Renal failure/rhabdomyolysis caused

Note in addition to the conditions listed, any cause of adrenal or renal failure, rhabdomyolysis, or hemolytic anemia may cause hyperkalemia. 

WARNING Cases of fulminant liver failure resulting in death have occurred Uses Adjunct to carbidopa/levodopa in Parkinson Dz Action COMT inhibitor slows levodopa metabolism Dose 100 mg PO tid w/ 1st daily levodopa/carbidopa dose, then dose 6 12 h later -1- w/ renal impair Caution [C, ] Contra Hqjatic impair, w/ nonselective MAOI Disp Tabs SE Constipation, XCTOstomia, vivid dreams, hallucinations, anorexia, N/D, orthostasis, liver failure, Rhabdomyolysis Interactions T Effects OF CNS dqjressants, SSRIs, TCAs, warfarin, EtOH t risk of hypotensive crisis W/ nonselective MAOIs (phenelzine, tranylc5 promine) EMS Has been associated w/ liver failure and death may experience hallucinations concurrent EtOH use can T CNS dqjression T effects of warfarin severe D is common sevoal wks afto starting OD May cause NA and dizziness... 

At the doses usually used by stimulant abusers, euphoria and wakefulness are accompanied by a sense of power and wellbeing. At higher doses, restlessness, agitation, and acute psychosis may occur, accompanied by hypertension and tachycardia. Prolonged muscular hyperactivity can cause dehydration and eventually hypotension. Seizures and muscle activity may contribute to hyperthermia and rhabdomyolysis. Body temperatures as high as 42°C (107.6°F) have been recorded. Hyperthermia can cause brain damage, hypotension, coagulopathy, and renal failure. 

The other type is non-myoglobinuric acute renal failure, in which intense exercise over a short period of time, such as sprinting, causes minimal rhabdomyolysis without myoglobinuria, i.e., acute renal failure syndrome with severe loin pain and patchy renal vasoconstriction [2]. A recent study showed that anaerobic exercise caused this syndrome, and proposed that Acute renal failure with severe Loin pain and Patchy renal ischemia after anaerobic Exercise (ALPE) (exercise-induced acute renal failure) was a new type of acute renal failure syndrome [4]. 

Simvastatin, like other inhibitors of HMG-CoA reductase, occasionally causes myopathy manifested as muscle pain, tenderness or weakness with creatine kinase (CK) 10 times above the upper limit of normal (ULN). Myopathy sometimes takes the form of rhabdomyolysis with or without acute renal failure secondary to myoglobinuria, and very rare fatalities have occurred. 

This is caused by excessive stimulation of CNS and peripheral serotonin receptors and is characterized by changes in mental state, autonomic hyperactivity (hypertension, tachycardia, hyperthermia, may be up to 4l°C, hyperactive bowel sounds, mydriasis, excessive sweating) and neuromuscular abnormality (tremor, clonus, ocular clonus, hypertonicity, hyperreflexia) the latter may lead to rhabdomyolysis with consequent risk of renal failure, hyperkalaemia and hypocalcaemia. Symptoms usually occur within 6 hours of taking the provoking drug, Tremor, akathisia and diarrhoea are early features. 

Shimada N, Omuro H, Saka S, Ebihara I, Koide H. [A case of acute renal failure with rhabdomyolysis caused by the interaction of theophylline and clarithromycin.] Nippon Jinzo Gakkai Shi 1999 41(4) 460-3. 

Adverse effects include increased risk of seizures, myocardial infarction, rhabdomyolysis, renal failure, and stroke. Other life-threatening adverse effects include hyperthermia, hypertension, vasoconstriction, tachycardia, cardiac ischemia, and paranoia. Prolonged cocaine abuse has been shown to cause cardiomyopathy. 

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. 

Metabolic acidosis with an increased SAG commonly results from increased endogenous organic acid production. In lactic acidosis, lactic acid accumulates as a by-product of anaerobic metabolism. Accumulation of the ketoacids /S-hydroxybutyric acid and acetoacetic acid defines the ketoacidosis of uncontrolled diabetes mellitus, alcohol intoxication, and starvation (see Table 51-5). In advanced renal failure, ac-cumulation of phosphate, sulfate, and organic anions is responsible for the increased SAG, which is usually less than 24 mEq/L." The severe metabolic acidosis seen in myoglobinuric acute renal failure caused by rhabdomyolysis may be caused by the metabolism of large amounts of sulfur-containing amino acids released from myoglobin. 

Rhabdomyolysis—The breakdown of muscle tissue and release of myoglobin and intracellular electrolytes into the circulation due to a variety of causes such as crush injuries, drug-induced immobilization, and status epilepticus. It often leads to acute renal failure. 

I The disorder evolves rapidly over 24-72 hours and lasts for 10-14 days if untreated. Between 5-20% of patients on oral medication and up to 30% of patients on depot formulations who develop the syndrome will die from the condition if imtreated. The usual cause of death is renal failure secondary to rhabdomyolysis. 

Rhabdomyolysis. This is a condition where the heat and mechanical stresses produced in the muscles causes the fibres to break down. This releases large quantities of myoglobin (a simpler form of haemoglobin found in muscles) into the blood stream which can overload the kidneys and lead to renal failure. 

Severe rhabdomyolysis, e.g. following injury, is an important cause of acute renal failure. 

B. Complications. Myoglobin released by damaged muscle cells may precipitate in the kidneys, causing acute tubular necrosis and renal failure. This is more likely when the semm CPK level exceeds several thousand lU/L and if the patient is dehydrated. With severe rhabdomyolysis, hyperkalemia, hyperphosphatemia, hypemricemia, and hypocalcemia may also occur. 

G. Renal failure. Examples of dmgs and toxins causing renal failure are listed in Table I-28. Renal failure may be caused by a direct nephrotoxic action of the poison or acute massive tubular precipitation of myoglobin (rhabdomyolysis), hemoglobin (hemolysis), or calcium oxalate crystals (ethylene glycol) or it may be secondary to shock caused by blood or fluid loss or cardiovascular collapse. 

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