Renal failure, acute, causes

Brivet EG, Kleinknecht DJ, Loirat P, Landais PJM, the French Study Group on Acute Renal Failure. Acute renal failure in intensive care units causes, outcome, and prognostic factors of hospital mortality a prospective, multicenter study. Crit Care Med 1996 24 192-198. 

Toxicology LD50 (IP, mouse) 830 mg/kg mod. toxic by IP route may cause changes in tubules incl. acute renal failure, acute tubular necrosis TSCA listed... 

The water solubiUty of glutaric acid fosters its toxicity. Glutaric acid is a known nephrotoxin. Renal failure has been documented ia rabbits adruinistered sodium glutarate subcutaneously (124). Dibasic ester (Du Pont), which contains primarily dimethyl glutarate, has low acute toxicity by inhalation and by ingestion, and is moderately toxic via dermal absorption. The acid is both a dermal and ocular irritant of humans. The ester is a severe skin irritant and may cause a rash ia humans (120). 

Renal Effects. Hemorrhage of the medullary layer of the kidneys was observed in an early report of three fatal cases of acute oral poisoning with endosulfan (Terziev et al. 1974). More recent studies have reported acute renal failure after ingestion of endosulfan as a major contributing cause of death in two individuals in both cases, postmortem examination showed extensive tubular necrosis (Blanco-Coronado et al. 1992 Lo et al. 1995). Neither case discussed the possible mechanism of endosulfan-induced acute renal failure, but in one case, the authors of the report indicate that the renal lesions may relate to sepsis and shock (Blanco-Coronado et al. 1992). Ingested doses were not determined in any of these cases, and it is not totally clear that the effects observed at autopsy were a direct result of endosulfan exposure, although based on results from acute animal studies, it seems likely. 

O Brien KL et al. Epidemic of pediatric deaths from acute renal failure caused by diethylene glycol poisoning. Journal of the American Medical Association, 1998, 279(15) 175-78. 

Causes of hypocalcemia include hypoparathyroidism, hypomagnesemia, alcoholism, hyperphosphatemia, blood product infusion (due to chelation by the citrate buffers), chronic renal failure, vitamin D deficiency, acute pancreatitis, alkalosis, and hypoalbuminemia. Medications that cause hypocalcemia include phosphate replacement products, loop diuretics, phenytoin (Dilantin, available as generic), pheno-barbital (available as generic), corticosteroids, aminoglycoside antibiotics, and acetazolamide (available as generic).34,39,42... 

Osmotic diuretics such as mannitol act on the proximal tubule and, in particular, the descending limb of the Loop of Henle — portions of the tubule permeable to water. These drugs are freely filtered at the glomerulus, but not reabsorbed therefore, the drug remains in the tubular filtrate, increasing the osmolarity of this fluid. This increase in osmolarity keeps the water within the tubule, causing water diuresis. Because they primarily affect water and not sodium, the net effect is a reduction in total body water content more than cation content. Osmotic diuretics are poorly absorbed and must be administered intravenously. These drugs may be used to treat patients in acute renal failure and with dialysis disequilibrium syndrome. The latter disorder is caused by the excessively rapid removal of solutes from the extracellular fluid by hemodialysis. 

Acute drug-related hypersensitivity reactions (allergic responses) may cause tubulointerstitial nephritis, which will damage the tubules and interstitium. These reactions are most commonly observed with administration of methicillin and other synthetic antibiotics as well as furosemide and the thiazide diuretics. The onset of symptoms occurs in about 15 days. Symptoms include fever, eosinophilia, hematuria (blood in the urine), and proteinuria (proteins in the urine). Signs and symptoms of acute renal failure develop in about 50% of the cases. Discontinued use of the drug usually results in complete recovery however, some patients, especially the elderly, may experience permanent renal damage. 

The metabolic encephalopathies comprise a series of neurological disorders not caused by primary structural abnormalities rather, they result from systemic illness, such as diabetes, liver disease and renal failure. Metabolic encephalopathies usually develop acutely or subacutely and are reversible if the systemic disorder is treated. If left... 

Parathyroid hormone (PTH) produces CNS effects in normal subjects and neuropsychiatric symptoms are frequently encountered in patients with primary hyperparathyroidism, where EEG changes resemble those described in acute renal failure. Circulating PTH is not removed by hemodialysis. In uremic patients both EEG changes and neuropsychiatric symptoms are improved by either parathyroidectomy or medical suppression of PTH. The mechanism whereby PTH causes disturbances of CNS function is not well understood, but it has been suggested that increased PTH might facilitate the entry of Ca2+ into the cell resulting in cell death. 

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Monitoring changes in UOP can help diagnose the cause of ARF. Acute anuria (less than 50 mL urine/day) is secondary to complete urinary obstruction or a catastrophic event (e.g., shock). Oliguria (400 to 500 mL urine/day) suggests prerenal azotemia. Nonoliguric renal failure (more... 

Abnormality Causing Category Acute Renal Failure... 

TABLE 75-2 Diagnostic Parameters for Differentiating Causes of Acute Renal Failure ... 

Common laboratory tests are used to classify the cause of ARF. Functional ARF, which is not included in this table, would have laboratory values similar to those seen in prerenal azotemia. However, the urine osmolality-to-plasma osmolality ratios may not exceed 1.5, depending on the circulating levels of antidiuretic hormone. The laboratory results listed under acute intrinsic renal failure are those seen in acute tubular necrosis, the most common cause of acute intrinsic renal failure. 

Acute renal failure due to NSAIDs is usually due to prerenal causes but may be caused by acute interstitial nephritis. Usually the worsening in renal function does not depend on dose (Muhlberg and Platt 1999). Use of NSAID is thus risky and may affect the elimination of concomitant medications. 

A common cause of renal failure in the elderly is the use of NSAIDs and it occurs more frequently in women. One to five percent of treatment with NSAIDs leads to some kind of renal dysfunction and mostly vasomotor acute renal failure occurs (Bakris and Kern 1989, Griffin et al. 2000, Henry et al. 1997). 

These results suggest acute renal failure (ARF) due to tubular necrosis caused by phenol. Plasma sodium is low due mainly to impaired reabsorption in the nephron, although the slightly low albumin suggests haemodilution possibly as a result of excessive i.v. fluids. Potassium is raised due to poor exchange with sodium in the distal tubule and the acidosis (low pH and low bicarbonate concentration) arises from defective acidification of the glomerular filtrate acidosis is often associated with hyperkalaemia (raised plasma... 

Abdominal cramps, vomiting, and diarrhea occurred in a truck driver who was exposed to diesel fuel vapor for 10 days while driving a truck with a leaking fuel injector. Acute renal failure was also observed. One case study describes eye irritation in two individuals exposed to JP-5 fuel (kerosene) for approximately 1 hour while flying an airplane. Coordination and concentration difficulties were noted, as were headache, apparent intoxication, and anorexia. Inhalation of 140mg/m deodorized kerosene by six volunteers caused olfactory fatigue in three subjects and a taste sensation in... 

Death from pulmonary edema occurred within 2 hours in three of six workers splashed with 70% solution, despite prompt showering with water. The HF concentration in the breathing zone was estimated to be above 10,000 ppm. A chemist exposed to HF splashes on the face and upper extremities developed pulmonary edema 3 hours after exposure and died 10 hours later. Persistent respiratory symptoms, including hoarseness, coughing fits, and nosebleeds, but with normal pulmonary function, were observed in one subject who survived a massive exposure. Acute renal failure of uncertain cause has also been documented after an ultimately fatal inhalation exposure." ... 

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