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      G-Protein β 3 Subunit C825T Variant, Nephropathy and Hypertension in Patients with Type 2 (Non-Insulin-Dependent) Diabetes mellitus

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          Background: There is substantial evidence that hereditary factors contribute to the predisposition to diabetic nephropathy. On the other hand, it has been suggested that genetics of diabetic nephropathy and hypertension may overlap. Recently, a C to T substitution (C825T) in the gene encoding for the guanine-nucleotide-binding protein β<sub>3</sub> subunit (GNB3) was identified, and this molecular variant was found to be associated with enhanced activation of G proteins and increased risk of the development of hypertension. The aim of the study was to test whether GNB3 C825T polymorphism contributes to the development of incipient or overt nephropathy or hypertension in type 2 diabetic patients. Methods: GNB3 genotype was determined in 130 type 2 diabetic patients with overt proteinuria or chronic renal failure, 155 diabetic patients with microalbuminuria and 163 control subjects with normoalbuminuria and known type 2 diabetes duration of at least 10 years. Results: No differences in GNB3 genotype distributions or allele frequencies between the study groups were found. Also, no differences between normotensive and hypertensive patients were demonstrated. Conclusion: The study provided evidence against the major impact of the GNB3 C825T polymorphism on the increased risk of the development of nephropathy or hypertension in type 2 diabetic patients.

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          Increased frequency of G-protein beta 3-subunit 825 T allele in dialyzed patients with type 2 diabetes.

          A polymorphism (C825T) in exon 10 of the gene encoding the beta 3 subunit of heterotrimeric G proteins (GN beta 3) has recently been described, and the T allele was found to be associated with late-onset hypertension. Because hypertension is a known risk factor for the development of clinically manifest progressive renal disease, we examined the C825T polymorphism in older hemodialysis patients suffering from nondiabetic renal disease or type 2 diabetes with presumed diabetic nephropathy, respectively, and in older healthy controls.
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            Association of increased erythrocyte Na+/H+ exchanger with renal Na+ retention in patients with essential hypertension.

            The goal of this study was to investigate the activity of the Na+/H+ exchanger in erythrocytes of patients with essential hypertension and its relation with urinary Na+ excretion. The study was performed in cells from 27 untreated hypertensive patients and 30 normotensive controls with similar age and sex distribution. All subjects were studied after 4 days on a controlled Na+ diet (145 mmol/day). The activity of the Na+/H+ exchanger was determined by acidifying cell pH and measuring the initial rate of the net Na(+)-dependent H+ efflux. The activity of the Na+/H+ exchanger was higher in hypertensive patients than in controls (301 +/- 45 v 162 +/- 23 mmol/L cells/h, mean +/- SEM; P < .01). With the upper limit of the normotensive population as a cut-off point (385 mmol/L cells/h), a subgroup of 12 hypertensive patients had an abnormally high activity of Na+/H+ exchanger. Compared with controls and with patients with normal exchanger activity, patients with increased exchanger activity were characterized by lower net (P < .01) and fractional (P < .05) Na+ excretion. The accumulative Na+ balance was higher (P < .01) in hypertensive patients with increased activity of the exchanger (39.90 +/- 3.47 mmol) than in the remaining hypertensive patients (0.59 +/- 6.96 mmol) or in the normotensive population (-5.71 +/- 6.12 mmol). After analyzing the relationship of renin activity with Na+ excretion it was observed that renin activity was inappropriately low in 9 (75%) patients with increased exchanger, in 6 (40%) patients with normal exchanger, and in 6 (20%) normotensives, these differences being significant (P<.01).

              Author and article information

              Am J Nephrol
              American Journal of Nephrology
              S. Karger AG
              August 2000
              01 September 2000
              : 20
              : 4
              : 305-310
              Department of Internal Medicine and Diabetoloy, Silesian School of Medicine, Zabrze, Poland
              13605 Am J Nephrol 2000;20:305–310
              © 2000 S. Karger AG, Basel

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              Tables: 3, References: 23, Pages: 6
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