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)

After mentioning insulin deficiency diabetes in animals produced by drugs such as Alloxan, Diazoxide or Streptozotocin only drugs are discussed, which are used in elderly patients and may either provoke diabetes mellitus (or temporary hyperglycemia) or may change the clinical course of diabetes. In the first group endocrine products such as corticosteroids, estrogens, somatotrophic hormone, thyroid hormone, glucagon, somatostatin, catecholamines and hormones with anabolic effects are listed. The second group comprises saluretics, salicylates, amphetamines, pentamidine, nicotinic acid and its derivatives, beta-receptor blockers and finally laxatives. Hypopotassemia alone can also be the cause of hyperglycemia. Speaking of the sulfonylureapreparations, their interaction with alcohol, with phenylbutazone, with some sulfonamides and the effect of the sulfonylureas on peripheric insulin-receptors is discussed. In case of severe diabetic vascular disease the use of anticoagulants may lead to hemorrhages. If such an hemorrhage occurs in the eyes, it may lead to blindness. In diabetic nephropathy the use of phenacetine and its derivatives should be substituted by another medication. This review is not at all complete but should only show some of the problems in the treatment of elderly diabetic patients.
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PMID:[Iatrogenic diabetes mellitus (side effects and interactions of drugs during clinical diabetes mellitus (author's transl)]. 612 38

Hyperhomocysteinemia is an established risk factor for cardiovascular disease. The modification of traditional cardiovascular risk factors has resulted in better morbidity and mortality outcomes, so the treatment of hyperhomocysteinemia is explored for a similar benefit. Vitamin B(6), vitamin B(12) and folate, as co-factors in the metabolism of homosyteine, are used in the treatment of hyperhomocysteinemia. Betaine, a methyl-donor in a separate homocysteine metabolism pathway, is also used to treat hyperhomocysteinemia. These supplements have been used in various doses and combinations for different periods of time, with favorable outcomes. There is still no concensus whether hyperhomocysteinemia can be treated with folic acid alone, or in combination with vitamin B(6) and vitamin B(12). The dose of the supplements required to normalize fasting homocysteine remains to be determined, especially in diabetic nephropathy, hemodialysis and renal transplant patients. The benefits from lowering homocysteine levels have mainly been demonstrated in surrogate cardiovascular outcomes. The treatment of hyperhomocysteinemia cannot be firmly advocated until there are trials that demonstrate a beneficial clinical endpoint. In patients who have cardiovascular disease in the absence of more established risk factors, investigation and treatment of hyperhomocysteinemia should be considered.
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PMID:Management of hyperhomocysteinemia. 1837 Jun 37

We have recently published that tubular epithelial cells affect the podocyte epigenome though nicotinic acid metabolism in diabetic nephropathy (DN), and we have named this relationship "proximal tubule-podocyte communication". In this review, we describe this novel mechanism in the early stage of DN, focusing on the function of renal tubular Sirt1 and Sirt1-related nicotinic acid metabolism. Mainly, we discuss the following three findings. First, we described the details of proximal tubule-podocyte communication. Second, we explained how Sirt1 regulates albuminuria via epigenetic mechanisms. This means that repeated high glucose stress triggers the initial changes in proximal tubules, which lead to the epigenetically irreversible glomerular damages. However, proximal tubular Sirt1 overexpression can rescue these changes. Our previous data indicated that the decrease in Sirt1 expression in proximal tubules caused the reduction in glomerular Sirt1 and the subsequent increase in glomerular Claudin-1. It seemed plausible that some humoral mediator is released from proximal tubules, migrates to podocytes and glomeruli, and affects Sirt1 expression in podocytes. Third, we mentioned a mediator connecting this communication, nicotinamide mononucleotide (NMN). We suggest the potential of Sirt1 or NMN as not only a therapeutic target but also as a prognostic marker of very early stage DN.
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PMID:Communication from Tubular Epithelial Cells to Podocytes through Sirt1 and Nicotinic Acid Metabolism. 2693 74