Acute renal failure injury

Acute tubular necrosis A form of acute renal failure that results from toxic or ischemic (insufficient oxygen) injury to the cells in the proximal tubule of the kidney. 

Renal impairment, including cases of acute renal failure and Fanconi syndrome (renal tubular injury with severe hypophosphatemia), has been reported in association with the use of tenofovir disoproxil fumarate. 

Ethanol. Alcohol (ethanol) ingestion has repeatedly been associated with potentiation of carbon tetrachloride-induced hepatic and renal injury in humans. In two cases in which men cleaned furniture and draperies with carbon tetrachloride, one man, a heavy drinker, became ill and died (Smetana 1939). His coworker, a nondrinker, suffered a headache and nausea but recovered quickly after breathing fresh air. Both men were subjected to the same carbon tetrachloride exposure, as they had been working in the same room for the same amount of time. In 19 cases of acute renal failure due to carbon tetrachloride inhalation or ingestion, 17 of 19 patients had been drinking alcoholic beverages at about the time of their carbon tetrachloride exposure (New et al. 

As their name suggests, osmotic diuretics such as mannitol (Osmitrol), isosorbide (Ismotic), and glycerin (Osmoglyn) draw fluid from the tissues of the body through principles of osmosis. Osmotic diuretics are typically given to treat or prevent acute renal failure (kidney failure). They may also be used to relieve intracranial pressure (swelling of the brain) in cases of head injury or hydrocephalus. 

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,... 

Lieberthal, W. and Nigam, S. K. (1998). Acute renal failure. I. Relative importance of proximal vs. distal tubular injury. Am. J. Physiol. 275 (5 Pt. 2), F623-F631. 

In 1982, we classified exercise-related acute renal failure into two types myoglobinuric acute renal failure, as had previously been reported, and non-myoglobin-related acute renal failure (exercise-induced acute renal failure). In 2002, the latter was named ALPE (Acute renal failure with severe Loin pain and Patchy renal ischemia after anaerobic Exercise) [4]. The term acute kidney injury (AKI) has recently been proposed as a patho-physiologically more correct alternative to the term acute renal failure. Therefore, exercise-induced acute renal failure in this book may be replaced by exercise-induced acute kidney injury. 

The protocol for inducing crescentic glomerulonephritis in mice was adapted from an earlier study (7), modified for our NTS to avoid rapid lethality from acute renal failure while ensuring adequate tissue injury for analysis (see Fig. 1). 

Stevens P (2007). Assessment of patients presenting with acute renal failure (acute kidney injury). Medicine 35 429-433... 

LiangosO, Perianayagam MC, Vaidya VS, Han WK, Wald R,Tighiouart H, MacKinnon RW, Li L, Balakrishnan VS, Pereira BJ, Bonventre JV, Jaber BL. Urinary N-acetyl-beta-(D)-glucosaminidase activity and kidney injury molecule-1 level are associated with adverse outcomes in acute renal failure J Am Soc Nephrol 2007 18 904-912. 

Drug-induced tubulointerstitial nephritides represent 1-10% of cases of acute renal failure and is characterized by infiltrates of mononuclear cells associated with tubular cell injury. A lot of drugs are incriminated, including antibiotics (P-lactams, sulfonamides, aminoglycosides, quinolones), antiepileptic drugs, diuretics, proton pump inhibitors, foscarnet and non-steroidal anti-inflammatory drugs [73]. Most often, withdrawal of the drug, with or without concomitant administration of steroids improves the renal functions. 

Racusen EC Renal histopathology and urine cytology and cytopathology in acute renal failure., chap. 9, in Acute renal failure. New concepts and therapeutic strategies, edited by Goligorsky MS, Stein JEI, New York, Churchill Eivingstone, 1995, p 194 Edelstein CL, Ling H, Schrier RW The nature of renal cell injury. Kidney Int 51 1341-1351,1997... 

Jennette JC, Falk RJ Acute renal failure secondary to leukocyte-mediated acute glomerular injury. Ren Fail. 14 395-399,1992... 

Endre ZEI, Ratcliffe PJ Patterns of ischaemic renal cell injury, in Acute Renal Failure, edited by Solez K, Racusen EC, New York, Marcel Dekker, 1990, pp 173-185... 

Zager RA, Johnson AC, Lund S, Flanson S, Acute renal failure determinants and characteristics ofthe injury-induced hyperinflam-matory response. Am J Physiol, 2006, 291 F546-56. 

Gordon JA, Gattone VH. Mitochondrial alterations In cisplatin-induced acute renal failure. Am J Physiol 1986 250 F991-8. Brady HR, Kone BC, StronIskI ME, Zeldel ML, Glebisch G, Gullans SR. Mitochondrial Injury an early event In cisplatin-toxicity to renal proximal tubules. Am J Physiol 1990 258 FI 181-7. 

Heyman SN, Brezis M, Reubinoff CA, Greenfeld Z, Lechene C, Epstein FH, Rosen S. Acute renal failure with selective medullary injury in the rat. J Clin Invest 1988 82 401 -412. 

Cases of anuria have been reported when EDTA was administered to treat lead poisoning. Such kidney injury is reversible and is probably not due to the chelate directly, but to the reabsorption of the metal in the tubules. Of 130 children that received dime-rcaprol and EDTA, 3% developed acute renal failure and 13% had biochemical evidence of nephrotoxicity. However, lead poisoning can cause kidney injury without EDTA therapy. In another study, 122 patients were given EDTA and none showed posttreatment increases in plasma creatinine. 

Hypoglycemia can be seen. Rhabdomyolysis, acute renal failure, disseminated intravascular coagulation, liver necrosis, and traumatic injury are reported complications. The anesthetic dose of phencyclidine is 0.25 mg kg intravenously. Doses of 1-5 mg are purported to cause euphoria and numbness, 5-10 mg cause excitation and hallucinations, and 20 mg or more cause coma and serious toxicity or death. Plasma concentrations of phencyclidine vary widely after overdose. Phencyclidine crosses the placenta resulting in hyperirritability, tremors and hypertonia, depressed reflexes, and nystagmus in neonates. 

A number of toxicants and drugs are known to induce renal injury resulting in acute renal failure, a prevalent clinical condition. These include... 

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