Disease relevance of DIANPH

• BACKGROUND: Diabetic nephropathy is the leading cause of end-stage renal disease [1].
• Susceptibility to diabetic nephropathy may be related to a predisposition to arterial hypertension [2].
• We investigated whether captopril, an angiotensin-converting-enzyme inhibitor, would reduce proteinuria in patients with advanced diabetic nephropathy [3].
• The primary outcome was the time to the onset of diabetic nephropathy, defined by persistent albuminuria in overnight specimens, with a urinary albumin excretion rate that was greater than 200 microg per minute and at least 30 percent higher than the base-line level [4].
• Restriction of dietary protein may slow the progression of renal failure in diverse renal diseases, but the extent to which such a diet is beneficial in patients with diabetic nephropathy is uncertain [5].

Psychiatry related information on DIANPH

• 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 [6].
• Using a stricter case definition based on advanced diabetic nephropathy, a comparable risk reduction of 24-32% was observed among the three subgroups, although statistical significance was reached only among Asians [7].
• Smoking cessation may slow nephropathy progression; given the additional health benefits of stopping smoking, this advice is an important part of the strategy of diabetic nephropathy treatment and prevention [8].
• In order to improve the basis upon which to advise women with diabetic nephropathy about pregnancy, we studied the effect of diabetic nephropathy on the course of pregnancy, perinatal outcome, infant development and long-term outcome of the mothers [9].
• Diabetic nephropathy (DNP) develops after latency periods that may vary by several years in approximately one third of patients with diabetes [10].

High impact information on DIANPH

• BACKGROUND: Microalbuminuria and hypertension are risk factors for diabetic nephropathy [4].
• The effect of irbesartan on the development of diabetic nephropathy in patients with type 2 diabetes [4].
• BACKGROUND: In patients with type I diabetes mellitus who do not have uremia and have not received a kidney transplant, pancreas transplantation does not ameliorate established lesions of diabetic nephropathy within five years after transplantation, but the effects of longer periods of normoglycemia are unknown [11].
• Reversal of lesions of diabetic nephropathy after pancreas transplantation [11].
• METHODS: We studied kidney function and performed renal biopsies before pancreas transplantation and 5 and 10 years thereafter in eight patients with type I diabetes but without uremia who had mild to advanced lesions of diabetic nephropathy at the time of transplantation [11].

Chemical compound and disease context of DIANPH

• Two of the diabetic patients had clinical diabetic nephropathy, including hypertension, marked albuminuria, and a substantially reduced creatinine clearance; the other five had normal renal function and only minor clinical indications of complications [12].
• OBJECTIVES: To evaluate the role of AGEs in the development of diabetic nephropathy and retinopathy, we studied pentosidine levels and the clinical characteristics of 48 subjects with insulin-dependent diabetes mellitus [13].
• The past medical history included liver transplantation followed by long term cyclosporin, features of thrombotic thrombocytopenic purpura (TTP) attributed to cyclosporin, type 1 diabetes mellitus and acute renal failure attributed to diabetic nephropathy [14].
• Glucose is a key factor in the development of diabetic complications, including diabetic nephropathy [15].
• Thus, a distinctive alteration that is found in human diabetic nephropathy also occurs in experimental (streptozotocin) diabetes in the rat [16].

Biological context of DIANPH

• The purpose of this study was to determine whether captopril has kidney-protecting properties independent of its effect on blood pressure in diabetic nephropathy [17].
• Familial clustering of diabetic kidney disease. Evidence for genetic susceptibility to diabetic nephropathy [18].
• Advanced glycosylation end products in patients with diabetic nephropathy [19].
• No tubular apoptosis was detected in renal-biopsy specimens from five patients with IgA nephropathy, three patients with nephrosclerosis, two patients with focal glomerulosclerosis, one patient with diabetic nephropathy, six patients with acute tubular necrosis, or four patients with acute and four patients with chronic renal-transplant rejection [20].
• The natural history and epidemiology of diabetic nephropathy. Implications for prevention and control [21].

Anatomical context of DIANPH

• Human and rat mesangial cell receptors for glucose-modified proteins: potential role in kidney tissue remodelling and diabetic nephropathy [22].
• Glomerulopathy in rats with streptozotocin diabetes. Accumulation of glomerular basement membrane analogous to human diabetic nephropathy [23].
• Since glomerular enlargement and accumulation of basement membrane are characteristic of human diabetic nephropathy, the findings also suggest that the streptozotocin-diabetic rat is an appropriate animal model for studies relating to the pathogenesis of this complication of diabetes [23].
• These findings suggest that podocyte loss contributes to the progression of diabetic nephropathy [24].
• Specific imidazolone immunoreactivity was detected in nodular lesions and expanded mesangial matrix of glomeruli, and renal arteries in an advanced stage of diabetic nephropathy, as well as in atherosclerotic lesions of aortas [25].

Associations of DIANPH with chemical compounds

• The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy [26].
• In one set, the probands (n = 11) had no evidence of diabetic nephropathy, with normal creatinine clearance and a urinary albumin excretion rate below 45 mg per day [18].
• Captopril protects against deterioration in renal function in insulin-dependent diabetic nephropathy and is significantly more effective than blood-pressure control alone [17].
• We propose that enhanced transglomerular trafficking of protein may predispose to sclerosis of glomeruli in those Pima Indians with NIDDM who ultimately develop diabetic nephropathy [27].
• Increased collagen-linked pentosidine levels and advanced glycosylation end products in early diabetic nephropathy [13].

Physical interactions of DIANPH

• BACKGROUND: GLUT1 upregulation and increased glucose transport activity may contribute to extracellullar matrix (ECM) accumulation characterizing diabetic nephropathy (DN) [28].
• A substitution (M235T) polymorphism in angiotensinogen (AGT) may interact with ACE I/D polymorphism for the risk of diabetic nephropathy, but their prognostic values have to be established by follow-up studies [29].

Regulatory relationships of DIANPH

• 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 [30].
• Local VEGF activity but not VEGF expression is tightly regulated during diabetic nephropathy in man [31].
• Thus progression of diabetic nephropathy may be promoted by PAI-1 upregulation mediated by the glycated albumin-induced Smad/DNA interactions [32].
• In situ hybridization revealed that hSGK transcription was markedly enhanced in diabetic nephropathy, with particularly high expression in mesangial cells, interstitial cells, and cells in thick ascending limbs of Henle's loop and distal tubules [33].
• TNF-alpha is a cytokine that induces apoptosis and has been implicated in the pathogenesis of diabetic nephropathy [34].

Other interactions of DIANPH

• Therefore, we investigated the association of these VEGF polymorphisms with proliferative diabetic retinopathy and diabetic nephropathy [35].
• These results suggest that the SLC12A3 gene locus is associated with ESRD due to diabetic nephropathy [36].
• These results suggest that the CCR5 promoter 59029 A genotype may be an independent risk factor for diabetic nephropathy in patients with type 2 diabetes [37].
• Chemokine receptor genotype is associated with diabetic nephropathy in Japanese with type 2 diabetes [37].
• Effects of mesangium glycation on matrix metalloproteinase activities: possible role in diabetic nephropathy [38].

Analytical, diagnostic and therapeutic context of DIANPH

• In the other set, the probands (n = 26) had undergone kidney transplantation because of diabetic nephropathy [18].
• CONCLUSIONS--This trial indicates a causal relationship between hyperglycemia and an important lesion of diabetic nephropathy, mesangial matrix expansion, in renal allografts transplanted into diabetic recipients [39].
• Moreover, as these changes persist in cultured lymphoblasts in vitro, these cells should provide a cell culture model to further define the basic mechanisms leading to NHE activation in diabetic nephropathy [40].
• 4.1% of the patients on renal replacement therapy at the end of 1984 were reported as having ESRF due to diabetic nephropathy [41].
• STUDY SELECTION: Randomized, controlled studies were selected for nondiabetic renal disease; randomized, controlled studies or time-controlled studies with nonrandomized crossover design were selected for diabetic nephropathy [42].

References