Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On 42 patients (25 males, 17 females) at the age of 46.1 +/- 13.4 years with a proliferative diabetic retinopathy clinical and laboratory examinations were performed for the proof of a renal lesion. This disease was found in 59.5% of the cases. In the foreground of the pathological findings were a proteinuria, a restriction of the creatinine clearance and of the concentration power of the kidneys as well as the hypertension. The diabetic nephropathy had its peak of frequency between the 50th and 60th year of age and showed significant relations to the duration of diabetes as well as to be early age of manifestation. Close ophthalmological and nephrological examinations, particularly of the juvenile diabetics, should render possible an early recognition and treatment of the diabetic microangiopathy.
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PMID:[Kidney changes in patients with proliferative diabetic retinopathy]. 648 27

In Caucasian patients with insulin-dependent diabetes mellitus (IDDM) proliferative diabetic retinopathy (PDR) and persistent proteinuria (PP) are associated, and major risk factors for development of microangiopathy have been identified. The aim of the present study was to evaluate whether these risk factors are also relevant and whether an association exists between the microangiopathic complications in Japanese IDDM-patients. A clinic-based cohort of 324 Japanese IDDM-patients was followed (a mean follow-up of 7 years). Annual examination for development of PDR and PP was performed. Fifty-eight patients developed PDR and 24 developed PP. Development of PDR was associated to high HbA1c-levels, i.e., the 4th quartile (RR 7.9, P < 0.0001), background retinopathy at admission (RR 9.9, P < 0.0001), high age at diabetes onset (RR 2.9, P < 0.0001) and female gender (RR 1.7, P < 0.05). Development of PP was associated to high HbA1c-levels (RR 2.8, P < 0.001) and background background retinopathy at admission (RR 7.9, P < 0.0001). The risk of developing PP was 9 times higher in patients developing PDR than in patients not developing PDR (P < 0.0001). The effect of metabolic control in our cohort was similar to that found in the DCCT and SDIS studies. In conclusion, development of PP is closely associated with PDR, also in Japanese IDDM-patients. The effect of metabolic control is the same as in Caucasian patients. Development of malignant angiopathy in IDDM-patients is not confined to Caucasian IDDM-patients, and the incidence rates are comparable to those found in Caucasian IDDM.
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PMID:Metabolic regulation and microangiopathy in a cohort of Japanese IDDM-patients. 859 14

Hypercholesterolemia is a major determinant of the decline of renal function in patients with diabetes. Apolipoprotein E polymorphism may influence the metabolism of lipoprotein in diabetic patients. The purpose of this study was to investigate the association between genetic polymorphisms in apolipoprotein E and the progression of diabetic nephropathy in patients with non-insulin-dependent diabetes mellitus over a 10-year period (13 to 37 years; median, 20 years). Subjects with a stable renal function without overt proteinuria had a higher cholesterol level, lower incidences of hypertension and proliferative diabetic retinopathy, and a higher frequency of the E4 allele than subjects with a decline in renal function (end-stage renal failure requiring dialysis treatment). In the diabetic patients, the apolipoprotein E4 carriers had a higher cholesterol level than did the noncarriers. The survival rate from renal disease in the apolipoprotein E4 carriers was higher than in the noncarriers among the diabetic patients. Apolipoprotein E polymorphism and hypertension were identified as independent risk factors for the progression to renal failure. Results indicate that apolipoprotein E polymorphism is associated with the progression of diabetic nephropathy. Presence of the apolipoprotein E4 allele is a protective factor, and other alleles are risk factors.
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PMID:Apolipoprotein E4 reduces risk of diabetic nephropathy in patients with NIDDM. 953 Nov 84

Starting from identical patients with type 2 diabetes, we compared the 20-year predictions of two computer simulation models, a 1998 version of the IMIB model and version 2.17 of the Global Diabetes Model (GDM). Primary measures of outcome were 20-year cumulative rates of: survival, first (incident) acute myocardial infarction (AMI), first stroke, proliferative diabetic retinopathy (PDR), macro-albuminuria (gross proteinuria, or GPR), and amputation. Standardized test patients were newly diagnosed males aged 45 or 75, with high and low levels of glycated hemoglobin (HbA(1c)), systolic blood pressure (SBP), and serum lipids. Both models generated realistic results and appropriate responses to changes in risk factors. Compared with the GDM, the IMIB model predicted much higher rates of mortality and AMI, and fewer strokes. These differences can be explained by differences in model architecture (Markov vs. microsimulation), different evidence bases for cardiovascular prediction (Framingham Heart Study cohort vs. Kaiser Permanente patients), and isolated versus interdependent prediction of cardiovascular events. Compared with IMIB, GDM predicted much higher lifetime costs, because of lower mortality and the use of a different costing method. It is feasible to cross-validate and explicate dissimilar diabetes simulation models using standardized patients. The wide differences in the model results that we observed demonstrate the need for cross-validation. We propose to hold a second 'Mt Hood Challenge' in 2001 and invite all diabetes modelers to attend.
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PMID:The Mt. Hood challenge: cross-testing two diabetes simulation models. 1108 May 63

A case of a 59-year-old male patient with advanced microangiopathic complications at the diagnosis of diabetes mellitus is reported. The patient was referred to ophthalmological investigation due to progressive loss of visual acuity. Although diabetes mellitus was not known, proliferative diabetic retinopathy with significant visual loss was found at fundus examination. Not only newly diagnosed diabetes mellitus (initial fasting blood glucose 19.0 mmol/, HbA1c: 11.6%) but the presence of advanced sensory, motor and autonomic diabetic neuropathy (nervus peroneus motor conduction velocity: 32.1 m/s, nervus suralis sensory conduction velocity could not be detected, postural decrease in systolic blood pressure: 20 mmHg, beat-to-beat variation 6 beats/min, 30:15 ratio 1.03) as well as signs of advanced diabetic nephropathy (daily urinary protein excretion: 1.2-5.7 g, serum creatinine value: 101 mumol/l, sitting blood pressure: 150/100-180/100 mmHg) could be documented by further investigations at Medical Department. Avoiding short-term strict metabolic control insulin therapy was initiated and adequate long-term diabetic control was achieved later (HbA1c: 6.5-6.2%). In order to classify the diabetes, repeated measurements of serum C-peptide, ICA, GADA and IA2-antibodies were performed and type 2 diabetes was diagnosed. After a transient deterioration the proliferative retinopathy remained unchanged. Although laser photocoagulation was performed, no improvement in the visual acuity could be achieved. Only a minor improvement of neurological alterations was documented by repeated electrophysiological investigation at follow-up. Although the antihypertensive treatment (ACE-inhibitor drug in combination with calcium channel blocker) resulted in a significant decrease of elevated blood pressure, only a transient improvement of proteinuria could be achieved. Despite regular control, the advanced microangiopathic complications of diabetes mellitus carry poor prognosis.
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PMID:[Advanced microangiopathic complications at the diagnosis of diabetes mellitus]. 1155 63

Three thousand and forty nine patients diagnosed with diabetes mellitus were examined in 13 community (district) hospitals in Lampang from January to December 2002. Complete eye examination with standard protocol was used to determine the prevalence and severity of diabetic retinopathy. The prevalence of the background or non-proliferative diabetic retinopathy (BDR or NPDR) was 18.9% and proliferative diabetic retinopathy (PDR) was 3% in all age groups. For the relationship of the duration of diabetes, it showed that the longer the duration of diabetes the higher the prevalence of diabetic retinopathy. In BDR or NPDR, the retinopathy varied from 13.11 to 22.91% in persons having diabetes for less than 10 years and up to 42.86% in those with diabetes for up to 20 years. In the PDR group, the prevalence was 2.15 to 2.42% in persons with diabetes for less than 10 years and up to 10.20% for those with diabetes for up to 20 years. The severity of retinopathy was found to be not only related to a longer duration of diabetes but also related to higher glycosylated hemoglobin levels, higher systolic blood pressure and the presence of proteinuria.
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PMID:Prevalence of diabetic retinopathy in relation to duration of diabetes mellitus in community hospitals of Lampang. 1582 7

Diabetic retinopathy is one of the leading causes of blindness in working-age individuals. Diabetic patients with proteinuria or those on dialysis usually present severe forms of diabetic retinopathy, but the association of diabetic retinopathy with early stages of diabetic nephropathy has not been entirely established. A cross-sectional study was conducted on 1214 type 2 diabetic patients to determine whether microalbuminuria is associated with proliferative diabetic retinopathy in these patients. Patients were evaluated by direct and indirect ophthalmoscopy and grouped according to the presence or absence of proliferative diabetic retinopathy. The agreement of diabetic retinopathy classification performed by ophthalmoscopy and by stereoscopic color fundus photographs was 95.1% (kappa = 0.735; P < 0.001). Demographic information, smoking history, anthropometric and blood pressure measurements, glycemic and lipid profile, and urinary albumin were evaluated. On multiple regression analysis, diabetic nephropathy (OR = 5.18, 95% CI = 2.91-9.22, P < 0.001), insulin use (OR = 2.52, 95% CI = 1.47-4.31, P = 0.001) and diabetes duration (OR = 1.04, 95% CI = 1.01-1.07, P = 0.011) were positively associated with proliferative diabetic retinopathy, and body mass index (OR = 0.90, 95% CI = 0.86-0.96, P < 0.001) was negatively associated with it. When patients with macroalbuminuria and on dialysis were excluded, microalbuminuria (OR = 3.3, 95% CI = 1.56-6.98, P = 0.002) remained associated with proliferative diabetic retinopathy. Therefore, type 2 diabetic patients with proliferative diabetic retinopathy more often presented renal involvement, including urinary albumin excretion within the microalbuminuria range. Therefore, all patients with proliferative diabetic retinopathy should undergo an evaluation of renal function including urinary albumin measurements.
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PMID:Proliferative diabetic retinopathy is associated with microalbuminuria in patients with type 2 diabetes. 1690 78

Vascular endothelial growth factor (VEGF) plays a key role in the development of both proliferative diabetic retinopathy (PDR) and diabetic macular oedema (DMO). In recent years, anti-VEGF agents have emerged as new approaches to the treatment of these devastating diabetic complications. Although Phase III studies in the diabetic population are needed, intravitreal anti-VEGF therapy is currently being used in clinical practice. Intravitreal injection is an effective means of delivering anti-VEGF drugs to the retina. However, this is an invasive procedure associated with potentially serious complications, such as endophthalmitis or retinal detachment, which may be significant for patients requiring serial treatment over many years. In addition, although delivered within the vitreous, anti-VEGF drugs could pass into the systemic circulation, which could potentially result in hypertension, proteinuria, increased cardiovascular events and impaired wound healing. Pegaptanib, ranibizumab and bevacizumab are the currently available anti-VEGF agents. Ranibizumab and bevacizumab block all VEGF isoforms, thus impairing both physiological and pathological neovascularisation. Pegaptanib only blocks the VEGF(165) isoform, and would therefore seem the best option for avoiding systemic adverse effects in diabetic patients, although this remains to be demonstrated in clinical trials. In this regard, head-to-head studies designed to evaluate not only the efficacy, but also the systemic adverse effects of these drugs in a high-risk population such as diabetic patients are warranted.
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PMID:Intravitreous anti-VEGF for diabetic retinopathy: hopes and fears for a new therapeutic strategy. 1860 60

The incidence of type 1 diabetes is increasing in Denmark as well as the rest of the world. Due to diabetes-related micro- and macrovascular complications, the morbidity and the mortality is higher among type 1 diabetic patients. The aim of this thesis was to examine a population-based cohort of 727 type 1 diabetic patients from Fyn County, Denmark, with an onset of diabetes before 1 July 1973 in order to: (1) Evaluate the all-cause mortality rates and the influence of sex, duration of diabetes and calendar year of diagnosis in a 33-year follow-up (Paper I). (2) Examine glycaemic regulation, lipids and renal dysfunction as risk factors for all-cause mortality, cardiovascular mortality and IHD (Paper II). (3) Estimate the prevalence of DR as well as the 25-year incidence of PDR and associated risk factors in long-time surviving patients (Paper III). (4) To compare the grading of DR between ETDRS seven standard field 30 degrees stereoscopic colour films and nine field 45 degrees monoscopic digital colour images in long-term surviving patients (Paper IV). In the years 1973-2006 an overall MR of 22.3 per 1000 person-years was found. Furthermore a relative mortality of 3.4 was found as compared to the general population in Denmark. The relative mortality was especially high for patients aged 30-39 (SMR 9.8). There was a tendency towards a better survival for patients diagnosed after 1964. This was especially seen for men. Diabetes was the most common cause of death for those who died in the group. In 1993-1996 blood samples were drawn and glycaemic regulation, lipids and renal markers were subsequently used as predictors of all-cause mortality, cardiovascular mortality and ischaemic heart disease. Glycaemic regulation, dyslipidaemia and creatinine were all significantly associated with all three endpoints. Furthermore, variations in glycaemic control were also identified as a risk factor for overall mortality. Two hundred and one patients were examined for diabetic retinopathy in 1981-1982 and 2007-2008. At follow-up, 97.0% had DR and 42.9% of all patients without PDR at baseline developed this during the follow-up period. Patients who had had a poor glycaemic regulation as well as those who had NPDR at baseline were more likely to develop PDR than the remaining patients. On the other hand, other risk factors such as high blood pressure and proteinuria did not predict PDR. In the comparative study between ETDRS seven standard field 30 degrees stereoscopic colour films and nine field 45 degrees monoscopic digital colour images, 43 eyes of 43 patients were examined in 2008. A poor correlation was found between the two methods: only 29.3% were graded alike. In the remaining, the level of DR was graded higher in the digital photos. Among these, PDR was detected in three eyes using digital photos but remained undetected on all films. This suggests that digital photos with wide fields are the best way to detect DR in long-term type 1 diabetic patients. Overall, it is concluded that mortality is still higher among type 1 diabetic patients. This depends, among other things, on glycaemic regulation, lipid status and, partly, renal dysfunction. Diabetic retinopathy is almost universal in long-term type 1 diabetic patients, and almost half of all patients will develop PDR in 25 years. Nine field digital photos provide the best grading of retinopathy in long-term type 1 diabetic patients.
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PMID:Long-term mortality and retinopathy in type 1 diabetes. 2050 Jul 31

The vascular endothelial growth factor (VEGF) plays a key role in the development of proliferative diabetic retinopathy (PDR) and diabetic macular edema (DME), resulting in a significant visual loss among patients with diabetes mellitus. Systemic VEGF-A and the interplay between membrane-bound VEGF receptors and VEGF-R1 (soluble form) are key to angiogenesis and vasculogenesis. Furthermore, patients with diabetes have a higher risk of hypertension and proteinuria, two surrogate markers of systemic VEGF inhibition. Pegaptanib, ranibizumab, bevacizumab and roboxistaurin are the currently available anti-VEGF agents. Agents with activity occurring later down the angiogenic pathway and those drugs with potential to synergize with anti-VEGF-A technologies are being developed. In recent years, inhibition of ocular VEGF has emerged as a promising treatment modality for diabetes and is currently undergoing evaluation in clinical trials. A potential role for these anti-VEGF agents in the prevention of PDR and DME are also emerging.
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PMID:Anti-angiogenesis drugs in diabetic retinopathy. 2093 97


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