Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated hypoaldosteronism is found in 75% diabetics where the disease has persisted for 10 or more years. Sporadically it is found in congenital autonomous neuropathy, in acute glomerulonephritis, in gouty kidney, tubulointerstitial nephritis, after transplantation of the kidney, on mytomycin etc. During dynamic testing of the response of plasma renin activity and aldosterone to the administration of furosemide and a vertical position in diabetics a significantly reduced response was recorded as compared with non-diabetic hypertonic subjects. In 18.3% no response was observed (decompensated form of IHH). Diabetic hypertonics behaved like control hypertonics on long-term beta-blocker treatment. In the decompensated form of IHH after administration of drugs interfering with the activity of SNS-RAAS activity (ACEI, spirolactone etc.) a hyperkalaemic crisis may develop which threatens the patient with acidosis, dehydration, myoplegia, muscular spasms, however, in particular with fatal disorders of the cardiac rhythm. A similar effect may be exerted also by blockers of prostaglandin synthetase (non-steroid antirheumatics) and other drugs. The cause of IHH in diabetics is the coincidence of several pathogenic factors: 1. hypersecretion of ANF with hyperosmolar hyperglycaemic hypervolaemia and hyperfiltration already at the onset of DN, 2. early development of autonomous neuropathy of the sympathetic nerve, 3. reduced renin and prostaglandin formation already in the early stages of DN, 4. reduced extrarenal isorenin formation, 5. reduced conversion of prorenin into active renin, 6. reduced reactivity of the zona glomerulosa to AII, hyperkalaemia and ACTH for its functional reconstruction as a result of periodic activation of contraregulative hormones by fluctuations of the blood sugar level in diabetic patients, 7. reduced response of the distal renal tubule to aldosterone because of tubulointerstitial changes. IHH is thus another serious but rarely diagnosed late complication of diabetes which depends only partly on the stage of DN. It must be, however, diagnosed and respected with regard to the selection of drugs for the treatment of arterial hypertension and the syndrome of insulin resistance and the 5H syndrome resp., i.e. the association of hyperinsulinism which compensates insulin resistance with hyperglycaemia (NIDDM), hypertension, hyperlipoproteinaemia and hirsutism in women (so-called Stein-Leventhal syndrome).
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PMID:[Diabetic nephropathy and isolated hyporeninemic hypoaldosteronism]. 892 9

Three hundred fifteen (315) elderly (> or = 60 years) patients with clinical renal diseases were evaluated for the evidence of glomerular diseases between November 1998 to June 2002. Glomerular diseases (GN) were observed in 20.6% (65/315) of the elderly patients. The age of the patients (male 56; female 9) ranged between 60-90 (mean 64.17 +/- 3.83) years. The clinical presentation of GN included: nephrotic syndrome 40 (61.5%), acute nephritic syndrome 19 (29.2%), rapidly progressive GN 4 (6.15%) and asymptomatic urinary abnormality 2 (3.0%). Overall, primary and secondary glomerular disease were seen in 47 (72.3%) and 18 (27.6%) elderly patients respectively. Idiopathic membranous nephropathy was the most common GN responsible for nephrotic syndrome in 11 (27.5%) of elderly patients. Diabetic Nephropathy related to type 2 diabetes mellitus was the second common cause 9 (22.5%) of nephrotic syndrome. Amyloidosis was noted in 6 (15%) patients. Nephrotic syndrome was related to leprosy in one patient. Amyloidosis occurred in association with multiple myeloma in 5 and carcinoma colon in 1 patient. Thus, primary and secondary GN were responsible for nephrotic syndrome in 60% and 40% of cases respectively. Endocapillary proliferative GN of post infectious etiology was the most prevalent (82.6%) form of acute GN in our elderly patients. Hypertension occurred in 78.2% of cases and edema in 69.5%. Pulmonary congestion (52.2%) and ARF (73.9%) were the dominant presenting feature of acute GN and 39% of patients required dialytic support. Glomerular crescents were seen in 4 (17.4%) patients with acute glomerulonephritis. Pauci-immune crescentic GN which is the commonest type of acute GN in the elderly in western countries was not observed in this study. Renal biopsy revealed mesangiocapillary GN (1) and mesangioproliferative GN (1) in two patients with asymptomatic urinary abnormalities. Thus, overall spectrum of glomerular disease in the Indian elderly population is similar to that of developed countries except in two ways: (1) post infectious endocapillary proliferative-GN was the commonest type of acute GN (2) rarity or absence of pauci-immune crescentic glomerulonephritis.
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PMID:Glomerular diseases in the elderly in India. 1507 10

Extracellular vesicles released into urine (uEVs) can represent interesting biomarkers of renal cell damage. CD133, a stem/progenitor cell marker expressed by renal progenitor cells, is highly expressed in uEVs of healthy individuals. In the present study, we evaluated the level of CD133 in the uEVs of patients with acute and chronic glomerular damage by cytofluorimetric analysis. The level of CD133+ uEVs was significantly decreased in pediatric patients with acute glomerulonephritis during the acute phase of renal damage, while it was restored after the subsequent recovery. A similar decrease was also observed in patients with chronic glomerulonephritis. Moreover, CD133+ uEVs significantly declined in patients with type 2 diabetes, used as validation group, with the lowest levels in patients with albuminuria with diabetic nephropathy. Indeed, receiver-operating characteristic curve analysis indicates the ability of CD133+ uEV values to discriminate the health condition from that of glomerular disease. In parallel, a significant decrease of CD133 in renal progenitor cells and in their derived EVs was observed in vitro after cell treatment with a combination of glucose and albumin overload, mimicking the diabetic condition. These data indicate that the level of CD133+ uEVs may represent an easily accessible marker of renal normal physiology and could provide information on the "reservoir" of regenerating cells within tubules.
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PMID:Acute and chronic glomerular damage is associated with reduced CD133 expression in urinary extracellular vesicles. 3186 43