Renal failure, acute mortality from

There are numerous abnormalities of cysteine metabolism. Cystine, lysine, arginine, and ornithine are excreted in cystine-lysinuria (cystinuria), a defect in renal reabsorption. Apart from cystine calculi, cystinuria is benign. The mixed disulfide of L-cysteine and L-homocysteine (Figure 30-9) excreted by cystinuric patients is more soluble than cystine and reduces formation of cystine calculi. Several metabolic defects result in vitamin Bg-responsive or -unresponsive ho-mocystinurias. Defective carrier-mediated transport of cystine results in cystinosis (cystine storage disease) with deposition of cystine crystals in tissues and early mortality from acute renal failure. Despite... 

Patients at greatest risk for mortality from acute pancreatitis are those who have multi-organ failure (e.g., hypotension, respiratory failure, or renal failure), pancreatic necrosis, obesity, volume depletion, greater than 70 years of age, and an elevated APACHE II score.3,4 The Acute Physiology, Age, and Chronic Health Evaluation (APACHE) II score is a rating scale of disease severity in critically ill patients. 

Clinical chemistry prior to death for both men revealed metabolic acidosis, acute renal and hepatic failure, skeletal muscle necrosis, and damage to other organ systems. Autolysis of viscera prevented complete characterization of lesions associated with mortality from these... 

Acute renal failure secondary to ischemia-reperfusion or nephro-toxins represents a major cause of morbidity and mortality in hospitalized patients, particularly in the intensive care unit setting. The proximal tubule region of the nephron suffers the most damage in acute renal injury and is therefore the target site of therapeutic interventions. While several experimental therapies have been attempted to prevent or hasten recovery from acute renal injury,... 

Recently, a case of vulture mortality was reported from the Indian subcontinent related to NS AID toxicity. Diclofenac is a widely available veterinary NS AID in the Indian subcontinent, used in domestic livestock. Vultures were exposed to the drug when they consumed carcasses of cattle that were treated with diclofenac shortly before death. Experimental studies of this drug in vultures showed marked nephrotoxicity. The gross observations were primarily deposits of urate on the surface of internal organs related to renal failure. Histopathological findings were acute necrosis of the proximal renal tubular epithelium with minimal inflammatory response and deposits of urate crystals (Oaks et al, 2004 Meteyer et al, 2005). 

Renal Effects. Rabbits, guinea pigs, rats, and mice dermally exposed to uranyl nitrate hexahydrate for 1 day showed proteinuria for up to 10 days, followed by recovery to control values. The degree of proteinuria did not correlate well with the applied dose of uranium. Rabbits had elevated blood NPN at doses over 270 mg U/kg. The animals that died from dermal exposure to uranium had microscopic renal damage typical of uranium poisoning. The kidneys of the animals that did not die were essentially normal, which may reflect repair of acute renal injury (Orcutt 1949). Chemically induced renal failure caused 100% mortality in male Wistar rats after 5 daily exposures to 237 or 1,928 mg U/kg/day as uranyl nitrate hexahydrate or ammonium uranyl tricarbonate, respectively, applied in a water-Vaseline emulsion (De Rey et al. 1983). Deaths from renal failure were also reported in this study for male Wistar rats that received daily apphcations of 1,965 mg U/kg as uranyl acetate dihydrate for 1-11 days. 

Ympa YP, Sakr Y, Reinhart K, Vincent J.L. Elas mortality from acute renal failure decreased A systematic review of the literature. Am J Med 2005 18 827-832). 

Acute renal failure occurs in approximately 5% of all hospitalized patients. The mortality rate of ARF patients who require renal replacement therapy ranges from 40% to as high as 80%. Severe malnutrition has been found in 42% of patients with ARF and is an independent predictor of in-hospital mortality and increased morbidity from sepsis, shock, dysrhythmias, and acute respiratory failure. Since malnutrition is an important contributor to mortality from ARF, nutrition support remains a cornerstone in the treatment of these patients. ... 

Within 10 years of the recognition of this outbreak of acute childhood lead poisoning, an increase in mortality from chronic renal failure was noted in this community and a strong belief grew up that this was a sequel to the acute childhood plumbism. By 1922, the greatly increased mortality from kidney disease throughout Queensland had been established and the Queensland branch of the British Medical Association... 

Impila toxicity is very sudden in onset, and it is suspected that many patients, especially those residing in rural areas, do not reach the hospital alive [1, 7, 8]. Documented cases indicate that symptom duration prior to hospital admission is less than 1 day in 40 % of patients [3, 6]. In fatal cases, death occurs either within a few hours (<24) from hypoglycemic coma [33] or within a few days (<4) from acute hepatic failure [3, 17, 34]. In a few cases, patients have succumbed after several days from uremia due to acute renal tubular necrosis [3, 6]. The chance of survival after severe Impila intoxication is low. It is estimated that 63 % of patients die within 24 h and a further 28 % die within 4 days thus, the total mortality from severe Impila poisoning is up to 91 % [3, 17]. 

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