Hemodynamic factors in the genesis of diabetic microangiopathy

Parving, Hans‐Henrik; Viberti, Giancarlo; Keen, H.; Christiansen, John; Lassen, Niels A.

doi:10.1016/0026-0495(83)90210-x

Cited by 319 publications

(163 citation statements)

References 60 publications

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“…Reduction of hydrostatic pressure in the microcirculation has been suggested as a likely factor. Direct [48] and indirect evidence suggest that capillary hydrostatic pressure is elevated in IDDM patients [47,49], while normal capillary pressure (finger nail fold) has been reported in normotensive NIDDM patients [50]. However, increased capillary pressure has been documented in essential hypertension [51] and hypertension was prominent in our NIDDM patients with (83 %) and without (30 %) diabetic nephropathy.…”

Section: Discussionmentioning

confidence: 65%

Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy

et al. 1996

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Insulin-dependent diabetic (IDDM) patients with incipient and overt diabetic nephropathy are characterized by a higher incidence and prevalence of retinopathy and cardiovascular diseases than normoalbuminuric IDDM patients [1,2]. The relative cardiovascular mortality is approximately 40 times higher in diabetic nephropathy as compared to the age-matched population [1]. Furthermore, the prevalence of

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Section: Discussionmentioning

confidence: 65%

Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy

et al. 1996

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“…Glomerular filtration rate (GFR) increases 50% as compared with nonpregnant levels (35) with subsequent decrease in serum creatinine, urea, and uric acid values (36). Also, increases in glomerular filtration rate and minor increases in urinary albumin excretion have been reported early in the course of diabetes (37,38). These events, could explain the lower total proteins, albumin, creatinine and urea levels found in GDM compared to control group.…”

Section: Discussionmentioning

confidence: 99%

Type 2 diabetes-associated genetic variants of FTO, LEPR, PPARg, and TCF7L2 in gestational diabetes in a Brazilian population

Anghebem-Oliveira

Martins

Alberton

et al. 2017

Arch. Endocrinol. Metab.

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Objective: Gestational diabetes mellitus (GDM) is a metabolic disorder that shares pathophysiologic features with type 2 diabetes mellitus. The aim of this study was to investigate the association of the polymorphisms fat mass and obesity-associated (FTO) rs1421085, leptin receptor (LEPR) rs1137100, rs1137101, peroxisome proliferator-activated receptor gamma (PPARg) rs1801282, and transcription factor 7-like 2 (TCF7L2) rs7901695 with GDM. Subjects and methods: 252 unrelated Euro-Brazilian pregnant women were classified into two groups according to the 2015 criteria of the American and Brazilian Diabetes Association: healthy pregnant women (n = 125) and pregnant women with GDM (n = 127), matched by age. The polymorphisms were genotyped using fluorescent probes (TaqMan ® ). Results: All groups were in Hardy-Weinberg equilibrium. The genotype and allele frequencies of the studied polymorphisms did not show significant differences between the groups (P > 0.05). In the healthy and GDM groups, the C allele frequencies (95% CI) of the FTO rs1421085 polymorphism were 36.8% [31-43%]

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“…It is suggested that elevation of intraglomerular capillary pressure, or "glomerular hypertension", is the principal haemodynamic perturbation responsible for glomerular damage [3][4][5][6][7][8]. The hypothesis has also been invoked to explain the progression of various glomerular disorders in man and the development of human diabetic nephropathy [9][10][11][12][13].…”

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confidence: 99%

Enalapril does not alter renal function in normotensive, normoalbuminuric, hyperfiltering Type 1 (insulin-dependent) diabetic children

et al. 1989

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Summary. Using a prospective randomised double-blind crossover design, the effect of the angiotensin converting enzyme inhibitor enalapril compared to a placebo was studied in 18 normotensive, normoalbuminuric Type 1 (insulin-dependent) diabetic children. Each patient had a high normal or dearly elevated glomerular filtration rate (145 ml.min -1. 1.73 m 2 or higher) in the 6 months prior to the study. Enalapril, 0.5 mg.kg -1. day -1, was given for 4 weeks followed by placebo for 4 weeks, or vice versa. At the end of each period, glomerular filtration rate, renal plasma flow, blood pressure, plasma renin activity, and converting enzyme activity were determined. Enalapril caused significant reduction (p= < 0.001) in blood pressure and converting enzyme activity and a rise in plasma renin activity. A slight but not significant rise in glomerular filtration rate and renal plasma flow without change in filtration fraction was observed. These data suggest that the renin angiotensin system is not involved in the glomerular hyperfiltration of Type 1 diabetes, and can be interpreted as showing no evidence for the presence of intraglomerular hypertension in these patients.

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Hemodynamic factors in the genesis of diabetic microangiopathy

Cited by 319 publications

References 60 publications

Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy

Macro-microangiopathy and endothelial dysfunction in NIDDM patients with and without diabetic nephropathy

Type 2 diabetes-associated genetic variants of FTO, LEPR, PPARg, and TCF7L2 in gestational diabetes in a Brazilian population

Enalapril does not alter renal function in normotensive, normoalbuminuric, hyperfiltering Type 1 (insulin-dependent) diabetic children

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