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Renal failure pathophysiology

De Vriese AS, Robbrecht DL, Vanholder RC, Vogelaers DP, Lameire NH. Rifampicin-associated acute renal failure pathophysiologic, immunologic, and clinical features. Am J Kidney Dis 1998 31(1) 108-15. [Pg.3048]

Apply knowledge of the pathophysiology of acute renal failure to the development of a treatment plan. [Pg.361]

These adaptations are lost as renal failure progresses. [Ca] X [POJ calcium-phosphorus product. (From Joy MS, Kshirsagar A, Paparello J. Chronic kidney disease Progression-modifying therapies. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 834, with permission.)... [Pg.388]

The pathophysiology, clinical manifestations, diagnosis, and treatment of acute renal failure and chronic kidney disease (CKD) or end-stage renal disease are discussed in Chaps. 75 and 76, respectively. [Pg.888]

Quigley s group in Cork, Ireland, have concluded that normal aging is associated with changes in motility but the pattern is varied and no clear clinical consequence can be identified (67). More important in their view are the pathophysiological influences, including depression (and treatment with anti-cholinergics and opiates), hypothyroidism, and chronic renal failure. [Pg.117]

Pathophysiologically normochromic and normo-cytic anaemia, as occurs in many clinical syndromes exemplified by renal failure, a number of cancers, rheumatoid arthritis and systemic lupus erythematosus, is typical. Initially erythrocytes are of normal size and degree of haemoglobinization. However, persistent impairment of iron supply, especially from mitochondria to globin in the cytoplasm, leads to them becoming hypochromic and microcytic. [Pg.734]

Osbourne CA, Finco DR, Low DG (1983) Pathophysiology of renal disease, renal failure and uremia. In Ettinger SJ (ed) Textbook of Veterinary Internal Medicine, 3rd edn. W.B. Saunders, Philadelphia, pp 1733-1798 Sharratt M, Frazer AC (1963) The sensitivity of function tests in detecting renal damage in the rat. Toxicol Appl Pharmacol 5 36 18... [Pg.108]

Rossen B, Steiness I. The pathophysiology of acute renal failure after chlorprothixene overdosage. Acta Med Scand 1981 209(6) 525-7. [Pg.253]

Traditionally, when searching for the etiology of AKI, the clinician s will subdivides the potential causes of a sudden decline of GFR into one of three general pathophysiologic processes pre renal failure, intrarenal failure or post renal failure [1]. Recently, Miet et al [ 52] in discussing drug-induce acute kidney injury detailed two additional mechanisms that need to be considered in addition to those outlined in Table 2. [Pg.9]

Lieberthal W, Levinsky NG. Acute renal failure. In The kidney physiology and pathophysiology. Seldin W, Giebish G (editors). Raven Press, New York 1992 p 3181-3225. [Pg.24]

Stein JH, Gottschall J, Osgood RW, Ferris TF Pathophysiology of a nephrotoxic model of acute renal failure. Kidney Int 8 27-41, 1975... [Pg.213]

Llach F, Felsenfeld AJ, Haussler MR.The pathophysiology of altered calcium metabolism in rhabdomyolysis-induced acute renal failure. N Engl J Med 1981 305 117-123. [Pg.614]

Hypercalcemia occurs in horses with chronic renal failure and in a few neoplastic conditions. The clinical signs are usually those of the underlying pathophysiology but soft tissue calcification may occur. In experimental ponies, hypercalcemia induced ventricular fibrillation or cardiac arrest at ionized calcium concentrations of 18.2-40mg/dl (4.55-10.0 mmol/1) (Glazier et al 1979). Treatment for severe hypercalcemia (ionized... [Pg.355]

Bames JL, McDowell EM, McNeil JS, et al. 1980. Studies on the pathophysiology of acute renal failure. V. Effect of chronic saline loading on the progression of proximal tubular injury and functional impairment following administration of mercuric chloride in the rat. Vichows Arch B 32 233-260. [Pg.583]

Figure 45-1 i Pathogenesis of ischemic acute renal failure. Hypoxic insults cause vascular responses and tubular damage. (From Bonventre Weinberg JM. Recent advances in the pathophysiology of ischemic acute renal failure. J Am Soc Nephrol 2003 14 2199-210.)... [Pg.1691]

Bonventre JV, Weinberg JM. Recent advances in the pathophysiology of ischemic acute renal failure. J Am Soc Nephrol 2003 14 2199-210. [Pg.1729]

There is epidemiologic evidence to suggest an increased prevalence of duodenal ulcers in patients with certain chronic diseases, but the pathophysiologic mechanisms of these associations are uncertain. A strong association exists in patients with systemic mastocytosis, multiple endocrine neoplasia type 1, chronic pulmonary diseases, chronic renal failure, kidney stones, hepatic cirrhosis, and ai-antitrypsin deficiency. An association may exist in patients with cystic fibrosis, chronic pancreatitis, Crohn s disease, coronary artery disease, polycythemia vera, and hyperparathyroidism. [Pg.632]

Hepatorenal syndrome, functional renal failure in the setting of cirrhosis in the absence of intrinsic renal disease, occurs in patients with cirrhosis as a result of intense vasoconstriction within the renal cortical vasculature. It is common and develops in approximately 40% of patients with cirrhosis and ascites within 5 years. The resultant reduction in blood supply to the kidneys causes avid sodium retention and oliguria. The vasoconstriction that occurs in the kidneys is in stark contrast to the state of systemic vasodilation that is characteristic of chronic liver failure. The pathophysiologic mechanism responsible for these effects is unknown, but is linked to the systemic vasodilation, hypovolemia, and hyperkinetic circulation seen in chronic liver failure. ... [Pg.707]


See other pages where Renal failure pathophysiology is mentioned: [Pg.130]    [Pg.362]    [Pg.370]    [Pg.426]    [Pg.273]    [Pg.355]    [Pg.734]    [Pg.220]    [Pg.234]    [Pg.282]    [Pg.12]    [Pg.1467]    [Pg.210]    [Pg.470]    [Pg.485]    [Pg.1683]    [Pg.1691]    [Pg.553]    [Pg.226]    [Pg.782]   
See also in sourсe #XX -- [ Pg.361 ]




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