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)

The relationship between erythrocyte cation transport systems, membrane and plasma lipids, plasma prorenin and microalbuminuria was examined in normal men and patients with insulin dependent diabetes mellitus (IDDM). Different measurements of erythrocyte transport systems were obtained in patients with IDDM and in age- and weight-matched healthy men: Na+/Li(+)-countertransport activity, Na+/K(+)-cotransport activity, Na+/K(+)-ATPase pump activity and the ground membrane permeability for Na+ and K+ as well as the intraerythrocyte Na+, K+ and Mg2+ concentration. Plasma prorenin, cholesterol, triglycerides, phospholipids, low and high density lipoprotein cholesterol and erythrocyte membrane cholesterol and phospholipids content were also obtained from the fasting subjects. The patients with IDDM had an elevated (p < 0.05 or less) erythrocyte Na+/Li(+)-countertransport activity, ground membrane leak for K+, intraerythrocyte K+ concentration, erythrocyte membrane cholesterol content, but a lower red blood cell phospholipids content. In single regression analysis the erythrocyte Na+/Li(+)-countertransport, Na+/K(+)-cotransport and Na+/K(+)-ATPase pump activity and ground membrane leak for Na+ and K+ were inversely related to the red cell membrane lipid content. The erythrocyte Na+/Li(+)-countertransport activity and K+ leak were also positively related to the plasma prorenin level and urinary microalbumin excretion. Our data in patients with IDDM show that an elevated erythrocyte membrane lipid content was accompanied by a lower erythrocyte Na+/Li(+)-countertransport, Na+/K(+)-cotransport or Na+/K(+)-ATPase pump activity. The elevated Na+/Li(+)-countertransport activity was also accompanied by a higher plasma prorenin level and microalbuminuria.
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PMID:Transmembrane cationic fluxes in erythrocytes of diabetics and normal men. 816 72

Magnesium concentrations in plasma, erythrocyte and platelet, and plasma and urine levels of the soluble form of Intercellular Adhesion Molecule-1 (sICAM-1) were evaluated in subjects with insulin dependent diabetes mellitus (IDDM) with or without microalbuminuria, and in a control group of healthy subjects. Using a recently introduced technique, we found that magnesium concentrations in platelets in diabetic subjects with microalbuminuria were lower than in diabetics with normal albuminuria (1.859 +/- 0.47 vs 2.065 +/- 0.62 mumol/10(8) cells; P < 0.05). Moreover, IDDM subjects had higher plasma sICAM-1 levels than control subjects; no difference, however, was found between sICAM-1 concentrations in the two groups of diabetics. An inverse correlation was found between intraplatelet magnesium and plasma sICAM-1 levels (r = - 0.64; P < 0.05) in the diabetics with microalbuminuria. It is concluded that the reduced intraplatelet magnesium content may contribute to the progression of the vascular complications in IDDM subjects with microalbuminuria.
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PMID:Altered platelet magnesium and plasma and urinary soluble form of intercellular adhesion molecule I (sICAM-1) concentrations in insulin dependent diabetes mellitus (IDDM) patients with microalbuminuria. 924 79

Extracellular matrix (ECM) accumulation in the glomerular mesangium is a characteristic feature of diabetic nephropathy. While transforming growth factor-beta1 (TGF-beta1) is the final mediator of ECM accumulation, reactive oxygen species (ROS) and protein kinase C (PKC) are the upstream signaling molecules that mediate hyperglycemia-induced ECM expansion. Magnesium lithospermate B (LAB) is an active component isolated from Salvia miltiorrhizae with known renoprotective properties due to its antioxidative effects. Thus, the present study examined the effects of LAB on renal injury in streptozotocin-induced diabetic rats (STZR) and on the activation of mesangial cells cultured under high glucose conditions. Ten micrtograms of LAB/kg per day was started 8 wk after streptozotocin injection and continued for a period of 8 wk. It significantly suppressed renal malondialdehyde (MDA), microalbuminuria, glomerular hypertrophy, mesangial expansion, and the upregulation of renal TGF-beta1, fibronectin, and collagen in STZR without significantly affecting plasma glucose. Both 30 mM of glucose and 100 uM of H(2)O(2) significantly increased TGF-beta1 and fibronectin protein secretion by mesangial cells. LAB at 10 micro g/ml inhibited high glucose- and H(2)O(2)-induced TGF-beta1 and fibronectin secretion. LAB also inhibited glucose-induced intracellular ROS generation and PKC activation in mesangial cells, but it did not directly inhibit PKC activity at dosages that inhibited ROS generation. The in vitro data of this study show that LAB inhibits ROS generation leading to PKC activation and TGF-beta1 and fibronectin upregulation in mesangial cells cultured under high glucose conditions. Moreover, delayed treatment with LAB was found to significantly suppress the progression of renal injury in STZR. LAB may become a new therapeutic agent for the treatment of diabetic nephropathy.
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PMID:Delayed treatment with lithospermate B attenuates experimental diabetic renal injury. 1259 7