Chronic Renal Failure Abstracts 1

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Chronic renal failure promotes severe variant of vitamin B12 deficiency
            (Duning et al., 2006) Download
The vitamin B12 deficiency in patients with chronic renal insufficiency is howev- er much more difficult to assess and poorly understood. There is evidence that patients with renal dysfunction might develop a vitamin B12 resistance. vitamin B12 serum concentrations within common reference ranges are not sufficient to deliver the vitamin into the cells indicating that supraphysiological doses could be necessary to ensure intracellular vitamin B12 delivery.

Prevalence of Helicobacter pylori in patients with chronic renal failure
            (Gladziwa et al., 1993) Download
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.


 

Hypothalamo-pituitary-adrenal axis in uraemia: evidence for primary adrenal dysfunction
            (Grant et al., 1993) Download
To study hypothalamo-pituitary-adrenal axis disturbances in chronic renal failure, we administered corticotrophin-releasing hormone to patients undergoing haemodialysis and CAPD and to normal controls. Cortisol, ACTH, and ACTH precursors were measured before and after corticotrophin-releasing hormone using sensitive and specific two-site assays. Baseline ACTH and cortisol were similar in all groups. Peak values occurred at 30 min (ACTH) and between 30 and 60 min (cortisol). The cortisol (but not the ACTH) responses were significantly reduced in patients with renal failure (P < 0.05). ACTH precursors did not change from baseline following corticotrophin-releasing hormone but were significantly elevated in patients with renal failure compared to controls (P < 0.01). The reduced cortisol response to corticotrophin-releasing hormone may reflect a primary defect of adrenal function in renal failure.

The effect of Helicobacter pylori on vitamin B 12 blood levels in chronic renal failure patients: a single blind control trial
            (Khedmat et al., 2013) Download
Helicobacter pylori (HP) is a common infection worldwide and has been associated with severe morbidity. The level of vitamin B 12 in HP-infected chronic kidney disease (CKD) patients is reported to be lower than in the general population. The present study has been designed to evaluate the vitamin B 12 level in HP-infected CKD patients. We assessed the serum levels of vitamin B 12 in 50 CKD patients with positive HP serology, one and three months after the eradication of HP infection. There were significant differences between the serum levels of vitamin B 12 in the study patients before (806.98 +/- 466.82) and after (760.36 +/- 433.93) eradication treatment (P <0.001). We conclude that our study suggests the correlation between vitamin B 12 deficiency in CKD patients and the HP infection status.

Rehmannia glutinosa ameliorates the progressive renal failure induced by 5/6 nephrectomy.
            (Lee et al., 2009) Download
AIM OF THE STUDY:  Rehmannia glutinosa, the steamed root of the Scrophulariaceae family, has been widely used in Asian countries for the treatment of renal diseases. In this study, we evaluated the renoprotective effect of aqueous extract of Rehmannia glutinosa in progressive renal failure. MATERIALS AND METHODS:  The effects of Rehmannia glutinosa on renal function, 24-h proteinuria, and the expression of angiotensin II, angiotensin II type 1 (AT(1)) receptor, TGF-beta1, and type IV collagen in renal cortex were analyzed in progressive renal failure rats induced by 5/6 nephrectomy. RESULTS:  Rehmannia glutinosa reduced the serum creatinine level, 24-h urinary protein excretion, and glomerulosclerosis, and it also inhibited the expression of angiotensin II, AT(1) receptor, TGF-beta1 and type IV collagen in the renal cortex. CONCLUSIONS:  These results suggest that the renoprotective effect of Rehmannia glutinosa might be mediated by suppressing the expression of angiotensin II and AT(1) receptor and by regulating TGF-beta1 and type IV collagen expression.

Hypergastrinemia and achlorhydria in chronic renal failure
            (Muto et al., 1985) Download
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.

Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in undialyzed and hemodialyzed patients
            (Muto et al., 1988a) Download
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.

Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in young patients with chronic renal failure
            (Muto et al., 1988b) Download
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.

Cellular uptake of vitamin B12 in patients with chronic renal failure
            (Obeid et al., 2005) Download
BACKGROUND/AIMS: Elevated concentration of plasma homocysteine (tHcy) is common in renal patients, however, the reason behind the resistance to vitamin B(12) and folate therapy are poorly understood. METHODS: We investigated vitamin B12 uptake by mononuclear cells (MC) from predialysis patients (n = 19) as compared to healthy controls (n = 15). Serum levels of tHcy, methylmalonic acid and cystathionine, holotranscobalamin (holoTC), total vitamin B12 and folate were also measured. RESULTS: The uptake of vitamin B12 by MC from renal patients was lower than that by MC from controls (9.3 vs. 12.5 pg/3 x 10(6) cells; p = 0.001). Nonetheless, the receptor-binding capacity was comparable between patients and controls (6.1 vs. 6.5 pg/3 x 10(6) cells; p = 0.627). Average reduction of vitamin B12 uptake in patients as compared to the controls was 18.1%. CONCLUSIONS: Our results show that vitamin B12 uptake is impaired in MC from renal patients, with no evidence that the surface receptor is down-regulated. High serum concentrations of holoTC are common in renal patients and might be related to a generalized resistance to this vitamin. Serum concentrations of vitamin B12 within the reference range are not likely to ensure vitamin delivery into the cells. Supraphysiological doses of vitamin B12 may be necessary to deliver a sufficient amount of the vitamins to the cells via mechanisms largely independent of holoTC receptor.


 

References

Duning, T., et al. (2006), ‘Chronic renal failure promotes severe variant of vitamin B12 deficiency’, Eur Neurol, 56 (1), 62-65. PubMed: 16921247
Gladziwa, U., et al. (1993), ‘Prevalence of Helicobacter pylori in patients with chronic renal failure’, Nephrol Dial Transplant, 8 (4), 301-6. PubMed: 8390002
Grant, AC, et al. (1993), ‘Hypothalamo-pituitary-adrenal axis in uraemia: evidence for primary adrenal dysfunction’, Nephrol Dial Transplant, 8 (4), 307-10. PubMed: 8390003
Khedmat, H., et al. (2013), ‘The effect of Helicobacter pylori on vitamin B 12 blood levels in chronic renal failure patients: a single blind control trial’, Saudi J Kidney Dis Transpl, 24 (4), 759-63. PubMed: 23816726
Lee, BC, et al. (2009), ‘Rehmannia glutinosa ameliorates the progressive renal failure induced by 5/6 nephrectomy.’, J Ethnopharmacol, 122 (1), 131-35. PubMed: 19146934
Muto, S., et al. (1985), ‘Hypergastrinemia and achlorhydria in chronic renal failure’, Nephron Clin Pract, 40 (2), 143-48. PubMed: 4000343
Muto, S., et al. (1988a), ‘Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in undialyzed and hemodialyzed patients’, Nephron Clin Pract, 50 (1), 10-13. PubMed: 3262834
——— (1988b), ‘Hypochlorhydria and hypergastrinemia and their association with gastrointestinal bleeding in young patients with chronic renal failure’, Nephron Clin Pract, 50 (1), 5-9. PubMed: 3173601
Obeid, R., et al. (2005), ‘Cellular uptake of vitamin B12 in patients with chronic renal failure’, Nephron Clin Pract, 99 (2), c42-8. PubMed: 15637428