Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Olfactory dysfunction has been reported in individuals with diabetes mellitus, but the etiology is unknown. Diabetes is often complicated by serious medical conditions which could be related to the development of decreased olfactory ability. Overall, our 111 subjects with diabetes showed deficiencies in their ability to identify odorants measured with the Odorant Confusion Matrix (mean = 67.8% correct). The presence of macrovascular disease was found to be associated with olfactory dysfunction. Glycemic control as well as the type and duration of diabetes were not related to olfactory ability. Also, there was no distinct association with the presence of neuropathy, retinopathy, nephropathy, hypertension, or impotence. Consistent with previous studies utilizing measures of odorant identification, performance decreased with increased age, females were somewhat superior to males, and smoking had a deleterious effect. Other nondiabetes-related medical conditions and medications had no apparent effect on the olfactory ability of our subjects. These results suggest that the sequelae associated with macrovascular disease, such as perhaps, ischemia, to the olfactory area, impact negatively on olfactory ability.
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PMID:Olfactory dysfunction in diabetes mellitus. 843 58

NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of arachidonic acid metabolism. Precipitous decrements in glomerular filtration and renal ischemia, manifested by increased serum creatinine and urea nitrogen, are possible. However, these effects are usually fully reversible with prompt discontinuation of the offending NSAID. Risk factors for the development of these acute renal effects are known. Acute interstitial nephritis with or without nephrotic syndrome is a rare form of renal toxicity that typically occurs between 2-18 months of use. Renal impairment may be so severe as to require temporary hemodialysis; however, renal function usually returns to normal upon discontinuation of the NSAID. The mechanism of acute interstitial nephritis is presumed to be of allergic origin but could also be caused by a reactive metabolite. Fenoprofen use appears to be associated with a much higher risk for its development. In contrast to the acute effects of NSAIDs, irreversible, analgesic-associated nephropathy manifested by papillary necrosis and chronic interstitial nephritis may occur following months to years of high doses of analgesic mixtures. The mechanism by which combination analgesics produce this form of renal injury is unknown and could be either a result of medullary ischemia or a direct effect of a reactive metabolite. An important issue to be resolved is the relationship between the acute, reversible, prostaglandin-mediated renal effects of the NSAIDs and chronic, irreversible destruction, if such a relationship exists. Theoretically, continual or repeated decrements in renal function in patients with predisposing risk factors could cause or contribute to progressive deterioration in renal function. Elevations in blood pressure or interference with the effects of antihypertensive medications could theoretically also contribute to long-term renal deterioration. In addition to renal syndromes caused by NSAIDs that result in renal impairment, other transient effects on electrolyte and water metabolism may also occur. Reduced secretion of sodium may result in formation of edema, exacerbation of heart failure, or increased blood pressure. Hyporeninemic-hypoaldosteronism may produce hyperkalemia. Finally, reduced excretion of water has rarely caused hyponatremia. It has been suggested that NSAIDs may be renoprotective in patients with nephrotic syndrome. Others have suggested that sulindac is "renal-sparing" because of a unique metabolic pathway that supposedly limits the exposure of the kidney to the active sulfide metabolite.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal toxicity of the nonsteroidal anti-inflammatory drugs. 849 47

Hypertension can be a cause as well as a consequence of renal disease. Fluid overload or activation of the renin angiotensin system by glomerular ischemia leads to an elevation of systemic blood pressure in acute as well as chronic renal disease. Furthermore in the latter disorder an increased activity of the sympathetic nervous system as well as metabolic disorders contribute to hypertension. Accordingly antihypertensive therapy in patients with renal insufficiency is diverse. Additionally in chronic kidney disease one has to consider the variable effects of different antihypertensive drugs on intrarenal hemodynamics.
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PMID:[Antihypertensive therapy in renal failure]. 857 52

When a melito-diabetic patient presents trophic infected injury on the limb, it is essential an evaluation of the circulatory conditions for therapeutic procedures orientation. In some circumstances, although arterial pulsation is absent, there is no ischemia of tissues. In these cases, the maintenance treatment, with eventual resection of the necrosed and infected tissues may be adopted. Evolution of 70 diabetic patients with trophic injuries on extremities were submitted to a maintenance treatment. Age of patients varied from 28 to 88 years, with an average of 56.8. The most occurrence was verified in women, with 42 cases. Diabetes non-dependent on insulin (type II) was observed in 64 patients (91.5%), being the remaining 6 patients of type I. Diabetic retinopathy was observed in 14 (20%) of the patients, neuropathy in 22 (31%) and nephropathy in 8 patients (11.4%). All the patients presented arterial pulsation until the popliteal region. They were divided in 2 groups, considering trunk arteries of legs: Group I, pervial legs arteries, composed by 48 patients; Group II, occluded legs arteries, with 22 patients. In what refers to the anatomic local of the injuries, patients were classified in three groups: Group A, formed by 32 patients (45.7%), presenting injuries in one or two toes only, without affecting the metatarsic region; Group B, formed by 16 patients (22.9%), trophic injuries affecting the metatarsic region and Group C, formed by 22 patients (31.4%), injuries affecting the calcaneous region. Injuries in both of the groups were caused by mechanical traumatism. Duration of the injury in the inferior member varied from 7 to 48 days, resulting in a 12 days average.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Maintenance treatment of diabetic patients, associating arterial obstructive tibio-peroneal disease. 857 80

Renovascular disease is the leading cause of surgically-curable arterial hypertension and one of the few cause of reversible chronic renal failure, but its exact prevalence remains unknown. Progression of atheromatous disease occurs in 50% of cases and it may result in bilateral stenosis (25%) or total occlusion (15%). By now, the main aim of renal revascularization is retrieval of impaired function or prevention of renal failure rather than control of hypertension. However, renal functional deterioration may result from cholesterol embolism or glomerulosclerosis in addition to ischemia. Correction of post-proximal stenosis is obtained by both surgery and percutaneous angioplasty. In favor of angioplasty are a higher acceptability and a modestly better cost-benefit ratio. Surgery may be preferred when the stenosis is proximal, complex or associated with aortic disease; in addition, analysis of published (mostly uncontrolled) series suggest that beneficial renal functional outcome is slightly better following surgery. Importantly, both diagnosis and prognosis of ischemic nephropathy are difficult to establish. Various predictors of recovery (renal size, renal vein renin ratio, alteration in scintigrams, angiography or biopsy) were shown to fail on an individual basis. Further controlled studies based on reliable methods of measuring renal function are warranted.
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PMID:[Preservation of renal function by revascularization in renovascular disease]. 858 40

Hypertension after renal transplantation continues to affect 50% or more of patients, despite use of modern immunosuppressive regimens. Relationships between poor control of blood pressure and reduced chronic allograft survival have been clearly demonstrated, and are analogous to the well-known acceleration of progressive renal disease by coexisting hypertension. It is likely, although to date it has not been formally proven by prospective study, that effective blood pressure control has a beneficial effect on chronic allograft outcome, as in progressive dysfunction of native kidneys. A further key question is whether differing classes of antihypertensive therapy may have differing effects on long-term graft outcome. It has been proposed that glomerular hypertension, hyperfiltration and hypertrophy, secondary both to inadequate nephron mass and to loss of functioning nephrons, may contribute to chronic allograft failure. If this is true, then use of converting enzyme inhibitors may particularly benefit long-term graft outcome. However, post-transplant hypertension in cyclosporine-treated patients is associated with sodium retention and renin system suppression, and a relative lack of renoprotective action of ACE inhibitors might be predicted in this context. An alternative hemodynamic factor underlying chronic allograft failure is glomerular ischemia, secondary to the vascular changes associated with chronic rejection and to cyclosporine-related afferent arteriolar vasoconstriction. In this setting, calcium channel blockers which lower systemic blood pressure in combination with afferent arteriolar vasodilatation may improve long-term allograft outcome. New strategies with a similar rationale include endothelin receptor antagonists and neutral endopeptidase inhibitors such as candoxatril, which in acute experimental and clinical studies reverse cyclosporine-induced reductions in renal blood flow and glomerular filtration rate. Long-term prospective controlled comparative studies are needed to assess the effect of all these differing therapeutic approaches on chronic allograft outcome.
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PMID:Does antihypertensive therapy modify chronic allograft failure? 858 70

Virtually no objective data exist regarding the natural history of arteriovenous (AV) dialysis access grafts placed in the lower extremity for routine hemodialysis. From March 1988 until October 1993, 45 consecutive lower extremity AV dialysis access grafts were placed in 39 patients (16 males; 23 females; mean age 58 years) at a large teaching community hospital. All 39 patients had long-standing end stage renal disease and had required chronic hemodialysis from 7 to 237 months mean, 72 months) prior to leg graft placement. Polytetrafluorethylene (n=39) or bovine (n=6) loop lower extremity dialysis grafts were placed after multiple upper extremity dialysis graft failures (mean, 2.7 previous grafts with 9.6 thrombectomies and/or access revisions per patient). There were no operative deaths; however, in follow-up (1-132 months; mean 20 months; median 18 months), 33 percent of the patients had died from systemic complications of their renal disease, and only 20 (44%) leg grafts are currently patent [correction of patient] . Graft complications, excluding graft thromboses, occurred in 20 grafts including graft infection (n=8; 18%), severe ipsilateral leg ischemia (n=7; 16%), graft aneurysmal degeneration requiring revision (n=3; 7%), fistula-induced congestive heart failure (n=2; 4%), and major lower extremity amputation (n=3; 7%). Primary patency by life-table analysis was 47 percent at 24 months. Fifteen (33%) grafts thrombosed at least once, and all but one were salvaged with thrombectomy. The need for lower extremity AV dialysis access appears to be a significant marker for late mortality in this group of chronically ill patients. They are associated with multiple complications and should probably be placed only if significant patient morbidity can be accepted and justified.
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PMID:Results and complications of arteriovenous access dialysis grafts in the lower extremity: a five year review. 860 76

Although successful simultaneous pancreas and kidney transplantation (SPK) achieves normoglycemia in the majority of diabetic recipients with end-stage renal disease, little is known about the factors that influence long-term endocrine function. In this prospective study of 48 bladder-drained SPK patients, 209 oral glucose tolerance tests were performed between 3 months and 6 years after transplantation. Normal fasting glucose levels and systemic hyperinsulinemia were stable for up to 6 years after SPK. Multivariate analysis revealed that increased area-under-curve (AUC) levels of C-peptide 3 months after transplantation were predicted by short surgical pancreas anastomosis time, greater recipient body weight, and total HLA mismatch score. Episodes of acute pancreas rejection were not associated with reduced allograft insulin output in the long term. Insulin output, stimulated by oral glucose tolerance tests and assessed by the ratio of AUC insulin to AUC glucose, fell gradually after transplantation and was decreased by an elevated serum calcium level and high cyclosporine dose. The ratio of fasting insulin to glucose, which acts as a marker of peripheral insulin resistance, fell with time after transplantation and was increased by greater body weight, higher prednisolone dose, and lower cyclosporine dose. The inhibitory effect of cyclosporine on both fasting and postprandial insulin output was, however, minor when quantified by multivariate analysis. Endocrine function of the transplanted pancreas was not correlated with its exocrine function measured by urinary amylase excretion, nor was there a correlation with change in renal function measured by isotopic glomerular filtration rate. In summary, simultaneous pancreas and kidney transplantation leads to excellent long-term glucose homeostasis maintained at the expense of systemic hyperinsulinemia. The key factors adversely affecting peripheral resistance in SPK were corticosteroid therapy, body weight, and time after transplantation. The susceptibility of islets to ischemia-reperfusion injury, as quantitated by surgical anastomosis time, may have implications for islet transplantation programs, as may the relative resistance of islets to allograft rejection. Glucose homeostasis after SPK, while remaining abnormal, may be used as the standard against which islet transplantation must be measured.
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PMID:Clinical determinants of glucose homeostasis after pancreas transplantation. 868 47

This review updates the advances in basic and clinical studies of adhesion molecules in renal disease that have appeared in 1995. The primary focus is on ischemia and transplantation.
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PMID:Adhesion molecules in renal disease. 873 61

Patients with end-stage renal disease often demonstrate retarded healing of surgical wounds, but the basis for spontaneous wound formation in these patients is less well understood. We report our experience with four patients with a unique clinical entity previously described as the uremic gangrene syndrome (also known as calciphylaxis) that involves spontaneously forming and insidiously progressive wounds of the skin and soft tissue in uremic patients with hyperparathyroidism. The importance of recognizing this phenomenon relates to the potential benefit to wound-healing efforts resulting from subtotal parathyroidectomy and adjustment of serum calcium and phosphate levels when severe hyperparathyroidism is present. Disrupted parathyroid homeostasis as a mechanism for soft-tissue ischemia and subsequent infarction is supported by wound biopsies demonstrating microarterial calcification. As experts in factors resulting in refractory wounds, plastic surgeons need be aware of this peculiar vulnerability for spontaneously forming wounds in uremic patients. Clinical and laboratory findings, success with wound treatment in four patients, and currently popular pathophysiologic mechanisms are discussed.
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PMID:The uremic gangrene syndrome: improved healing in spontaneously forming wounds following subtotal parathyroidectomy. 877 89


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