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 a 63-year-old woman with longstanding type I diabetes mellitus, CAD and chronic heart failure, a subacute myocardial infarction developed, together with decompensation of cardiac function and diabetes and concurrent pneumonia. Acute heart failure with acute renal failure on top of diabetic nephropathy, and interstitial pulmonary edema was initially treated with hemofiltration and catechol amines together with antibiotic and perfusor-regulated insulin therapy, and systemic heparinization. Subsequent chronic treatment with digitalis, acetyl salicylic acid, insulin and a combination of an ACE inhibitor and a loop diuretic resulted in an improvement of heart failure to NYHA functional class II where PTCA of coronary multi-vessel disease could be performed with low risk.
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PMID:[Heart failure after myocardial infarct in decompensated diabetes mellitus. Acute therapy with catecholamines--long-term therapy with ACE inhibitor-loop diuretic combination]. 937 33

In type 2 diabetic patients with or without nephropathy, we examined relationships between plasma concentrations of total homocysteine (tHcy) and clinical macroangiopathy, as well as endothelial dysfunction indicated by plasma thrombomodulin (TM) concentrations. We studied 103 type 2 diabetic patients including 26 with macroangiopathy (12 patients with coronary artery disease [CAD], 10 with stroke, and 4 with peripheral vascular disease [PVD]). Plasma tHcy was measured by high-performance liquid chromatography. Plasma TM was determined by enzyme immunoassay. As an index of glomerular filtration rate, creatinine clearance (Ccr) also was determined in a 24-hour urine collection. Considering all diabetic patients, plasma tHcy concentrations were significantly higher in those with macroangiopathy than in those without (10.4 +/- 3.7 v 8.5 +/- 2.8 micromol/L, P=.0077). By univariate and multivariate analyses, plasma tHcy was correlated inversely with Ccr. Plasma tHcy concentrations were significantly higher in the patients with overt albuminuria than in those with normoalbuminuria or microalbuminuria. After exclusion of patients with renal insufficiency (Ccr<60 mL/min), differences in plasma tHcy concentrations between patients with and without macroangiopathy were abolished. By multivariate analysis, total cholesterol, urinary albumin, Ccr, C-peptide, and tHcy retained significant influence on the plasma TM. Even in patients with normal renal function (Ccr > or = 80 mL/min), plasma tHcy was correlated positively with plasma TM. In conclusions, diabetic nephropathy is a main determinant of plasma tHcy elevation in type 2 diabetic patients. Since plasma TM is independently associated with plasma tHcy, in diabetic patients with overt nephropathy, elevation of tHcy reflecting reduced clearance is a likely cause of endothelial dysfunction, resulting in the atherosclerosis underlying development of cardiovascular disease.
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PMID:High plasma homocysteine concentrations are associated with plasma concentrations of thrombomodulin in patients with type 2 diabetes and link diabetic nephropathy to macroangiopathy. 1462 17

Chronic kidney disease (CKD) has become a major health-care problem of global proportions. Progression to end-stage renal disease (ESRD), the need for renal replacement therapy, and the high annual death rate of dialysis patients are the most noticeable outcomes of CKD. Less appreciated, however, is the fact that most patients with CKD actually die mainly from cardiovascular disease, rather than progress to ESRD. Coronary artery calcification (CAC), a surrogate marker of atherosclerosis, is common in dialysis and CKD patients. Coronary artery calcium scores, as measured by ultrafast computed tomography, is an independent predictor of future cardiac events. Using this technique, several studies have documented extensive calcification in dialysis patients, a subject of several exhaustive reviews. Unfortunately, much less attention has been paid to calcification in nondialyzed patients with CKD. In this review, I will emphasize the fact that CVC is common in patients with CKD not yet on dialysis, develops early in the course of CKD, and worsens with the decline in renal function particularly among diabetics who progressed to ESRD. I will also discuss the pathogenesis of CVC in CKD patients and highlight the lack of a major role for abnormalities of mineral metabolism in the pathogenesis of calcification in CKD patients. In addition to the high prevalence of traditional risk factors for CAD, the presence of proteinuria, reduced renal function, diabetic nephropathy, and the rate of progression to ESRD may represent the main uremia-related factors that increase the risk for calcification in CKD. Finally, I will review the protective role of inhibitors of calcification in CKD.
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PMID:Cardiovascular calcification in nondialyzed patients with chronic kidney disease. 1737 87