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Renal failure, acute risk factors

Gastrointestinal complaints (eg, nausea, diarrhea, vomiting, flatulence) are the most common adverse effects but rarely require discontinuation of therapy. Other potential adverse effects include headache and asthenia. Tenofbvir-associated proximal renal tubulopathy causes excessive renal phosphate and calcium losses and 1-hydroxylation defects of vitamin D, and preclinical studies in several animal species have demonstrated bone toxicity (eg, osteomalacia). Monitoring of bone mineral density should be considered with long-term use in those with risk factors for or with known osteoporosis, as well as in children. Reduction of renal function over time, as well as cases of acute renal failure and Fanconi s syndrome, have been reported in patients receiving tenofovir alone or in combination with emtricitabine. For this reason, tenofovir should be used with caution in patients at risk for renal dysfunction. Tenofovir may compete with other drugs that are actively secreted by the kidneys, such as cidofovir, acyclovir, and ganciclovir. [Pg.1078]

Diabetes is a major risk factor for deterioration in renal function after angiography (2,7,13). Other factors variably associated with increased rates of CIN include age over 75 years, anemia, female gender, periprocedural volume depletion, heart failure, cirrhosis, hypertension, proteinuria, concomitant use of nonsteroidal anti-inflammatory drugs, and intra-arteriai injection (2,4,5,7,10,13,14,19,43,44). In the setting of acute myocardial infarction or PCI, hypotension or use of an intra-aortic balloon pump has been associated with a higher rate of acute renal failure after exposure to a contrast medium (13,50). Finally, high doses of CM also increase the likelihood of renal dysfunction (51). [Pg.495]

McCullough PA, Wolyn R, Rocher LL, et al. Acute renal failure after coronary intervention incidence, risk factors, and relationship to mortality. Am J Med 1997 103 368-375. [Pg.500]

As shown in Fig. 54, the types of exercise taken by the patients consisted of a track race (a short-distance sprint such as a 200-m race), soccer, a swimming race, baseball, weightlifting, and a bicycle race, in all of which an intense power output per second or per minute is repeated. However, a single 100-m race was less likely to cause exercise-induced acute renal failure (ALPE). Several 200-m or 100-m races frequently caused ALPE. Repeated anaerobic exercise may be a risk factor. [Pg.56]

Risk factors for exercise-induced acute renal failure (ALPE) include anaerobic exercise, renal hypouricemia, administration of antipyretic analgesics for cold, and dehydration. We review renal hypouricemia here and in Chap.10. [Pg.61]

Dehydration is a risk factor for all types of acute renal failure. It promotes the onset of ALPE, but may not be an important factor. The significance of dehydration in the pathogenesis of ALPE remains to be clarified. [Pg.70]

A previous medical history of non-insulin dependent diabetes mellitus and hypertension are added risk factors for developing acute renal failure, as they will predispose the patient to having a degree of chronically impaired renal function. [Pg.372]

The nonsalicylate NSAIDs can also affect renal function. Risk factors fc>r NSAID-induced acute renal failure include congestive heart feilure, glomerulonephritis, chronic renal insufficiency, cirrhosis, systemic lupus erythematosus, diabetes mellitus, significant atherosclerotic disease in the elderly and use of diuretics. NSAIDs can adversely affect cardiovascular homeostasis and can be a risk factor for the onset or exacerbation of heart feilure. [Pg.102]

In contrast, published case reports and case series have provided more insight into the potential nephrotoxicity associated with COX-2-selective inhibitors. Taken together, these case reports suggest that COX-2 inhibitors, like non-selective NSAIDs, produce similar and consistent renal adverse effects in patients with one or more risk factors that induce prostaglandin-dependent renal function (that is patients with renal and cardiovascular disease and taking a number of culprit medications, such as diuretics and ACE inhibitors). Acute renal insufficiency, disturbances in volume status (edema, heart failure), metabolic acidosis, hyperkalemia, and hyponatremia have been commonly described. The duration of treatment with COX-2 inhibitors before the development of chnically recognized renal impairment ranged from a few days to 3-4 weeks. Withdrawal of COX-2 inhibitors and supportive therapy most often resulted in resolution of renal dysfunction, but in some patients hemodialysis was required (102,108-112). [Pg.1009]

Boldt J. Hydroxyethylstarch as a risk factor for acute renal failure is a change of clinical practice indicated Drug Saf 2002 25(12) 837-46. [Pg.1294]

The actual risk of NSAID-associated acute renal dysfunction also continues to be the subject of controversy. There is adequate evidence that underlying renal insufficiency, congestive heart failure, or hepatic cirrhosis are conditions that carry a high risk of NSAID-related renal functional impairment. It is still not known whether old age is a risk factor, whether the risk of renal impairment varies with different NSAIDs, or whether renal function continues to deteriorate, stabilize, or even improve in affected patients with continued use of NSAIDs. Three cases of renal insufficiency caused by topical NSAIDs have been described (SEDA-18,100). [Pg.2567]

Rasmussen HH, Ibels LS. Acute renal failure multi variant analysis of causes and risk factors. Am J Med 1982 73 211-218. [Pg.22]

Shusterman N, Strom BL, Murray TG, Morrison G, West SL, and Maislin G. 1987. Risk factors and outcome of hospital-acquired acute renal failure. Clinical epidemiologic study. Am7Med83 65-71. [Pg.40]

Anderson LG, Ekroth R, Bratteby EE, Hallhagen S, and Wesslen 0.1993. Acute renal failure after coronary surgery-a study of Incidence and risk factors In 2009 consecutive patients. Thorac Cardiovasc Surg 41 237-241. [Pg.41]

Lima EQ,Zanetta DM, Castro i, Massarollo PC, MiesS, Machado MM, Yu L. Risk factors for development of acute renal failure after liver transplantation. Ren Eail 2003 25 553-560. [Pg.662]

Hingorani SR, Guthrie K, Batchelder A, Schoch G, Aboulhosn N, Manchion J, McDonald GB. Acute renal failure after myeloablative hematopoietic cell transplant incidence and risk factors. Kidney int 2005 67 272-277. [Pg.662]

Nephrotoxicity induced by radiographic contrast media is the third leading cause of hospital-acquired acute renal failure.The incidence rises from <2% in patients with low risk to 40% to 50% in high-risk patients such as those with pre-existent renal insufficiency or diabetes melhtus. " " The risk of contrast nephropathy increases as the number of risk factors increases, and diabetic patients with renal insufficiency have the greatest risk." " ... [Pg.876]

The major risk factor for acute renal failure is an elevated lithium concentration, particularly in association with dehydration. Concomitant therapy with neuroleptic agents may contribute. Chronic nephrotoxicity may result from cumulative damage due to repeated episodes of acute renal injury. [Pg.885]


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See also in sourсe #XX -- [ Pg.372 ]




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