Renal failure, acute functional

Amphetamines have also been associated with a syndrome of acute kidney injury and rhabdomyolysis. Several series have described patients following intravenous injection of methamphetamine or phenmetrazine who presented with hyperactivity, fever, chills, sweats, abdominal cramps, diarrhea, and hypotension [177,178]. The patients have developed acute kidney injury which is usually oliguric and associated with classic rhabdomyolysis, similar to cases of cocaine-induced rhabdomyolysis. Several patients have had disseminated intravascular coagulation and liver function abnormalities as well. Methamphetamine abuse has also been associated with accelerated hypertension, unexplained chronic renal failure, acute lead poisoning (a common reagent used in its production utilizes lead acetate) and at least one case of biopsy proven interstitial nephritis the latter patient responded to intravenous corticosteroids but whether the nephritis was truly due to amphetamines remains unproven [179]. 

Provide intensive supportive care. Including hemodialysis if needed, for acute renal failure. Kidney function Is usually regained in 2-3 weeks. 

The nurse immediately reportsany signs of acetaminophen toxicity, such as nausea, vomiting, anorexia, malaise, diaphoresis abdominal pain, confusion, liver tenderness hypotension, arrhythmias jaundice, and acute hepatic and renal failure. Early diagnoss is important because liver failure may be reversible. Toxicity is treated with gastric lavage, preferably within 4 hours of ingestion of the acetaminophen. Liver function studiesare perform ed frequently. Acetylcysteine (Mucomyst) is an antidote to acetaminophen toxicity and acts by protect-... 

Renal—hematuria, cystitis, elevated blood urea nitrogen, polyuria, dysuria, oliguria, and acute renal failure in those with impaired renal function... 

O Equations to estimate creatinine clearance that incorporate a single creatinine concentration (e.g., Cockcroft-Gault) may underestimate or overestimate kidney function depending on whether acute renal failure is worsening or resolving. 

Mehta RL, Pascual MT, Soroko S, et al. Diuretics, mortality, and nonrecovery of renal function in acute renal failure. JAMA 2002 288 2547-2553. 

The initial dose of allopurinol is based on the patient s renal function. Patients with creatinine clearances of 50 mL/minute or less should receive a starting dose of less than 300 mg/day to minimize adverse effects. The relationship between dose of allopurinol and its most severe side effects is controversial. However, the dose can be adjusted upward as needed and tolerated. It is reasonable to reduce the dose temporarily in patients who develop reversible acute renal failure. 

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. 

Acute renal failure is a rare but serious side effect of ACE inhibitors preexisting kidney disease increases the risk. Bilateral renal artery stenosis or unilateral stenosis of a solitary functioning kidney renders patients dependent on the vasoconstrictive effect of angiotensin II on efferent arterioles, making these patients particularly susceptible to 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. 

Assessment of renal function is not required prior to first administration to man or even during clinical development however, based on the potential implications of acute renal failure and the challenges in assessing it in normal healthy animals or humans, it would make sense to consider a proper assessment of renal function prior to first administration to humans. 

Neither P840 nor iodixanol had major deleterious consequences on the GFR up to 90 min following injection (Table 9). The selected doses were different for P840 and iodixanol since the expected clinical dose of the SCBPA is lower than that of a classic NS-CA. Since acute renal failure is defined as a rapid and sustained decrease in renal function and since renal function is best evaluated by measurement of the GFR [36], such a parameter appears to be of particular clinical interest. 

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." ... 

In patients with severe CHF whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, treatment with ACEIs may be associated with oliguria or progressive azotemia and, rarely, with acute renal failure or death. Impaired renal function decreases lisinopril elimination. The elimination half-life of quinaprilat increases as Ccr decreases. Dosage adjustment may be necessary for quinapril, benazepril, ramipril, and lisinopril. Impaired renal function decreases... 

Renai function impairment Dosage reduction is recommended with renal impairment (see Administration and Dosage). Acute renal failure and CNS symptoms have been reported in patients with underlying renal disease who have received inappropriately high doses for their level of renal function. Exercise similar caution when administering valacyclovir to elderly patients and patients receiving potentially nephrotoxic agents. 

Renal function impairment Renal impairment, including cases of acute renal failure and Fanconi syndrome, has been reported in association with the use of tenofovir. Avoid tenofovir with concurrent or recent use of a nephrotoxic agent. Carefully monitor patients at risk for, or with a history of, renal dysfunction and patients... 

Renal - Methotrexate may cause renal damage that may lead to acute renal failure. Close attention to renal function including adequate hydration, urine alkalinization and measurement of serum methotrexate and creatinine levels are essential for safe administration. 

Lithium intoxication can be precipitated by the use of diuretics, particularly thiazides and metola-zone, and ACE inhibitors. NSAIDs can also precipitate lithium toxicity, mainly due to NSAID inhibition of prostaglandin-dependent renal excretion mechanisms. NSAIDs also impair renal function and cause sodium and water retention, effects which can predispose to interactions. Many case reports describe the antagonistic effects of NSAIDs on diuretics and antihypertensive drugs. The combination of triamterene and indomethacin appears particularly hazardous as it may result in acute renal failure. NSAIDs may also interfere with the beneficial effects of diuretics and ACE inhibitors in heart failure. It is not unusual to see patients whose heart failure has deteriorated in spite of increased doses of frusemide who are also concurrently taking an NSAID. 

Baseline electrolytes, renal function tests, and urinalysis baseline and at least BUN, creatinine, potassium within 2 weeks after initiation of therapy (increased levels may indicate acute renal failure)... 

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