Hemodynamically mediated glomerular injury and the progressive nature of kidney disease

Bm, Brenner

doi:10.1038/ki.1983.72

Cited by 572 publications

(269 citation statements)

References 52 publications

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“…Alternatively, the lesion could reflect a compensatory response to nephron loss caused by the vascular and interstitial effects of cyclosporine and tacrolimus. Thus, it is believed that compensatory glomerular hypertrophy can result in capillary hyperfiltration, endothelial injury, mesangial dysfunction, and progressive segmental or global glomerulosclerosis (114). A possible link between glomerulosclerosis and local activation of the renin angiotensin system is suggested by experiments demonstrating stimulation of extracellular matrix protein synthesis by rat glomerular mesangial cells exposed to angiotensin II (115).…”

Section: Glomerular Pathologymentioning

confidence: 97%

Tacrolimus (FK506)-Associated Renal Pathology

Randhawa¹,

Starzl

Demetris³

1997

Advances in Anatomic Pathology

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Section: Glomerular Pathologymentioning

confidence: 97%

Tacrolimus (FK506)-Associated Renal Pathology

Randhawa¹,

Starzl

Demetris³

1997

Advances in Anatomic Pathology

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“…2 Glomerular and tubular theories for the development of hyperfiltration (HF) in diabetes early decreases in whole-kidney GFR may reflect a generalised decrease in single-nephron GFR. By contrast, at later stages of nephropathy, nephron dropout leads to compensatory hyperfiltration in remaining nephrons [5].…”

Section: Hyperfiltration At Whole-kidney and Single-nephron Levelmentioning

confidence: 99%

“…However, it remains uncertain whether hyperfiltration is merely a marker of glycaemic control or whether it exerts a pathogenetic role in human diabetic nephropathy, independently of factors such as HbA 1c , blood pressure, age and pubertal status, duration of diabetes, AER and smoking [3,4]. Experimental models of hyperfiltration include hyperfiltration at the single-nephron level, in the whole kidney in the intact animal and in the remnant kidney after subtotal nephrectomy [5,6]. The latter has a human counterpart in advanced kidney disease.…”

Section: Introductionmentioning

confidence: 99%

The clinical significance of hyperfiltration in diabetes

et al. 2010

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Glomerular filtration rate is commonly elevated in early diabetes and patients with this symptom are arbitrarily considered to have hyperfiltration. The prevalence of hyperfiltration in type 1 diabetes varies from less than 25% to more than 75%. The corresponding figures in type 2 diabetes are significantly lower, ranging between 0% and more than 40%. Several factors, methodological and biological, may contribute to the wide variation in estimates of hyperfiltration prevalence. Methodological differences in measurement and evaluation of GFR apply in particular to the handling of plasma disappearance curves of filtration markers. Biological factors that may influence GFR in the hyperfiltration range include glycaemic control, diabetes duration, BMI, sex, pubertal status in type 1 diabetes and age in type 2 diabetes. Hyperglycaemia may influence GFR and albuminuria, and may therefore confound the evaluation of hyperfiltration as an independent risk factor for diabetic nephropathy. Adequate assessment of the relationship between glycaemic control, GFR and AER therefore requires serial measurements of all three variables followed by multivariate analysis. A recent meta-analysis of ten type 1 diabetes studies concluded that the presence of hyperfiltration at baseline more than doubled the risk of developing micro-or macroalbuminuria at follow-up. However, not all studies allowed for confounding factors or regression dilution bias. Future studies will therefore need to address the independent role of hyperfiltration, not only in the evolution of albuminuria, but also in the subsequent decline of GFR.

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“…In kidney diseases, up-regulation of VEGF and its receptor suggests that VEGF participates in stimulating endothelial cell proliferation after glomerular injury [53]. After the induction of experimental diabetes, the glomerular capillary tuft undergoes hypertrophy accompanied by increased blood flow [54]. These early changes are possibly pathogenetically linked to the subsequent expansion of mesangial ECM and increased permeability to macromolecules [55].…”

Section: Discussionmentioning

confidence: 99%