Diabetic nephropathy. An update

Reddi, Alluru S.; Camerini-Dávalos, Rafael A.

doi:10.1001/archinte.150.1.31

Cited by 44 publications

(14 citation statements)

References 136 publications

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“…This trend continued and at 1 year diabetic kidney weight averages exceeded controls by 27%. Similarly, Abrass et al (1988) and Reddi and Camerini-Davalos (1990) demonstrated that whole kidneys in streptozotocininduced diabetic rats enlarge shortly after onset of hyperglycemia. Although clear explanations for diabetic renal hypertrophy remain elusive, it has been suggested that at least in streptozotocin-induced diabetes, depressed proteolysis contributed to increase kidney protein content (Shechter et al, 1994).…”

Section: Kidney Weightsmentioning

confidence: 87%

Significant glomerular basement membrane thickening in hyperglycemic and normoglycemic diabetic‐prone BB Wistar rats

et al. 2004

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The diabetic-prone BioBreeding Wistar rat (BB/DP) is an autoimmune model of insulindependent diabetes mellitus. Approximately 80 -90% of the animals are hyperglycemic (BB/ DP h ) by 90 -120 days of age while those that do not become diabetic in adolescence (BB/DP n ) remain normoglycemic for life. Likewise, rats in the diabetes-resistant (BB/DR) strain are normoglycemic. Although renal morphological studies have been carried out in this model, ultrastructural observations of age-and diabetes-related extracellular matrix (ECM) changes, including glomerular basement membrane (GBM) morphometry, are not available. Moreover, possible renal changes in the relatively uncommon BB/DP n control animals have not been reported. The current electron microscopic study was carried out to investigate temporal changes in detergent-treated acellular ECM in BB/DP h rats at 2 weeks, 3 months, 6 months, and 1 year postonset of moderate hyperglycemia. Age-matched BB/DR and BB/DP n control animals were also examined. Our data demonstrate age-and diabetes-related alterations in mesangial matrix distributions and GBM widths and show for the first time significant increases in GBM thickening in both hyperglycemic (BB/DP h ) and normoglycemic (BB/DP n ) rats when compared to age-matched BB/DR controls. Surprisingly, the rate of increase is greatest in BB/DP n animals. Although the pathogenesis of diabetic basement membrane disease is not completely understood, GBM thickening is widely regarded as a morphological consequence of hyperglycemia. However, data in the current investigation show that ECM alterations, including significantly increased GBM thickness, may occur in genetically diabetic animals in the absence of hyperglycemia. © 2004 Wiley-Liss, Inc. Key words: diabetes; glomerular basement membrane thickness; BB Wistar ratsThe BioBreeding Wistar rat (BB rat) is an autoimmune model of insulin-dependent diabetes mellitus (IDDM) discovered in 1974 in a colony of pathogen-free Wistar rats (Chappel and Chappel, 1983). Like human IDDM, the onset of clinical symptoms in diabetes-prone (BB/DP) BB rats appear during adolescence, generally between 60 and 120 days of age (Butler et al., 1983;Chappel and Chappel, 1983). These are characterized by rapid weight loss, polyuria, polydipsia, ketonuria, and finally death unless exogenous insulin is administered (Chappel and Chappel, 1983;Like and Rossini, 1984). The incidence of diabetes through 120 days of age is 60 -90% in most colonies and averaged 86% in a viral antibody-free NIH colony in Worcester, Massachusetts (Crisa et al., 1992). The diabetes exhibited by BB rats is not attributed to a single dominant or recessive gene, but the etiology seems to include a genetic component (Chappel and Chappel, 1983).

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Section: Kidney Weightsmentioning

confidence: 87%

Significant glomerular basement membrane thickening in hyperglycemic and normoglycemic diabetic‐prone BB Wistar rats

et al. 2004

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“…Furthermore, in patients with CRF due to diabetic nephropathy, anemia is also affected by metabolic disorders. EPO treatment is often ineffective for diabetic nephropathy (15,16), but the precise reason for this blunted effect is not clear.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic use of continuous subcutaneous infusion of recombinant human erythropoietin in malnourished predialysis anemic patients with diabetic nephropathy

Sohmiya

Kakiba

Kato

1998

European Journal of Endocrinology

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We compared the effect of recombinant human erythropoietin (rhEPO) administration by continuous s.c. infusion (CSI) with that of a weekly bolus s.c. injection (SBI) in five malnourished predialysis anemic patients with diabetic nephropathy. rhEPO was either continuously infused at a flow rate of 6000 IU per week (36 IU/h) (CSI group) or injected s.c. at a dose of 6000 IU once a week (SBI group) for 4 weeks, in a cross-over comparative study with a washout period of 4 weeks. Mean Ϯ S.D. plasma EPO levels increased from a basal value of 18.0 Ϯ 4.9 mIU/ml to a steady state value of 70.5 Ϯ 38.9 mIU/ml 2 weeks after the start of CSI of rhEPO (P < 0.05). Increases in reticulocyte count above the basal value were greater in the CSI group than the SBI group at 3 weeks after the start of treatment (0.94 Ϯ 0.35% vs ¹0.03 Ϯ 0.46%, P < 0.05). Increases in Hb concentration above the basal value were much greater in the CSI group than the SBI group at 4 weeks after the start of treatment (2.56 Ϯ 0.77 g/dl vs 0.28 Ϯ 0.62 g/dl, P < 0.05). These findings suggest that rhEPO administration by CSI is more effective than by SBI for improving anemia in malnourished predialysis patients with diabetic nephropathy.

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“…It is characterized by thickening of the basement membranes, mesangial expansion and proliferation, and tubulointerstitial fibrosis (1)(2)(3). The histologic characteristics are caused by excessive deposition of extracellular matrix (ECM) proteins, which are induced by the hyperglycemic milieu (4 -6) via the induction of various growth factors.…”

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confidence: 99%

Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

et al. 2003

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Tubulointerstitial fibrosis is an important component in the development of diabetic nephropathy. Various renal cell types, including fibroblasts, contribute to the excessive matrix deposition in the kidney. Although transforming growth factor-␤ (TGF-␤) has been thought to play a major role during fibrosis, other growth factors are also involved. Here we examined the effects of connective tissue growth factor (CTGF) and IGF-I on collagen type I and III production by human renal fibroblasts and their involvement in glucose-induced matrix accumulation. We have demonstrated that both CTGF and IGF-I expressions were increased in renal fibroblasts under hyperglycemic conditions, also in the absence of TGF-␤ signaling. Although CTGF alone had no effect on collagen secretion, combined stimulation with IGF-I enhanced collagen accumulation. Furthermore, IGF-I also had a synergistic effect with glucose on the induction of collagens. Moreover, we observed a partial inhibition in glucose-induced collagen secretion with neutralizing anti-CTGF antibodies, thereby demonstrating for the first time the involvement of endogenous CTGF in glucose-induced effects in human renal fibroblasts. Therefore, the cooperation between CTGF and IGF-I might be involved in glucose-induced matrix accumulation in tubulointerstitial fibrosis and might contribute to the pathogenesis of diabetic nephropathy.

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Diabetic nephropathy. An update

Cited by 44 publications

References 136 publications

Significant glomerular basement membrane thickening in hyperglycemic and normoglycemic diabetic‐prone BB Wistar rats

Significant glomerular basement membrane thickening in hyperglycemic and normoglycemic diabetic‐prone BB Wistar rats

Therapeutic use of continuous subcutaneous infusion of recombinant human erythropoietin in malnourished predialysis anemic patients with diabetic nephropathy

Connective Tissue Growth Factor and IGF-I Are Produced by Human Renal Fibroblasts and Cooperate in the Induction of Collagen Production by High Glucose

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