Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0730345 (microalbuminuria)
 4,018 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normalbuminuric patients who have long-standing IDDM have a wide range of renal structure, from within normal limits to advanced lesions that overlap those of patients who have high levels of MA and border on those seen in patients who have overt DN. Patients who have low-level MA have reduced glomerular structure similar to that of patients who have NA. Low GFR, hypertension, or both can occur in patients who have NA or low-level MA and are associated with more advanced lesions. Patients who have MA and AER greater than 45 mg/24 hr have more advanced lesions than do patients with NA or low-level MA, but similar lesions are present in these patients whether AER is greater than or less than 100 mg/24 hr. Increasing AER in NA and MA patients who have long-standing IDDM is associated with GBM and mesangial expansion. A structural basis for MA cannot currently be deduced from studies of glomerular epithelial cell fine structure, capillary wall charge site analysis, or immunohistochemical studies of renal ECM composition. Hemodynamic adaptations to mesangial expansion and reduced filtration surface and, perhaps, hydraulic conductivity may accelerate glomerular damage, as expressed by increasing AER. Microalbuminuria derives its clinical utility in IDDM, as it identifies a population of patients at statistically increased risk of progression to overt DN by acting as a marker of already well-established DN lesions. Although MA is currently the best of the widely used indicators of DN risk, it is not precise. Therapies that reduce MA may ultimately slow or prevent progression toward ESRD, but this finding requires confirmation by demonstrating that a given treatment strategy can preserve GFR.
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PMID:Glomerular changes in normo- and microalbuminuric patients with long-standing insulin-dependent diabetes mellitus. 892 36

Diabetic nephropathy (DN) is one of the major microvascular diseases and most common in diabetic patient, finally results in kidney failure. The main features of DN are basement membrane thickening, microalbuminuria, proteinuria, glomerular, mesangial hypertrophy and ECM protein accumulation. Recent discoveries have been shown that numerous pathways are activated during the development of DN in Diabetes mellitus. The small non-coding miRNA plays an important role in regulating the pathway which is involved in DN. In our study we consolidate different pathways which regulated by miRNAs in molecular signaling which results in causing DN. We embedded entire pathway in the form of regulatory network and we could able to understand that some of the miRNAs like miR-29 family, miR-377 and miR-25 would be able to control DN.
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PMID:Molecular signaling cascade of miRNAs in causing Diabetes Nephropathy. 2375 89

Diabetic nephropathy, a major complication of diabetes mellitus (DM), is increasing worldwide and the large majority of patients have type 2 DM. Microalbuminuria has been used as a diagnostic marker of diabetic nephropathy. But owing to its insufficient sensitivity and specificity, other biomarkers are being sought. In addition, the pathophysiology of diabetic nephropathy is not fully understood and declines in renal function occur even without microalbuminuria. In this study, we investigated urinary proteins from three study groups (controls, and type 2 diabetic subjects with or without microalbuminuria). Non-targeted label-free Nano-LC QTOF analysis was conducted to discover underlying mechanisms and protein networks, and targeted label-free Nano-LC QTOF with SWATH was performed to qualify discovered protein candidates. Twenty-eight proteins were identified as candidates and functionally analyzed via String DB, gene ontology and pathway analysis. Four predictive mechanisms were analyzed: i) response to stimulus, ii) platelet activation, signaling and aggregation, iii) ECM-receptor interaction, and iv) angiogenesis. These mechanisms can provoke kidney dysfunction in type 2 diabetic patients via endothelial cell damage and glomerulus structural alteration. Based on these analyses, three proteins (kininogen-1, basement membrane-specific heparan sulfate proteoglycan core protein, and roundabout homolog 4) were proposed for further study as potential biomarkers. Our findings provide insights that may improve methods for both prevention and diagnosis of diabetic nephropathy.
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PMID:Roles of kininogen-1, basement membrane specific heparan sulfate proteoglycan core protein, and roundabout homolog 4 as potential urinary protein biomarkers in diabetic nephropathy. 3266 74