Renal failure functional

The 23-valent pneumococcal polysaccharide vaccine is recommended for use in all adults 65 years of age or older and adults less than 65 years who have medical comorbidities that increase the risk for serious complications from S. pneumoniae infection, such as chronic pulmonary disorders, cardiovascular disease, diabetes mellitus, chronic liver disease, chronic renal failure, functional or anatomic asplenia, and immunosuppressive disorders. Alaskan natives and certain Native American populations are also at increased risk. Children over the age of 2 years may be vaccinated with the 23-valent pneumococcal polysaccharide vaccine if they are at increased risk for invasive S. pneumoniae infections, such as children with sickle cell anemia or those receiving cochlear implants. 

Common laboratory tests are used to classify the cause of acute renal failure. Functional acute renal failure, 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. 

Sotalol is rapidly and almost completely (>90%) absorbed. Bioavahabhity of absorbed dmg is 89—100%. Peak plasma levels are achieved in 2—4 h. Sotalol is 50% bound to plasma proteins. Plasma half-life of the compound is about 5.2 h. No metabolites of sotalol have been identified indicating littie metabolism. The dmg is excreted mainly by the kidneys (80—90%) and about 10% is eliminated in the feces. The plasma half-life is prolonged in patients having renal failure. Kinetics of the compound are not affected by changes in liver function (1,2). Sotalol has ah the adverse effects of -adrenoceptor blockers including myocardial depression, bradycardia, transient hypotension, and proarrhythmic effects (1,2). 

FLUCONAZOLE Because older adults are more likely to have decreased renal function, they are at increased risk for further renal impairment or renal failure. 

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... 

Death from overdose of barbiturates may occur and is more likely when more than 10 times the hypnotic dose is ingested. The barbiturates with high lipid solubility and short half-lives are the most toxic. Thus the lethal dose of phenobarbital is 6—10 g, whereas that of secobarbital, pentobarbital, or amo-barbital is 2-3 g. Symptoms of barbiturate poisoning include CNS depression, coma, depressed reflex activity, a positive Babinski reflex, contracted pupils (with hypoxia there may be paralytic dilation), altered respiration, hypothermia, depressed cardiac function, hypotension, shock, pulmonary complications, and renal failure. 

All patients with major patterns are monitored for rhabdomyolysis and renal failure. An early sign of rhabdomyolysis is an elevated serum uric acid, associated with an increase in serum CK. Within 8 to 12 hours, the serum tests are repeated. If the uric acid falls and the CK rises, rhabdomyolysis is likely. Renal function tests may also be increased at this time. When the diagnosis of rhabdomyolysis is made, the patient is treated with 40 mg furose-mide IV once, and IV fluids. Urine myoglobin concentrations are obtained. If the patient develops renal failure, hemodialysis or peritoneal dialysis may be necessary. In all cases, multiple drug intoxication, trauma, and rhabdomyolysis are ruled out or treated. All patients are kept under observation until they are asymptomatic. 

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. 

The primary goals of treatment are correction of the intraabdominal disease processes or injuries that have caused infection and drainage of collections of purulent material (abscess). A secondary objective is to resolve the infection without major organ system complications (e.g., pulmonary, hepatic, cardiovascular, or renal failure) or adverse drug effects. Ideally, the patient should be discharged from the hospital with full function for self-care and routine daily activities. 

The primary goals of management of tumor lysis syndrome are (1) prevention of renal failure and (2) prevention of electrolyte imbalances. Thus the best treatment for tumor lysis syndrome is prophylaxis to enable delivery of cytotoxic therapy for the underlying malignancy. For patients who present with or develop tumor lysis syndrome despite prophylaxis, treatment goals include (1) decrease uric acid levels, (2) correct electrolyte imbalances, and (3) prevent compromised renal function. These goals should be achieved in a cost-effective manner. 

Potassium is the second most abundant cation in the body and is found primarily in the intracellular fluid. Potassium has many important physiologic functions, including regulation of cell membrane electrical action potential (especially in the myocardium), muscular function, cellular metabolism, and glycogen and protein synthesis. Potassium in PN can be provided as chloride, acetate, and phosphate salts. One millimole of potassium phosphate provides 1.47 mEq of elemental potassium. Generally, the concentration of potassium in peripheral PN (PPN) admixtures should not exceed 80 mEq/L (80 mmol/L). While it is safer to also stick to the 80 mEq/L (80 mmol/L) limit for administration through a central vein, the maximum recommended potassium concentration for infusion via a central vein is 150 mEq/L (150 mmol/L).14 Patients with abnormal potassium losses (e.g., loop or thiazide diuretic therapy) may have higher requirements, and patients with renal failure may require potassium restriction. 

Although determination of creatinine clearance rate is a standard clinical procedure, it is difficult to carry out mainly because accurate collection of total urine output over a 24-hour period is required. It can never be certain that this requirement has been met. Since creatinine is produced continuously in muscle and is cleared by the kidney, renal failure is characterized by elevated serum creatinine levels. The degree of elevation is directly related to the degree of renal failure—if it is assumed that the production of creatinine in the muscle mass is constant and that renal function is stable. When these assumptions are valid, there is a direct relationship between serum creatinine level and kanamycin half-life, as shown in Fig. 9. The equation of the line in Fig. 9 is... 

The answer is d. (Hardman, p 7502) The most consistent of the toxicides of ACT inhibitors is impairment of renal function, as evidenced by proteinuria. Elevations of blood urea nitrogen (BUN) and creatinine occur frequently, especially when stenosis of the renal artery or severe heart failure exists Hyperkalemia also may occur These drugs are to be used very cautiously where prior renal failure is present and in the elderly Other toxicides include persistent dry cough, neutropenia, and angioedema. Hepatic toxicity has not been reported... 

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. 

Hyperoxaluria type 1 is due to functional efficiency of the liver specific peroxisomal enzyme alanine-glyoxylate aminotransferase. It leads to severe renal failure. The nervous system is not affected. 

IV colchicine should be avoided because it is associated with serious adverse effects (e.g., bone marrow suppression, tissue necrosis from local extravasation, disseminated intravascular coagulation, hepatocellular toxicity, and renal failure). If considered necessary, the recommended initial IV dose is 2 mg (if renal function is normal) diluted in 10 to 20 mL of normal saline administered slowly over 10 to 20 minutes in a secure, free-flowing IV line to avoid extravasation. This may be followed by two additional doses of 1 mg each at 6-hour intervals, with the total dose not exceeding 4 mg. After a full IV course, patients should not receive colchicine by any route for at least 7 days. 

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. 

For urethral overactivity and/or bladder underactivity, digital rectal exam or transrectal ultrasound should be performed to rule out prostate enlargement. Renal function tests should be performed to rule out renal failure. 

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