hemodialysis did not significantly alter predialysis serum gastrin, cholecystokinin, or glucagon concentration, but the serum gastric inhibitory polypeptide concentration decreased by 30% (P less than 0.01) after hemodialysis. The disproportionate increases of hormones with antagonistic actions may alter gastrointestinal function in renal insufficiency.

Topics: Adult; Aged; Cholecystokinin; Creatinine; Female; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis

Topics: Acute Kidney Injury; Cholecystokinin; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Kidney Failure, Chronic; Secretin

In 18 patients with acute renal failure and 11 patients with chronic renal insufficiency serum gastrin levels were estimated before and after a test meal. The results were compared with those obtained in a group of 52 healthy subjects. It was stated that patients with acute as well as chronic renal failure display a "physiological" increase of serum gastrin after stimulation by a test meal. In contrast to healthy subjects the post-test meal gastrin curves in patients with chronic and acute renal insufficiency during the anuric/oliguric phase started from significantly higher fasting values. From the results obtained it seems that diminished renal clearance of gastrin by the insufficient kidneys is only partially responsible for the elevated fasting values found in anuric/oliguric patients with acute renal failure or patients with chronic renal insufficiency.

Topics: Acute Kidney Injury; Adult; Creatinine; Fasting; Female; Gastrins; Humans; Kidney; Kidney Failure, Chronic; Male; Middle Aged

Topics: Adult; Aged; Blood Pressure; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Lithium; Male; Middle Aged; Pepsin A; Peptic Ulcer; Permeability; Polyethylene Glycols; Renal Dialysis; Uremia

In twelve patients on chronic haemodialysis, a relationship was established between gastric acid secretion on the one hand, and certain parameters of calcium metabolism on the other hand: in a multifactorial statistical analysis, plasma calcium before dialysis (p less than 0,05), plasma parathormone levels before dialysis (p less than 0,05) and plasma calcitonin before dialysis (p less than 0,05) were variable explicatives of basal gastric acid secretion according to a direct relationship, whilst plasma calcium (p less than 0,05) was the only explicative variable of maximal gastric acid secretion after pentagastrin, with an inverse relationship. These preliminary results suggest that gastric acid secretion in the haemodialysis patient must be interpreted in the light of the state of calcium metabolism. Thus hypocalcaemia may be accompanied by decreased basal acid secretion and by contrast by an increased maximal acid secretion. These results require confirmation in a larger number of patients.

Topics: Adult; Calcitonin; Calcium; Female; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis

Many alterations in metabolic and endocrine function occur in end-stage renal disease. Glucose intolerance is almost always present with uremia; it improves shortly after institution of regular hemodialysis. Hyperlipidemia (type IV) is prevalent, and atherosclerotic cardiovascular disease causes death in about 50% of patients receiving long-term hemodialysis. Although plasma levels of growth hormone usually are elevated, children with chronic renal failure show growth retardation. The occurrence of thyroid disorders is difficult to determine, since many clinical features of uremia are similar to those of hyperthyroidism and hypothyroidism. The incidence of duodenal ulcer is high, possibly due to high gastrin levels. Sex hormone disturbances are common. Anemia is a constant feature of chronic renal failure; patients usually tolerate it well.

Topics: Anemia; Blood Glucose; Gastrins; Gonadal Steroid Hormones; Growth Hormone; Humans; Hyperlipidemias; Insulin; Kidney Failure, Chronic; Renal Dialysis; Thyroid Diseases; Triglycerides; Uremia

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.

Topics: Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Insulin; Kidney Failure, Chronic; Renal Dialysis; Secretin; Vasoactive Intestinal Peptide

Topics: Adult; Calcitonin; Calcium; Female; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Parathyroid Hormone; Renal Dialysis

High levels of serum calcitonin were found in patients with chronic renal failure. Serum calcitonin correlated directly with the phosphate to total calcium ratio; calcitonin levels correlated inversely with serum calcium in those patients on dialysis and directly with serum calcium in nondialysis patients. All patients had elevated serum gastrin. The high levels of serum calcitonin usually decreased following successful kidney transplantation. The pathophysiology of this hypercalcitonemia and its relationship to renal osteodystrophy and the disordered calcium metabolism of uremia remains to be elucidated.

Topics: Adult; Calcitonin; Calcium; Diabetic Nephropathies; Female; Gastrins; Glomerulonephritis; Humans; Hypertension, Renal; Kidney Diseases, Cystic; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Phosphates; Pyelonephritis; Renal Dialysis

Topics: Calcitonin; Calcium; Circadian Rhythm; Ethanol; Gastrins; Glomerular Filtration Rate; Humans; Insulin; Kidney Failure, Chronic; Parathyroid Hormone; Phosphates; Propranolol

Peptic ulcer is a common problem in advanced renal failure, but most drugs for ulcers are hazardous in this condition. In a small open study cimetidine was given to nine patients with acid hypersecretion and endoscopically diagnosed duodenal ulceration who were undergoing haemodialysis. The patients obtained good pain relief and suffered no serious side effects. Both basal and stimulated acid output fell considerably and the plasma gastrin response to food increased during treatment. Two patients with recurrent vomiting during haemodialysis had a striking response to cimetidine, which suggested that such vomiting may be acid-mediated in some patients. These preliminary results suggest that cimetidine may prove to be an advance in the management of peptic ulcer in uraemic patients.

Topics: Adolescent; Adult; Cimetidine; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastrins; Guanidines; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Vomiting

Topics: Acute Kidney Injury; Anemia, Pernicious; Duodenal Ulcer; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Kidney Failure, Chronic; Zollinger-Ellison Syndrome

In 50 patients (10 anephric, 10 with chronic renal failure, and 30 with acute renal failure) the correlation was studied between basal PG levels and basal and stimulated gastric acid secretion. a) The mean PG level in all 3 groups was significantly higher than in the control group, with the highest values in the anephric, which decreased to normal after kidney transplantation. b) In the patients with ARF and after transplantation there was a very positive correlation between PG levels and kidney function. c) Hemodialysis decreased PG levels moderately but significantly. d) Gastric acid studies showed in all groups a very low BAO and basal intragastric pH, with a significant release of gastric acid after pentagastrin stimulation, especially in the anephric.

Topics: Acute Kidney Injury; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Kidney Transplantation; Nephrectomy; Postoperative Complications; Transplantation, Homologous

Both gastrin and acid responses to antral stimulation by meat extracts (Oxo) were studied in 15 undialysed males with chronic renal failure (CRF). Eighteen sex and age-matched duodenal ulcers (DU) served as controls. Oxo increased acid and plasma gastrin in both groups. The rise in plasma gastrin was larger in CRF than in DU. The pattern of gastrin response in CRF suggests accumulation of gastrin in the plasma probably related to impaired renal inactivation of the hormone. Five CRF had large acid responses representing 40 to 90 percent of their maximal secretory capacity. Antral function should be measured in CRF before haemodialysis or renal transplantation.

Topics: Adult; Duodenal Ulcer; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Male; Meat; Middle Aged; Pyloric Antrum

Topics: Gastrins; Humans; Kidney Failure, Chronic; Molecular Conformation

Gastric secretion was evaluated in 9 male patients with chronic renal failure on maintenance hemodialysis. Five secreted low or normal quantities of acid and 4 exhibited hypersecretion, 2 of whom had associated peptic ulcer disease. Serum gastrin responses to a protein meal were comparable to control subjects. Calcium infusion in two basal hypersecretors depressed acid secretion. The only statistically significant correlation observed was between basal acid output ans serum levels of parathormone. These studies suggest that while acid secretory abnormalities vary in patients with chronic renal failure on hemodialysis, there is no apparent sensitivity of the gastrin-secreting cells to protein or calcium ion which might account for acid hypersecretion. Secondary hyperparathyroidism may influence the occurrence of acid secretory abnormalities.

Topics: Adult; Aged; Calcium; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Stomach Ulcer

Topics: Female; Gastrins; Humans; Kidney Failure, Chronic; Male

Topics: Acute Kidney Injury; Adolescent; Adult; Aged; Blood Urea Nitrogen; Child; Creatinine; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Iodine Radioisotopes; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Radioimmunoassay; Renal Dialysis; Transplantation, Homologous

Topics: Anemia, Pernicious; Bicarbonates; Duodenal Ulcer; Endocrine System Diseases; Esophagitis, Peptic; Esophagus; Gastric Juice; Gastrins; Humans; Hyperplasia; Intestines; Kidney Failure, Chronic; Pancreas; Pheochromocytoma; Pyloric Antrum; Stomach; Stomach Neoplasms; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Serum gastrin radioimmunoassay (RIA) is a sensitive and specific method suitable for measurement of circulating concentrations of this peptide hormone, which is a major regulator of gastric acid secretion. When performed under optimal conditions this RIA permits measurement of low and normal serum gastrin levels and changes that occur after physiologic stimulation. Hypergastrinemia may be secondary to atrophy of the acid-secreting gastric mucosa. This form of pypergastrinemia is appropriate and leads to no seriousequences. Hypergastrinemia associated with gastric acid hypersecretion is inappropriate. The major cause is a gastrinsecreting tumor (gastrinoma) that produces the clinical picture of the Aollinger-Ellison syndrome. The differential diagnosis of inappropraite hypergastrinemia includes antral G-cell hyperplasia and ISOLATED RETAINED ANTRUM. Accurate diagnosis of these conditions may be aided by ancillary studies including feeding, secretin, and calcium stimulation tests. Distinction among these conditions is important in planning appropriate surgical tratment.

Topics: Antibody Specificity; Arthritis, Rheumatoid; Catecholamines; Duodenal Ulcer; Gastrectomy; Gastrins; Humans; Kidney Failure, Chronic; Pentagastrin; Pheochromocytoma; Pyloric Antrum; Radioimmunoassay; Stimulation, Chemical; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

The effects of somatostatin (growth hormone release inhibiting hormone) on basal gastrin were studied in patients suffering from pernicious anaemia and chronic renal and liver disease, and during sequential arginine/insulin-stimulated gastrin release in normal subjects. When basal gastrin concentrations were normal (10-50 pg/ml) in controls and in patients who were in renal and liver failure, somatostatin had no effect on gastrin levels. Raised basal gastrin levels in pernicious anaemia and in 2 cases of chronic renal disease, were significantly inhibited by somatostatin with a half-life (T 1/2) of 3-4 minutes. Arginine infusion caused an insignificant rise in serum gastrin which was unaffected by somatostatin, whereas insulin hypoglycaemia significantly stimulated gastrin release, which was inhibited by somatostatin.

Topics: Adult; Anemia, Pernicious; Arginine; Chronic Disease; Depression, Chemical; Gastrins; Humans; Insulin Antagonists; Kidney Failure, Chronic; Liver Diseases; Secretory Rate; Somatostatin; Stimulation, Chemical

Topics: Adult; Aged; Female; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged

Topics: Gastrins; Humans; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Postoperative Complications; Radioimmunoassay; Transplantation, Homologous

Topics: Calcium; Gastric Juice; Gastrins; Humans; Hyperparathyroidism; Kidney Failure, Chronic; Parathyroid Glands; Postoperative Care; Renal Dialysis

Topics: Calcium; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Long-Term Care; Parathyroid Glands; Renal Dialysis

Fasting serum gastrin was measured by radioimmunoassay in 89 patients with chronic renal failure. When the serum creatinine level was used as an index of the degree of renal impairment serum gastrin rose proportionately with the degree of renal failure. Haemodialysis did not significantly alter serum gastrin levels but renal transplantation tended to return them towards normal. This study indicates that the kidney has a role in the degradation of gastrin.

Topics: Adult; Creatinine; Gastrins; Humans; Kidney; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Radioimmunoassay; Renal Dialysis; Transplantation, Homologous

Topics: Adrenal Cortex Hormones; Gastrins; Humans; Hydrogen-Ion Concentration; Immunosuppression Therapy; Kidney Failure, Chronic; Kidney Transplantation; Peptic Ulcer; Postoperative Complications; Transplantation, Homologous; Uremia

Topics: Anemia, Pernicious; Animals; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Kidney Failure, Chronic; Radioimmunoassay; Zollinger-Ellison Syndrome