High blood pressure is a risk factor for the development of microalbuminuria in Japanese subjects with non-insulin-dependent diabetes mellitus

Haneda, Masakazu; Kikkawa, Ryuichi; Togawa, Masaki; Koya, Daisuke; Kajiwara, Nobuyuki; Uzu, Takashi; Shigeta, Yukio

doi:10.1016/1056-8727(92)90034-i

Cited by 35 publications

(22 citation statements)

References 15 publications

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“…These additional variables could include age, diabetes duration, blood pressure (including 24-h blood pressure monitoring), GFR, HbA 1c , retinopathy, and renal biopsy measurements. Prospective studies in type 1 and type 2 diabetic patients generally support the concept that normoalbuminuric and MA patients who progress have significantly higher baseline levels of blood pressure (25,39,43,44,47,(75)(76)(77) and HbA 1c (14,21,22,25,39,40,(43)(44)(45)47,(77)(78)(79) compared with patients that do not progress. However, there is still controversy as to whether increased baseline GFR is a predictor of progression (9,24,(80)(81)(82)(83)(84)(85).…”

Section: Need For New Markers and Predictors Of Diabetic Nephropathy mentioning

confidence: 98%

“…One produced similar (43) and the other produced higher values (44) of progression to proteinuria than the group A studies (Table 3). Five papers (38,(45)(46)(47)(48) were in group C because of the MA definition used (Table 3). Progression from normoalbuminuria to MA varied markedly from 5.9 to 57.6%, whereas progression from normoalbuminuria to proteinuria varied from 0 to 11.8%.…”

Section: Type 2 Diabetesmentioning

confidence: 99%

“…Gall., H.-H. Parving, personal communication) observed, after 5 years of follow-up, approximately the same progression rate to proteinuria as seen in group A studies, but return to normoalbuminuria was not defined in this cohort (Table 4). Five studies were classified as group C because of MA definitions (38,45,47,48,54) (Table 4). In these studies, the progression rates from MA to proteinuria ranged from 0 to 40%, and these articles were not used in the risk calculations.…”

Section: Type 2 Diabetesmentioning

confidence: 99%

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The need for early predictors of diabetic nephropathy risk: is albumin excretion rate sufficient?

2000

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Initial studies showing an ~80% rate of progression from microalbuminuria (MA) to proteinuria in type 1 diabetic patients led to the broad acceptance of MA as a useful clinical predictor of increased diabetic nephropathy (DN) risk. Some MA patients, however, have quite advanced renal structural changes, and MA may, in these cases, be a marker rather than a predictor of DN. More recent studies have observed only about a 30-45% risk of progression of MA to proteinuria over 10 years, while about 30% of type 1 diabetic patients with MA became normoalbuminuric and the rest remained microalbuminuric. The finding that some MA patients have only mild diabetic renal lesions is consistent with the lower than originally estimated risk of progression from MA to proteinuria and with the notion that some MA patients revert to normoalbuminuria. To increase the complexity of the scenario, some normoalbuminuric long-standing type 1 diabetic patients have well-established DN lesions and ~40% of all patients destined to progress to proteinuria are normoalbuminuric at initial screening, despite many years of diabetes. A similar picture is emerging in type 2 diabetic patients, although fewer studies have been conducted. Thus, the predictive precision for MA to progress to overt nephropathy over the subsequent decade or so is considerably less than originally described. It is unclear whether this is due to changes in the natural history of DN resulting from improved glycemia and blood pressure control, or whether there were overestimates of risk in the original studies due to the small sample sizes, post hoc analyses, and variable MA definitions. Albumin excretion rate (AER) remains the best available noninvasive predictor of DN risk and should be regularly measured according to established guidelines. However, AER may be unable to define patients who are safe from or at risk of DN with an accuracy that is adequate for optimal clinical decision making or for the design of certain clinical trials. Investigations into new risk markers or into the combined use of several currently available predictive parameters are needed.

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Section: Need For New Markers and Predictors Of Diabetic Nephropathy mentioning

confidence: 98%

Section: Type 2 Diabetesmentioning

confidence: 99%

Section: Type 2 Diabetesmentioning

confidence: 99%

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The need for early predictors of diabetic nephropathy risk: is albumin excretion rate sufficient?

2000

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“…Thus, the role of the ⑀2 allele as the prognostic factor for DN should be confirmed by a cohort study. Also, the role of this polymorphism on the onset of microalbuminuria, which is a powerful predictor of the late development of persistent overt proteinuria and ESRD in subjects with type 2 diabetes (18,19), has not been established in previous studies.…”

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confidence: 99%

APOE Polymorphism and the Progression of Diabetic Nephropathy in Japanese Subjects With Type 2 Diabetes

et al. 2003

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OBJECTIVE -The aim of this study is to clarify the conflicting results of the ⑀2/⑀3/⑀4 APOE polymorphism as a risk factor on diabetic nephropathy by a cohort study. RESEARCH DESIGN AND METHODS-A total of 429 Japanese subjects with type 2 diabetes and with normoalbuminuria (n ϭ 299) or with microalbuminuria (n ϭ 130) were enrolled in a prospective observational follow-up study during 1995-1998 and followed until 2001 (for at least 3 years). The endpoint was the occurrence of a renal event defined as the progression to a higher stage of diabetic nephropathy.RESULTS -During the study (the mean follow-up period: 4.4 Ϯ 1.0 years), 31 of 429 subjects progressed: 21 from normoalbuminuria to microalbuminuria and 10 from microalbuminuria to overt proteinuria. The allele frequency of the APOE polymorphism was significantly different between the progressors and the nonprogressors. Eight of 42 ⑀2 carriers (19%) progressed, whereas 23 of 387 noncarriers (6%) progressed with a relative risk of 3.2 (95% CI 1.5-6.7). When subjects were stratified by renal status at baseline, each relative risk for the progression in the ⑀2 carriers was 2.7 (0.99 -7.4) in those with normoalbuminuria and 4.2 (1.3-13.3) in those with microalbuminuria. Furthermore, when analyzed only in subjects with normoalbuminuria and short duration of diabetes (Ͻ15 years) at baseline, the risk in the ⑀2 carriers became higher to 3.2 (1.2-8.8).CONCLUSIONS -Our follow-up study indicates that the ⑀2 allele of the APOE polymorphism is a prognostic risk factor for both the onset and the progression of diabetic nephropathy in Japanese type 2 diabetes. Diabetes Care 26:2416 -2420, 2003D iabetic nephropathy (DN) associated with type 2 diabetes is a leading cause of end-stage renal disease (ESRD) in Japan and the U.S. (1,2). Although long-standing hyperglycemia is an important risk factor for the development of DN, epidemiologic and family studies suggest that genetic susceptibility to this complication is also required (3). The abnormalities of lipid metabolism have been proposed as one plausible mechanism in the pathogenesis of the development of DN (4). Thus, the genes encoding components of this pathway that regulate lipid metabolism can be considered as candidate genes susceptible to DN (5).Apolipoprotein E (apoE) is a 299-amino acid glycoprotein that plays a central role in lipid metabolism. ApoE is well known to consist of three common isoforms (E2, E3, E4) encoded by three alleles (⑀2, ⑀3, ⑀4) in exon 4 of the apoE gene (APOE) (6). The lipid profiles or atherogenic factors are, in part, determined by this genetic variation of APOE (6). Carriers of apoE4 have higher plasma levels of total cholesterol and low-density lipoprotein cholesterol than carriers of apoE2 or apoE3 homozygotes (6). On the other hand, the binding of apoE2 to lipoprotein receptors is defective in comparison with that of E3 or E4 and results in delayed clearance of triglyceride (TG)-rich lipoprotein.Recently, this ⑀2/⑀3/⑀4 polymorphism of APOE has been investigated for the association with DN ...

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“…This complication develops in less than half of all diabetic patients [4, 5]and is classically preceded by a period of microalbuminuria, i.e., a slight elevation in urinary albumin excretion rate (UAER) [2, 6]. Poor glycemic control [7], hypertension [8, 9], and altered renal hemodynamics [10, 11, 12]only partially, but not entirely, explain the development of diabetic nephropathy. Evidence that diabetic nephropathy clusters within families both in IDDM and NIDDM suggests the influence of genetic factors [13, 14].…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism and Diabetic Albuminuria in Patients with NIDDM Followed Up for 9 Years

Xiao-hong¹,

Rantalaiho

Wirta

et al. 1998

Nephron

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Nephropathy is a major cause of premature morbidity and mortality in patients with non-insulin-dependent diabetes mellitus (NIDDM). The insertion/deletion (I/D) polymorphism of angiotensin-converting enzyme (ACE) is a genetic determinant of plasma ACE levels. Recent studies have found I/D polymorphism of the ACE gene to be associated with nephropathy in NIDDM. This association has not been evaluated in prospective studies. We, therefore, studied the relationship between ACE gene I/D polymorphism and diabetic albuminuria and glomerular filtration rate (GFR) in 83 NIDDM patients followed up for 9 years. At baseline, 29% (24 of 83) of the diabetic patients had an increased (>30 mg/24 h) urinary albumin excretion rate (UAER) and the prevalence of albuminuria at the 9-year examination was 35% (29 of 83). During the follow-up period, systolic blood pressure (p = 0.044), prevalence of hypertension (p < 0.01), and fasting blood glucose levels (p < 0.01) increased, while high-density lipoprotein cholesterol (p < 0.01) decreased. The declines of GFR during the follow-up period were 8.5, 14.1, and 16.3% within genotype groups of II, ID, and DD, respectively (p values for decreases: NS for II, <0.001 for ID, and <0.001 for DD). Patients with the DD genotype tended to have a steeper decrease of GFR, but the change was not statistically significant between the genotype groups. The increases of UAER during the follow-up period were 35.1, 8.3, and 122.4% within genotype groups of II, ID, and DD, respectively, but p values for all increases were not significant. Parallel to GFR, patients with the DD genotype tended to have a steeper increase of UAER, but the change was not statistically significant between the genotype groups. There were no differences in the ACE genotype distribution and allele frequencies between the patients with or without albuminuria either at follow-up or in cross-sectional settings. In conclusion, this 9-year follow-up study does not support the hypothesis that the ACE I/D polymorphism is a major genetic marker of diabetic nephropathy in NIDDM patients.

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High blood pressure is a risk factor for the development of microalbuminuria in Japanese subjects with non-insulin-dependent diabetes mellitus

Cited by 35 publications

References 15 publications

The need for early predictors of diabetic nephropathy risk: is albumin excretion rate sufficient?

The need for early predictors of diabetic nephropathy risk: is albumin excretion rate sufficient?

APOE Polymorphism and the Progression of Diabetic Nephropathy in Japanese Subjects With Type 2 Diabetes

Angiotensin-Converting Enzyme Insertion/Deletion Polymorphism and Diabetic Albuminuria in Patients with NIDDM Followed Up for 9 Years

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