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Renal failure and

The most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. [Pg.177]

In the treatment of hypertension, ACE inhibitors are as effective as diuretics, (3-adrenoceptor antagonists, or calcium channel blockers in lowering blood pressure. However, increased survival rates have only been demonstrated for diuretics and (3-adrenoceptor antagonists. ACE inhibitors are approved for monotherapy as well as for combinational regimes. ACE inhibitors are the dtugs of choice for the treatment of hypertension with renal diseases, particularly diabetic nephropathy, because they prevent the progression of renal failure and improve proteinuria more efficiently than the other diugs. [Pg.10]

Erythropoietin is a growth factor produced by interstitial cells of the kidney in response to hypoxia. Erythropoietin stimulates haematopoiesis in the bone marrow. Recombinant human erythropoietin is used to treat anemias, e.g. anemia caused by chronic renal failure and anemia in AIDS and cancer patients. [Pg.483]

Poorly treated hyperthermia may lead to metabolic acidosis, rhabdomyolysis, elevated aminotransferases, seizures, renal failure, and disseminated intravascular coagulation (DIC)... [Pg.146]

Identifying patients at high risk for development of acute renal failure and implementing preventive methods to decrease its occurrence or severity is critical. [Pg.361]

Protonated THAM (with CP or HCO, ) is excreted in the urine at a rate that is slightly higher than creatinine clearance. As such, THAM augments the buffering capacity of the blood without generating excess C02. THAM is less effective in patients with renal failure and toxicities may include hyperkalemia, hypoglycemia, and possible respiratory depression. [Pg.427]

Surgical intervention should be reserved for patients with severe lower urinary tract symptoms of benign prostatic hyperplasia or those with complications of disease (such as recurrent urinary tract infections, renal failure, and bladder calculi). [Pg.791]

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. [Pg.1467]

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. [Pg.1487]

For patients with fluid deficits, it is safer and more cost-effective to correct fluid abnormalities using standard intravenous fluids (e.g., sodium chloride 0.9% in water, dextrose 5% in water, and lactated Ringer s solution). Minimizing fluid volume in PN may be indicated in patients with fluid overload, such as critically ill patients who receive large-volume resuscitation fluids, patients with oliguric (urine output less than 400 mL/day) or anuric (urine output less than 50 mL/day) renal failure, and those with congestive heart failure. It is reasonable to... [Pg.1496]

Hemolytic uremic syndrome A syndrome characterized by microangiopathic hemolytic anemia, acute renal failure, and a low platelet count (thrombocytopenia). [Pg.1567]

There have been many sporadic reports that lipo-PGEj is effective in fulminant hepatitis, neuralgia associated with herpes zoster, multiple spinal canal stenosis, cerebral infarction, myocardial infarction, chronic renal failure, and bed sores as well as for its registered indications. [Pg.267]

Phenols are carcinogenic [39-42] and mutagenic thus affect the central nervous system. Long term contact to phenol may even paralyze the body and damage liver, kidneys [41] and heart [43]. Phenol and its vapour are corrosive to the eyes, skin and respiratory tract [44], Renal failure and pulmonary toxicity has been reported with overdose of 89% injectable phenol solution [45]. According to Central Pollution Control Board (CPCB) the discharge limit of phenol in inland water should be lower than 1 mg/1 [46],... [Pg.289]

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. [Pg.324]

Based upon the available data, derivation of AEGL-1 values was considered inappropriate. The continuum of arsine-induced toxicity does not appear to include effects consistent with the AEGL-1 definition. The available human and animal data affirm that there is a very narrow margin between exposures that result in little or no signs or symptoms of toxicity and those that result in lethality. The mechanism of arsine toxicity (hemolysis that results in renal failure and death), and the fact that toxicity in humans and animals has been reported at concentrations at or below odor detection levels (-0.5 parts per million (ppm)) also support such a conclusion. The use of analytical detection limits (0.01 to 0.05 ppm) was considered as a basis for AEGL-1 values but was considered to be inconsistent with the AEGL-1 definition. [Pg.85]

Reference The available human and animal data indicate that there is very little margin between seemingly inconsequential exposures and lethal exposures. The mechanism of arsine toxicity (hemolysis and subsequent renal failure) and the fact that toxicity has been demonstrated at or below the odor threshold justify the inappropriateness of AEGL-1 values for any exposure period. [Pg.127]

Signs and Symptoms Abdominal pain, cramps, diarrhea, fever, vomiting, tenesmus, and blood, pus, or mucus in stools. Infections also cause mucosal ulceration, rectal bleeding, drastic dehydration. Serious less frequent complications include sepsis, seizures, convulsions, rectal prolapse, toxic megacolon, intestinal perforation, renal failure, and hemolytic uremic syndrome. [Pg.517]

Neorecormon (tradename, also known as epoetin beta) is a recombinant human EPO first approved for medical use in the EU in 1997. It is indicated for the treatment of anaemia associated with various medical conditions, most commonly chronic renal failure and cancer patients receiving chemotherapy. Neorecormon is produced by recombinant DNA technology in a CHO cell line and is manufactured as outlined in Figure 10.5. It is presented in lyophilized format at various strengths (500-10 000 IU/vial) and contains phosphate buffer, sodium chloride, calcium chloride, urea, polysorbate and various amino acids as excipients. [Pg.276]

Ingestion — but not necessarily swallowing — of about 15 mL ( mouthful ) of a 20% solution 4->40 mg/kg BW Ingestion of 30 mg/kg BW Fatal dose (Kimbrough 1974) Acute oral LD50 (Manzo etal. 1979 Summers 1980) Associated with hepatic, cardiac, or renal failure, and sometimes death (Dasta 1978)... [Pg.1180]

ACE inhibitors are absolutely contraindicated in pregnancy because of possible major congenital malformations associated with exposure in the first trimester and serious neonatal problems, including renal failure and death in the infant, from exposure during the second and third trimesters. [Pg.132]

The principal infecting organism is Escherichia coli, but Proteus mirabilis and Klebsiella pneumoniae account for some infections. Untreated bacteri-uria may result in pyelonephritis, preterm labor, preeclampsia, transient renal failure, and low birth weight. [Pg.369]

Modified amino acid solutions are designed for patients with altered protein requirements associated with hepatic encephalopathy, renal failure, and metabolic stress or trauma. However, these solutions are expensive and their role in disease-specific PN regimens is controversial. [Pg.685]

The pathophysiology, clinical manifestations, diagnosis, and treatment of acute renal failure and chronic kidney disease (CKD) or end-stage renal disease are discussed in Chaps. 75 and 76, respectively. [Pg.888]


See other pages where Renal failure and is mentioned: [Pg.274]    [Pg.130]    [Pg.210]    [Pg.136]    [Pg.183]    [Pg.202]    [Pg.673]    [Pg.63]    [Pg.115]    [Pg.368]    [Pg.1188]    [Pg.1263]    [Pg.1455]    [Pg.280]    [Pg.341]    [Pg.112]    [Pg.541]    [Pg.547]    [Pg.570]    [Pg.588]    [Pg.687]    [Pg.1178]    [Pg.434]   
See also in sourсe #XX -- [ Pg.39 ]




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