Necrosis, acute tubular

ChanJ. 1995. Acute tubular necrosis following endosulfan insecticide poisoning Author s reply. Clin Toxicol 33(4) 377-378. 

Lo RSK, Chan JC, Cockram CS, etal. 1995. Acute tubular necrosis following endosulphan insecticide poisoning. J Toxicol Clin Toxicol 33(l) 67-69. 

Proximal tubule cells are exquisitely sensitive to vasculat disturbances and acute tubular necrosis (ATN) can occur naturally in areas of poor perfusion resulting from falling blood pressure, or vasospasm of renal vessels or arterioles. In other words hypoxia associated with partial ischaemia can cause severe damage. It is not then surprising that anoxia associated with iatrogenic, surgically induced total ischaemia produces irreversible damage within a short time unless steps are taken to prevent it. 

Loop diuretics (dose depends on severity of renal insufficiency) ° Not directly beneficial in established acute tubular necrosis. 

During phase I, each seizure causes a sharp increase in autonomic activity with increases in epinephrine, norepinephrine, and steroid plasma concentrations, resulting in hypertension, tachycardia, hyperglycemia, hyperthermia, sweating, and salivation. Cerebral blood flow is also increased to preserve the oxygen supply to the brain during this period of high metabolic demand. Increases in sympathetic and parasympathetic stimulation with muscle hypoxia can lead to ventricular arrhythmias, severe acidosis, and rhabdomyolysis. These, in turn, could lead to hypotension, shock, hyperkalemia, and acute tubular necrosis. 

Tubular and interstitial diseases (e.g., analgesic nephropathy, drug-induced nephritis, oxalate nephropathy, radiation nephritis, acute tubular necrosis, and sarcoidosis)... 

ADHD Attention-deficit hyperactivity disorder ATN Acute tubular necrosis... 

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. 

There is evidence that y-aminobutyric acid A receptors may be modified during SE and become less responsive to endogenous agonists and antagonists. Two phases of GCSE have been identified. During phase I, each seizure produces marked increases in plasma epinephrine, norepinephrine, and steroid concentrations that may cause hypertension, tachycardia, and cardiac arrhythmias. Muscle contractions and hypoxia can cause acidosis, and hypotension, shock, rhabdomyolysis, secondary hyperkalemia, and acute tubular necrosis may ensue. 

Acute tubular necrosis Ischemic Hypotension Vasoconstriction Exogenous toxins Contrast dye Heavy metals Drugs (amphotericin B, aminoglycosides, etc.) (continued)... 

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. 

Tubular epithelial cell damage Acute tubular necrosis Pentamidine... 

The nephropathy induced by accumulation of this protein has not been noted in female rats, female mice (studies conducted on male mice were not located), or dogs of either sex when exposed under similar conditions to either JP-5 or marine diesel fuel vapors (Bruner 1984 Cowan and Jenkins 1981 Gaworski et al. 1984). There is no evidence of renal necrosis in humans acutely exposed to JP-5 vapor (Porter 1990). In a case report, one individual exposed to an unspecified diesel fuel for several weeks exhibited acute tubular necrosis (Crisp et al. 1979). However, renal necrosis did not occur in two other individuals acutely exposed to diesel fuel vapor (Barrientos et al. 1977 Reidenberg et al. 1964), although they did... 

Crisp AJ, Bhalla AK, Hoffbrand BJ. 1979. Acute tubular necrosis after exposure to diesel fuel. Br Med J 2 177. 

Acute tubular necrosis (ATN) Drug dosing of nephrotoxic agents Diabetes meUitus... 

Cresols are rapidly absorbed through the skin, producing systemic effects. About 20ml of a 90% cresol solution accidentally poured over an infant s head caused chemical burns, cyanosis, unconsciousness, and death within 4 hours. Histopathologic examination showed hepatic necrosis, cerebral edema, acute tubular necrosis of the kidneys, and hemorrhagic effusions from the peritoneum, pleura, and pericardium. The blood contained 12 mg cresol/lOOdl. 

Aseptic meningitis syndrome-The incidence of this syndrome was 6%. Fever, headache, meningismus, and photophobia were the most commonly reported symptoms a combination of these 4 symptoms occurred in 5% of patients. Headache - Headache is frequently seen after any of the first few doses and may occur in any of the aforementioned neurologic syndromes or by itself. Seizures - Seizures, some accompanied by loss of consciousness or cardiorespiratory arrest, or death, have occurred independently or in conjunction with any of the neurologic syndromes described below. Patients predisposed to seizures may include those with the following conditions Acute tubular necrosis/uremia fever infection a precipitous fall in serum calcium fluid overload hypertension hypoglycemia, history of seizures and electrolyte imbalances those who are taking a medication concomitantly that may, by itself, cause seizures. 

Patients should be warned that rifampicin colors urine, tears and other body fluids reddish-orange. Adverse effects further include rashes and pruritus and gastrointestinal complaints like nausea, anorexia and diarrhoea. With intermittent therapy a probably allergic hypersensitivity reaction can occur which mostly manifests itself as a flu-like syndrome with fever but can also result in nephritis and acute tubular necrosis. Elevation of serum transaminase levels occur frequently but clinical hepatitis is rare. Fatal outcome has been reported however. 

Chemically induced kidney damage is typically seen as acute tubular necrosis (ATN). The cells in the proximal tubule are affected. Reabsorption of water, elec-... 

Inorganic Hg+ (less toxic) Hg2+ (more toxic) Gastrointestinal, skin (minor) Soft tissues, especially kidney Acute tubular necrosis gastroenteritis CNS effects (rare) Inhibits enzymes alters membranes Urine... 

In a 23-year-old woman, a kidney allograft recipient with recurrent lymphoceles treated with povidone-iodine irrigations (50 ml of a 1% solution bd for 6 days), a metabolic acidosis occurred and renal function deteriorated. After a few days, despite suspension of irrigation, the patient developed oliguria, and dialysis was needed. A renal biopsy showed acute tubular necrosis. 

Adverse Effects. The primary problem associated with foscarnet is impaired renal function, including acute tubular necrosis. Hematologic disorders (anemia, granulocytopenia, leukopenia), gastrointestinal disturbances (cramps, nausea, vomiting), and CNS toxicity (confusion, dizziness) may also occur during foscarnet treatment. 

Patients with nephrotic syndrome can develop acute renal failure as a consequence of intravascular hypovolemia and/or sepsis with subsequent prerenal azotemia or acute tubular necrosis. Renal hypoperfusion in these patients can be potentiated by the administration of diuretics, inhibitors of angiotensin-converting... 

Fig. 4. Kidney biopsy. The findings suggested acute tubular necrosis (p. 4)...

Fig. 1. Acute tubular necrosis (acute renal failure) due to myoglobinuria (rhabdomyolysis) after Shorinji Kenpo...

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