Microalbuminuria, blood pressure and diabetic renal disease: origin and development of ideas

Mogensen, Carl Erik

doi:10.1007/s001250051151

Cited by 250 publications

(143 citation statements)

References 340 publications

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“…Detection of early decline in GFR has been possible at the stage of new onset microalbuminuria, well before the onset of overt nephropathy. In type 2 diabetes, the onset of hypertension promotes a rise in AER and a decline in GFR [7]. In our study we have correlated the degree of albuminuria with respect to eGFR in type 2 diabetics and hypertensives.…”

Section: Introductionmentioning

confidence: 85%

Correlation of Microalbuminuria with Estimated GFR (eGFR) by Cockcroft–Gault and MDRD Formula in Type 2 Diabetics and Hypertensives

et al. 2014

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Increase in urine albumin excretion rate (AER) precede a fall in glomerular filtration rate in patients developing diabetic chronic kidney disease (CKD). Our results have shown that 7 (50 %) of diabetic and hypertensive individuals with decreased GFR do not have increased AER. In this cross-sectional study, we measured AER of 75 patients with type 2 diabetes and hypertension by immunoturbidimetric method. We correlated the results with eGFR values obtained by Cockcroft-Gault and MDRD method. The method used was not a compensated method. We measured serum creatinine by modified Jaffe's kinetic method in autoanalyzer XL-600. Analysis of data showed positive correlation between eGFR and microalbuminuria by both the methods with eGFR \60 mL/min/ 1.73 m 2 . Pearson's correlation co-efficient (r) was 0.9 (p = 0.0001) by Cockcroft-Gault formula and 0.69 (p = 0.0063) by MDRD formula. Our results concluded that there was positive correlation between AER and eGFR \60 mL/min/1.73 m 2 . We have recognized that these two parameters provide a complimentary benefit in management of cases with CKD.

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Section: Introductionmentioning

confidence: 85%

Correlation of Microalbuminuria with Estimated GFR (eGFR) by Cockcroft–Gault and MDRD Formula in Type 2 Diabetics and Hypertensives

et al. 2014

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“…This might well contribute to the increased leakiness of the glomerular capillaries, in particular if the filter is not of a completely normal composition as in the diabetic glomerulopathy. The arteriolar hyalinosis could thereby be part of the structural explanation of the higher albumin excretion [24]. Also, in situations with hypotension or during increased sympathetic tone or other vasoconstrictive stimulation such segments are probably not able to dilate, which could then lead to damage due to hypoperfusion and hypofiltration.…”

Section: Discussionmentioning

confidence: 99%

Structural changes in renal arterioles in Type I diabetic patients

Østerby

Hartmann

Bangstad³

2002

Diabetologia

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Abnormalities of arteriolar structure in the diabetic kidney were described in histological studies in the 1940's and 1950's (reviewed in [1]). The lesion consisting of a homogeneous material in the vessel wall was termed arteriolar hyalinosis due to the appearance of the PAS-positive a-cellular material. Staining characteristics were similar to those of glomerular fibrinoid caps and capsular drops. All these changes were therefore referred to one group, the exudative lesions [2], and increased leakage of plasma protein into the arteriolar wall was considered an important pathogenetic mechanism [3].Arteriolar hyalinosis is also observed in the kidneys of elderly non-diabetic patients and in hyperten- Diabetologia (2002) Abstract Aims/hypothesis. We aimed to obtain data on arteriolar structure in a follow-up study of microalbuminuric diabetic patients. Methods. Kidney biopsies were obtained at baseline and after 8 years in 18 Type I (insulin-dependent) diabetic patients. Albumin excretion rate, blood pressure and HbA 1C were measured regularly, and the glomerular filtration rate (GFR) was measured at the time of the kidney biopsy. The biopsy was embedded into plastic blocks and serially sectioned with 1 mm sections. In levels 25 mm apart, afferent and efferent arteriolar profiles were identified and digitised in the electron microscope. The extra-cellular matrix as volume fraction of the media was measured, and estimates of thickness of matrix, media, endothelium and lumen were obtained. Baseline and follow-up biopsies were studied concomitantly. Results. A large increase was seen in matrix volume fraction in afferent (p = 0.0001) and in efferent arterioles (p = 0.0004). Estimated thickness of media and matrix increased, whereas endothelial cell thickness decreased, over the 8 years. There was a correlation between the parameters of diabetic glomerulopathy and arteriolar parameters in the biopsies done at 8 years, basement membrane thickness compared with afferent matrix volume fraction: r = 0.74, p = 0.0005. Also aggravation of glomerulopathy and arteriolar structure over 8 years showed positive correlation. Arteriolar parameters correlated with the albumin excretion rate (AER) and inversely with GFR. Conclusion/interpretation. The arteriolar accumulation of matrix parallels that taking place in glomeruli and shows association with functional parameters over 8 years in Type I diabetic patients with microalbuminuria. These changes are considered an important part of the structural lesions in the diabetic kidney underlying the development of diabetic nephropathy. [Diabetologia (2002) 45:542±549]

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“…It is considered to be an early indicator of renal and cardiovascular disease risk, 2,3 as well as of an increased risk of all-cause mortality. 4,5 Thus, microalbuminuria is an indication for aggressive intervention to improve glycaemic and blood pressure (BP) control and to reduce cardiovascular risk factors.…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone reduces urinary albumin excretion in type II diabetes

et al. 2003

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This study examines the effect of rosiglitazone on urinary albumin excretion (UAE) in patients with type II diabetes. Urinary albumin : creatinine ratio (ACR) was measured in a 52-week, open-label, cardiac safety study comparing rosiglitazone and glyburide. Patients were randomised to treatment with rosiglitazone 4 mg b.i.d. or glyburide. ACR was measured at baseline and after 28 and 52 weeks of treatment. Statistically significant reductions from baseline in ACR were observed in both treatment groups at week 28. By week 52, only the rosiglitazone group showed a significant reduction from baseline. Similar results were observed for the overall study population and for the subset of patients with baseline microalbuminuria. For patients with microalbuminuria at baseline, reductions in ACR did not correlate strongly with reductions in glycosylated haemoglobin, or fasting plasma glucose, but showed strong correlation with changes in mean 24-h systolic and diastolic blood pressure for rosiglitazone-treated patients (DACR vs Dmean 24-h systolic blood pressure, r ¼ 0.875; DACR vs Dmean 24-h diastolic blood pressure, r ¼ 0.755; Po0.05 for both). No such correlation was observed for glyburide-treated patients. In conclusion, rosiglitazone treatment was associated with a decrease in urinary albumin excretion. These findings suggest a potential beneficial effect of rosiglitazone in the treatment or prevention of renal and vascular complications of type II diabetes.

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Microalbuminuria, blood pressure and diabetic renal disease: origin and development of ideas

Cited by 250 publications

References 340 publications

Correlation of Microalbuminuria with Estimated GFR (eGFR) by Cockcroft–Gault and MDRD Formula in Type 2 Diabetics and Hypertensives

Correlation of Microalbuminuria with Estimated GFR (eGFR) by Cockcroft–Gault and MDRD Formula in Type 2 Diabetics and Hypertensives

Structural changes in renal arterioles in Type I diabetic patients

Rosiglitazone reduces urinary albumin excretion in type II diabetes

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