UMLS:C0011881 - FACTA Search

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Query: UMLS:C0011881 (diabetic nephropathy)
10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The less rigorous attention to the management of the complications of chronic renal insufficiency (CRI) and its comorbid conditions has potentially tragic consequences. In fact, with early recognition and intervention, many of the complications of CRI and its comorbid conditions can be ameliorated or prevented. We review here the most prevalent, troublesome, and potentially preventable complications and comorbidities of CRI with a view toward developing high-quality, cost-effective strategies for delivering early interventional care. Complications of CRI include malnutrition, anemia, disorders of divalent ion metabolism and osteodystrophy, metabolic acidosis, and dyslipidemia. Important comorbid conditions of CRI are hypertension, diabetes mellitus, and cardiovascular disease. Clinical intuition suggests that early intervention will avert morbidity related to the hypoalbuminemia and other nutritional disorders of CRI, the metabolic acidosis, and the dyslipidemias, but prospective data are lacking at present. Correction of anemia, usually with recombinant human erythropoietin, may be key to the prevention of cardiac disease and other comorbidities of CRI. Incipient disorders of bone and mineral metabolism are managed prospectively using such measures as protein restriction to reduce phosphorus intake, phosphate binders, calcium supplementation, and vitamin D analogues. Hypertension, whatever its original etiology, is clearly an important risk factor for the progression of kidney failure and for the development of diffuse vascular disease; appropriate and aggressive treatment is essential. In patients with diabetic nephropathy, the principles of both primary and secondary prevention have been validated in several large trials of glycemic and blood pressure control. The seeds of these insidious, challenging, and costly comorbid conditions are sown very early in CRI, at a time when they are-in theory-most amenable to intervention. We therefore must be as proactive as possible in the timely implementation of relatively simple therapies that have the potential to prevent some of these adverse outcomes of CRI.
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PMID:Complications of chronic renal insufficiency: beyond cardiovascular disease. 1111 56

In this paper a sensitive, rapid and simple HPLC method for the simultaneous determination of creatinine (Cr), pseudouridine (Pu) and uric acid(UA) has been established. We have evaluated clinical value of the method in the early diagnosis of diabetic nephropathy (DN). Separation was obtained using Shim-pack CLC-ODS 15 x 0.6 cm column and mobile phase of buffer solution of phosphate (pH 3.0, 0.02 mol/L) with flow rate of 1 mL/min. Detection was performed with UV detector at an automatic adjustment of wavelength. The recoveries of Cr, Pu and UA were 101.4%, 104.9% and 105.0% respectively. The calibration curves were linear within the concentration range of 8.6-274.6 mumol/L for Cr, 0.72-22.93 mumol/L for Pu and 19.1-612.7 mumol/L for UA (n = 6, r > 0.999, p < 0.01). The CV for within day and between day measurements were < 2.5% and < 5.0% respectively. In addition, Pu, Cr and UA were simultaneously determined in serum and urine of 39 patients with diabetic mellitus (DM). 15 patients with nephrotic syndrome (NS) and 53 normal subjects by the method. Results include: 1. the levels of serum Pu in all DM patients (100%) with microalbuminuria (MiAU) and macroalbuminuria (MaAU) were greater than maximum of normal subjects (X + 2S). In addition, in 9 DM patients (41%) with normal albuminuria (NAU) the levels were also greater than the maximum. 2. In patients with DM, there was no correlation between the serum Pu and the urinary albumin excretion (UAE), whereas the serum Pu correlated closely with the serum Cr. However, the incidence for serum Pu increase was significantly greater in patients. 3. The levels of serum Pu in patients with NS were greater than those in control subjects and patients with DM. Conclusion is that the determination of serum Pu could be used as sensitivity index for the early diagnosis of DN.
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PMID:[Simultaneous determination of creatinine, pseudouridine and uric acid in serum and urine by high performance liquid chromatography]. 1132 82

Maintenance hemodialysis (HD) in Yugoslavia started in the sixties and followed the dialysis trends in the Western Europe. However, in the last decade the development of renal replacement therapy (RRT) slowed down. In this report the epidemiology of ESRD from 1997-1999 and the survey of the status of HD treatment in Yugoslavia in 1999 are presented. Epidemiological data are obtained by the annual center questionnaires (response rate: 92.6 -94.2%). The survey of HD status is based on a specific questionnaire and covered 2108 patients (65%). At the end of 1999 there were 56 RRT centers in Yugoslavia treating 3939 patients: 3232 (82%) patients by HD, 248 (6.3%) by peritoneal dialysis, and 459 (11.7%) living with transplanted kidney. In a three year period, incidence of ESRD ranged from 108-128 pmp, point prevalence from 435-463 pmp and mortality rate from 20.7-17.9. Numerous refugee patients were treated over the last 10 years. Main causes of ESRD were glomerulonephritis (30%); Balkan nephropathy represented 11% and diabetic nephropathy 7% of all primary renal diseases. Cardiovascular and cerebrovascular diseases were the most common causes of death of RRT patients. Most centers are overcrowded and HD machines are worn out. Mean Kt/V was 1.19+/-0.08, mean URR% 58.8+/-7.4. The shortage of drugs prevented adequate management: 83% of HD patients had hemoglobin level less than 100 g/L but only 10.3 -17.8% were treated with rHuEpo; 64.5% of patients had phosphate levels higher than 1.7 mmol/L but only 33.5% used phosphate binders; 47% of patients had hypertension despite the antihypertensive therapy. The prevalence of hepatitis B remained unchanged (about 14%) in HD population during the last three years, but the prevalence of anti-HCV positive patients decreased (31-23%). In conclusion, there is a well developed dialysis service in Yugoslavia but insufficient conditions for adequate treatment.
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PMID:Epidemiology of end-stage renal disease and current status of hemodialysis in Yugoslavia. 1240 1

A new high-performance capillary zone electrophoretic assay for creatine (Cr), creatinine (Cn), urea (U) and uric acid (Ua), markers of human diabetic nephropathy, both in plasma and urine has been developed with UV detection at 200 nm. The plasma sample was deproteinized with trichloroacetic acid and centrifuged at 10 000 rpm for 10 min. The urine sample was diluted 20-fold with buffer before analysis. The optimum separation conditions for the markers was investigated with respect to the concentration of the buffer, the pH, the voltage and the capillary temperature. Baseline separation was achieved in 25 mmol/L phosphate buffer (pH 3.45) using a 21 cm x 75 microm I.D. fused-silica capillary at 40 degrees C with an electric field of 1190 V/cm. The calibration curves showed good linearity in the range 3.5-1000, 0.18-700, 500-5000 and 2-800 microM (r2 min > 0.998) for Cr, Cn, U and Ua, respectively. The proposed method also has a high reproducibility (peak area RSD max < 3%) and has been successfully applied to the determination of clinical samples.
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PMID:High-performance capillary zone electrophoretic assay for markers of diabetic nephropathy in plasma and urine. 1261 44

Glutamine-fructose-6-phosphate transaminase 1 (GFAT) is the rate-limiting enzyme of the hexosamine pathway that has been implicated in the pathogenesis of diabetic nephropathy. As such, we hypothesized that GFPT1, which encodes for GFAT, may confer genetic susceptibility to this complication among Caucasians. Screening of all known functional regions of GFPT1 revealed six single nucleotide polymorphisms (SNPs) that were located in the promoter, introns, and 3' untranslated region. The approximately 60 kb GFPT1 locus was encompassed in a single conserved haplotype block, and two tagging SNPs were sufficient to capture >90% of the haplotype diversity. Analysis of these SNPs in a case-control study made up of type 1 diabetic subjects (324 case subjects with diabetic nephropathy and 289 control subjects with normoalbuminuria despite >15 years of diabetes) revealed no significant association even after stratification by sex, diabetes duration, glucose control, and blood pressure. Similar results were obtained among type 2 diabetic subjects (202 case and 114 control subjects). Genetic variation in GFPT1 is thus unlikely to have a major impact on susceptibility to diabetic nephropathy.
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PMID:Scrutiny of the glutamine-fructose-6-phosphate transaminase 1 (GFPT1) locus reveals conserved haplotype block structure not associated with diabetic nephropathy. 1498 77

Patients with end-stage renal disease have a high mortality, with the majority of deaths due to vascular disease. The prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure (CRF) is poorly characterized. The aim of the present study was to determine the prevalence of vascular risk factors and clinically overt vascular disease in an Australian cohort of patients with predialysis CRF. We performed a retrospective chart review of outpatients with CRF and noted demographic data, the cause of renal failure, the presence or otherwise of vascular risk factors and vascular disease and calculated glomerular filtration rate. The prevalence of overt vascular disease and modifiable vascular risk factors was calculated. One hundred and eighty patients completed the study. Eighty-nine per cent of patients had hypertension, 68% had dyslipidaemia, 32% were diabetic and 38% were previous smokers. The subgroup with diabetic nephropathy had significantly more risk factors (P < 0.001) than other groups. Twenty-seven per cent of the group had cardiovascular disease, 22% had cerebrovascular disease, 23% had peripheral vascular disease and 9% had renal artery stenosis. Patients with ischaemic nephropathy had significantly more vascular disease than other groups (P < 0.001). Patients with overt vascular disease were older, had a higher number of risk factors and a higher calcium phosphate product than those without vascular disease. In conclusion, the present study suggests a high prevalence of vascular risk factors and vascular disease in predialysis CRF. Early detection provides an opportunity for early intervention and may help reduce the development of vascular disease, and the associated mortality, once these patients progress to dialysis.
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PMID:Prevalence of vascular risk factors and vascular disease in predialysis chronic renal failure. 1501 97

Diabetic nephropathy has become the most prevalent cause of end-stage renal disease (ESRD) in many countries. ESRD patients with diabetes have a particularly poor prognosis compared with patients without diabetes. The course of diabetic nephropathy can be modified with early management of the condition and it is important that diabetes patients are screened regularly for early signs of kidney damage. Blood pressure control and use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers have been shown to slow the progression of chronic kidney disease. Patients with diabetes are at considerable risk of cardiovascular complications, and modifiable cardiovascular risk factors, such as anaemia and dyslipidaemia, should be treated at an early stage. Correction of anaemia with recombinant human erythropoietin is associated with improvements in quality of life, functional status, and cardiovascular morbidity and mortality, and may slow the progression of renal disease. Abnormalities in calcium and phosphate metabolism and acidosis may also occur in patients with diabetes and nephropathy and these should be monitored regularly. It is important that patients with kidney disease are detected promptly to allow intervention to slow renal disease progression and to treat modifiable cardiovascular risk factors. Improved collaboration between diabetologists and nephrologists will also ensure that patients receive optimal care.
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PMID:Screening and management of patients with early chronic kidney disease. 1510 42

Advanced glycation end-products (AGE) are generated by chronic hyperglycaemia and may cause diabetic microvascular complications such as diabetic nephropathy. Many factors influence the development of diabetic nephropathy; however, dysregulation of mesangial cell (MC) proliferation appears to play an early and crucial role. In this study, we investigated the effects of AGE on rat MC proliferation and the involvement of sphingolipids in the AGE response. Results show a bimodal effect of AGE on MC proliferation. Thus, low AGE concentrations (<1 microm) induced a significant increase (+26%) of MC proliferation, whereas higher concentrations (10 microm) markedly reduced it (-24%). In parallel, AGE exerted biphasic effects on neutral ceramidase expression and activity. Low AGE concentrations increased neutral ceramidase activity and expression, whereas high AGE concentrations showed opposite effects. Surprisingly, neutral ceramidase modulation did not result in changes of ceramide levels. However, the AGE (10 microm)-inhibitory effect on MC proliferation was associated with accumulation of sphingosine and was specifically prevented by blocking glucosylceramide synthesis, suggesting that the high AGE concentration effects are mediated by sphingosine and/or glycolipids. On the other hand, treatment of cells with low AGE concentrations led to an increase of sphingosine kinase activity and sphingosine-1-phosphate production that drove the increase of MC proliferation. Interestingly, in glomeruli isolated from streptozotocin-diabetic rats, a time-dependent modulation of ceramidase activity was observed as compared with controls. These results suggest that AGE regulate MC growth by modulating neutral ceramidase and endogenous sphingolipids.
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PMID:Bimodal effect of advanced glycation end products on mesangial cell proliferation is mediated by neutral ceramidase regulation and endogenous sphingolipids. 1518 94

Increased glucose metabolism through the hexosamine pathway may result in insulin resistance, impaired insulin secretion, and diabetic nephropathy. We hypothesized that variants of GFPT1 encoding glutamine-fructose-6-phosphate amidotransferase, the rate limiting enzyme in this pathway, could increase GFPT1 gene expression and thus susceptibility to diabetes and diabetic nephropathy. To test this hypothesis, we screened for variation in the GFPT1 and flanking regions in Caucasian and African-American individuals. We tested each variant with over 5% allele frequency for an association with type 2 diabetes in Caucasian and African-American populations, and for an association with diabetic nephropathy in African-American subjects. We measured allele specific levels of GFPT1 mRNA and we compared mRNA levels across diagnostic categories for each ethnic group using RNA derived from transformed lymphocytes. None of the 8 variants detected altered the coding sequence or was present in a known regulatory region. We found a marginal association (p = 0.044) of 1/6 variants with diabetes in Caucasian subjects, and marginal associations of 2/7 variants with diabetic nephropathy among African-American subjects (p = 0.025, p = 0.041). Alleles marked by a variant in the 3' untranslated region were equally expressed, but in a small sample, GFPT1 mRNA levels were increased by 60% in Caucasians with diabetic nephropathy compared to diabetic individuals without nephropathy. Variants in the GFPT1 gene show suggestive evidence of an association with diabetic nephropathy among African-American individuals, and increased GFPT1 gene expression may characterize Caucasian subjects with diabetic nephropathy. Both findings need to be confirmed in other populations.
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PMID:Molecular screening of the human glutamine-fructose-6-phosphate amidotransferase 1 (GFPT1) gene and association studies with diabetes and diabetic nephropathy. 1530 30

In this study, the effects of short-term diabetes (4 days) on rat renal glomerular cells proliferation and the potential involvement of sphingolipids in this process were investigated. Immunohistochemical analysis showed that streptozotocin (STZ)-induced diabetes promoted increased intra-glomerular hyperplasia, particularly marked for mesangial cells. This was associated with a concomitant increase in neutral ceramidase and sphingosine-kinase activities and the accumulation of the pro-proliferative sphingolipid sphingosine-1-phosphate, in glomeruli isolated from kidney cortex of STZ-treated rats. These results suggest a possible involvement of sphingolipid metabolites in the glomerular proliferative response during the early stages of diabetic nephropathy.
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PMID:Glomerular proliferation during early stages of diabetic nephropathy is associated with local increase of sphingosine-1-phosphate levels. 1571 Apr 21

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