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)

The aim of the study was to clarify whether antihypertensive treatment could affect the systolic blood pressure (SBP) and urinary albumin excretion (UAE) in diabetics during exercise (450 kpm/min, followed by 600 kpm/min, 20 min each). Young male insulin-dependent diabetics with normal UAE (n = 9) and diabetics with incipient nephropathy (n = 7) were examined in an acute study. Five patients with incipient diabetic nephropathy participated in a long-term study. Incipient diabetic nephropathy is defined as persistently elevated UAE (greater than 15 micrograms/min), but no clinical proteinuria. In the acute study, using placebo/metoprolol 10 mg i.v. in patients with normal UAE, the maximal SBP at 600 kpm/min was reduced by 17 mmHg +/- 10 (SD) (2p less than 1.0%) and the maximal SBP at 600 kpm/min in the patients with incipient nephropathy was reduced by 15 mmHg +/- 11 (SD) (2p less than 1.0%). However, no difference was observed in UAE, in patients with normal UAE or those with incipient nephropathy. Five of the patients with incipient nephropathy were followed with repeated exercise tests before and during 2.6 years of antihypertensive treatment, using metoprolol 200 mg/24 h and subsequently also hydroflumethiazid 25 mg/24 h. The maximal SBP at 600 kpm/min at the end of the study compared to the pretreatment level was reduced by 38 mmHg +/- 12 (SD) (2p less than 1.0%), and furthermore the exercise-induced elevated UAE was reduced by 61% +/- 29 (SD) (2p = 2.0%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute and long-term effect of antihypertensive treatment on exercise-induced albuminuria in incipient diabetic nephropathy. 353 2

Diabetic nephropathy is a microvascular complication, as well as retinopathy and neuropathy of type 1 and type 2 diabetes mellitus. The pathogenesis directly correlates with hyperglycemia. The direct glucose toxicity, hypercoagulability, oxidative stress and endothelial dysfunctions play a role. Strict glycemic control with HbA1c levels <7% for 10 yrs is associated with a 25% microvascular end point reduction. Patients underwent pancreas transplantation, and after 10 yrs the present nephropathy and functional and structural abnormalities have regressed. Diabetic nephropathy alters the pharmacokinetic profile of almost all oral anti-diabetic agents, as well as insulin metabolism; therefore, it is imperative to determine creatinine clearance. Renal failure requires insulin therapy. Incipient diabetic nephropathy allows very limited indications to oral anti-diabetic agents because of the altered pharmacokinetic profile and side effects (hypoglycemia with secretagogues agents, lactic-acidosis with metformin and other biguanides, and hydric retention and weight gain with thiazolidinediones). Moreover, oral anti-diabetic agents reduce the percentage of HbA1c by no more than 1.5%. Insulin therapy is preferred, with a dose reduction when creatinine clearance is <60 mL/m. To control better the post-prandial glycemic peak, it is useful to use bolus insulin analogues at each meal and basal intermediate-acting insulin at bedtime to mimic the natural insulin patterns as far as possible.
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PMID:[Diabetic nephropathy: oral anti-diabetic agents or insulin?]. 1663 98