Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to evaluate tubular function 99mTc-DMS dynamic kidney scintigraphy and 99mTc-DMS uptake determinations were performed in 55 patients with endemic nephropathy, diabetic nephropathy and glomerulo nephritis. From 64-656th segment of computerized radiorenograms 99mTc-DMS uptake and curve slope were assessed and compared with the corresponding parameters of 20 healthy subjects. Both parameters were decreased in patients of all three groups. Tubular uptake of 99mTc-DMS measured during 60 sec. 4 hours after 99mTc-DMS administration, was decreased in endemic nephropathy and diabetic nephropathy, but without a significant difference in glomerulonephritic patients. The study of the relationship between 4 hour 99mTc-DMS tubular fixation and glomerular filtration rate, estimated by 99mTc-DTPA clearance, showed a positive correlation only in patients with diabetic nephropathy. Patients with renal failure from all three groups had more seriously impaired tubular handling of 99mTc-DMS, that correlated with reduction of the glomerular filtration rate. The present data showed more severe impairment of tubular function in patients with endemic nephropathy and diabetic nephropathy than in glomerulonephritic patients. The method was suitable for estimation of the tubular function.
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PMID:[Fixation of tubules with radioactive technetium dimercaptosuccinate in parenchymal diseases of the kidney]. 772 48

There remains a need for robust mouse models of diabetic nephropathy (DN) that mimic key features of advanced human DN. The recently developed mouse strain BTBR with the ob/ob leptin-deficiency mutation develops severe type 2 diabetes, hypercholesterolemia, elevated triglycerides, and insulin resistance, but the renal phenotype has not been characterized. Here, we show that these obese, diabetic mice rapidly develop morphologic renal lesions characteristic of both early and advanced human DN. BTBR ob/ob mice developed progressive proteinuria beginning at 4 weeks. Glomerular hypertrophy and accumulation of mesangial matrix, characteristic of early DN, were present by 8 weeks, and glomerular lesions similar to those of advanced human DN were present by 20 weeks. By 22 weeks, we observed an approximately 20% increase in basement membrane thickness and a >50% increase in mesangial matrix. Diffuse mesangial sclerosis (focally approaching nodular glomerulosclerosis), focal arteriolar hyalinosis, mesangiolysis, and focal mild interstitial fibrosis were present. Loss of podocytes was present early and persisted. In summary, BTBR ob/ob mice develop a constellation of abnormalities that closely resemble advanced human DN more rapidly than most other murine models, making this strain particularly attractive for testing therapeutic interventions.
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PMID:BTBR Ob/Ob mutant mice model progressive diabetic nephropathy. 2070 6