Effects of Helicobacter pylori eradication on proteinuria: a prospective study.

BACKGROUND: Helicobacter pylori is one of the most common bacterial infections, seen in humans worldwide and its possible relationship to different diseases is a focus of attention nowadays. The aim of this study was to analyse the effects of H. Pylori eradication on proteinuria. METHODS: Ninety-nine patients suffering from dyspeptic complaints were recruited in this prospective study. The patients were divided into two groups according to the presence of H. pylori infection. Thus, a total of 67 H. pylori positive and 32 H. pylori negative patients were studied. The H. pylori positive patients' group was divided into two groups according to response toH. pylori eradication treatment. A total of three groups were formed, viz; group 1 comprises of patients who are H. pylori positive and responds positively toH. pylori eradication therapy, group 2 comprises of patients who are H. pylori positive and responds negatively toH. pylori eradication therapy and group 3 is the control group and comprises of patients that are H. pylori negative. Urine samples to obtain the protein/creatinine ratio were collected initially and at the end of the study from all patients. RESULTS: Mean difference levels (pre- and post-treatment difference) of urine protein/creatinine ratio was 0.055 ± 0.13 in group 1. The ratio was - 0.0007 ± 0.0067 in group 2 and - 0.0022 ± 0.008 in group 3. A statistically significant difference was found in group 1 compared to the other groups in terms of mean difference levels of protein/creatinine ratios (p < 0.001). CONCLUSION: As a result of our study, treatment of H. pylori eradication significantly reduced the proteinuria within the normal limits.

Relation between serum thyroid hormone and 'nondipper' circadian blood pressure variability.

Currently, the pathogenesis of nondipper hypertension remains largely unclear in patients without any renal or endocrine pathology. It is well known that overt hypothyroidism is strongly associated with diastolic hypertension. However, no study has addressed the pathogenic role of TSH, free T3 (FT3), and free T4 (FT4) in nondipper hypertension. The aim of the present investigation is to evaluate if higher TSH, low FT3 and FT4 would be associated with a nondipper hypertension profile, in patients with normal renal function and without any overt thyroid hormone disorder. 131 subjects were screened and those who met the following inclusion criteria were enrolled: (1) glomerular filtration rate (GFR) >60 ml/min; (2) no history of thyroid disorders; (3) no history of thyroid hormone medication. All subjects underwent 24-hour ambulatory blood pressure monitoring on a usual working day. Of the total population, 59 patients (45%) were classified as dippers and 72 (55%) were classified as nondippers. The only significant differences between dipper and nondipper patients appear to be related to FT3 levels and GFR. Nondipper patients had lower FT3 levels (4.5 +/- 0.6 vs. 4.0 +/- 0.9 pmol/l, p = 0.02) and low GFR (80.5 +/- 12.2 vs. 86.9 +/- 16.9 ml/min, p = 0.03), compared to dipper patients. The final regression model included serum TSH, FT3 levels, and GFR; the only independent predictor of nondipper hypertension was FT3 (p = 0.04). In conclusion, even if the mechanisms of our findings remain incompletely understood, we demonstrate a graded independent relation between lower level of FT3 and the risk of nondipping. Further studies are warranted to confirm this relationship and to elucidate the pathogenetic mechanisms of this relationship.

Relation between serum calcium, phosphate, parathyroid hormone and 'nondipper' circadian blood pressure variability profile in patients with normal renal function.

BACKGROUND AND AIMS: In patients with renal disease, an association between abnormal circadian blood pressure profile and abnormalities in bone and mineral metabolism, including vascular calcifications, is well known. However, such a link has not yet been reported in hypertensive patients with normal renal function. We aimed to evaluate if higher serum phosphate, calcium, parathyroid hormone (PTH) level and the calcium x phosphate (Ca x P) product would be associated with a nondipper hypertension, in patients with normal renal function and without any PTH disorder. METHODS: 190 hypertensive subjects with the following inclusion criteria were enrolled: (1) normal phosphate and PTH levels; (2) glomerular filtration rate (GFR) >60 ml/min, and (3) no history of calcium, phosphate, vitamin D medication and hyperparathyroidism. RESULTS: Of the total population, 76 patients (40%) were classified as dippers and 114 (60%) as nondippers. Nondipper patients had higher levels of phosphate (3.70 +/- 0.61 vs. 3.35 +/- 0.44 mg/dl, p = 0.001), Ca x P product (35.4 +/- 6.5 vs. 31.5 +/- 5.0, p = 0.001) and PTH (75.7 +/- 28.8 vs. 46.6 +/- 17.1 pg/ml, p = 0.000) compared to dipper patients. Independent predictors (multiple regression) for nondipper hypertension were PTH (beta = 0.43, p = 0.001) and phosphate (beta = 0.9, p = 0.03). CONCLUSION: We demonstrate a graded independent relation between higher levels of phosphate, PTH, Ca x P product and the risk of nondipping in hypertensive patients with an estimated GFR of >60 ml/min and normal mineral metabolism.