Kidney-compromised

Know the metabolism and clearance of your muscle relaxant choice. Does your patient have liver or kidney compromise (Table 89.1) ... 

Kidney Function. Prostanoids influence a variety of kidney functions including renal blood flow, secretion of renin, glomerular filtration rate, and salt and water excretion. They do not have a critical role in modulating normal kidney function but play an important role when the kidney is under stress. Eor example, PGE2 and -I2 are renal vasodilators (70,71) and both are released as a result of various vasoconstrictor stimuli. They thus counterbalance the vasoconstrictor effects of the stimulus and prevent renal ischemia. The renal side effects of NSAIDS are primarily observed when normal kidney function is compromised. 

In contrast to chlordiazepoxide and diazepam, lorazepam and oxazepam are not metabolized into active compounds in the liver. Instead, they are excreted by the kidneys following glucuronidation. This is important because many alcohol-dependent patients have compromised liver function. Therefore, when treatment is initiated before the results of blood tests for liver function are known, as is often the case in outpatient clinics, lorazepam and oxazepam may be preferred. Patients with liver disease may still be treated with diazepam and chlordiazepoxide, but at lower doses. This can be accommodated with the loading technique, although hourly dosing with 5 mg of diazepam or 25 mg of chlordiazepoxide may be sufficient. 

The Leggett Model simulates the age-dependence of lead kinetics on such factors as bone turnover rates, partitioning between soft tissues and excreta, removal half-times in liver, kidneys, and red blood cells, and the deposition fraction in brain. The model structure represents a compromise between biological realism and practical considerations regarding the quantity and quality of information available to determine parameter values (Leggett 1993). 

No studies were located regarding populations that are unusually susceptible to hexachloroethane toxicity. Because the kidney and liver are the primary target tissues, individuals with compromised liver or kidney function would have an increased risk from exposure. Susceptibility to pulmonary infections could be increased by exposure to hexachloroethane vapors and, thus, individuals that suffer from chronic respiratory problems could also have an increased risk from hexachloroethane exposure. 

The anorexia suffered by cancer patients is likely to arise from a combination of psychological stress, altered senses of taste and smell and increased levels of cytokines, which influence the appetite and satiety centres in the hypothalamus. There are several consequences micronutrient intake will be diminished and this may contribute to the signs and symptoms of the disease. Plasma amino acid levels will fall, as in starvation (Chapter 16). Synthesis of glutamine (by muscle, adipose and lung), aspartate (by liver), glutathione (by the intestine) and arginine (by the kidney) will all be compromised. The metabolic significance of all of these is discussed in Chapter 18. 

While most lipophilic and large molecules are primarily excreted by the hepatobiliary system, the kidney is the major excretory organ for many small organic and inorganic molecules, drugs and hydrophilic metabolites, maintenance of fluid balance, and bone metabolism. These functions expose the kidney to a number of clinical, physiological, and pathological conditions that may compromise renal function. Some renal disorders that necessitate clinical intervention are listed in Table 2. 

Fluid load Lower concentrations of nitroglycerin IV and nitroglycerin in dextrose injection increase the potential precision of dosing, but these concentrations increase the total fluid volume that must be delivered to patients. Total fluid load may be a dominant consideration in patients with compromised function of the heart, liver, and/or kidneys. 

Studies in animals revealed that hexachlorobutadiene causes damage to the proximal tubules of the kidney and, to a lesser extent, to the liver. Accordingly, people with preexisting kidney and liver damage may have compromised organ functions and are expected to be more vulnerable to chemical insult than people with normal kidney and liver functions. Infants are more likely to be... 

Cyanide poisoning poses some risk however, this is minimized both by the kinetic inertness of both Fe and Fe " cyano complexes and the high affinity of these ions for cyanide ([Fe"(CN)6] , fi6 10 [Fe "(CN)6] , Bg 10 [7, 35]. Small amounts of cyanide, which are released by photolysis and reduction products of nitroprusside, can usually be metabolized in the liver and kidneys by the enzyme rhodanase, which converts CN" to SCN [7, 36]. Cyanide can also be taken up by hydroxocobalamin to generate cy-anocobalamin (B12). As the conversion of cyanide to thiocyanate is dependent on the availability of sulfur, thiosulfate can be administered as an antidote [37]. Monitoring thiocyanate levels as an indicator of cyanide toxicity is no longer routine, but is done on patients with severe hepatic compromise who have been... 

Although asparaginase therapy has proved effective, a number of side-effects have been associated with initiation of therapy. These have included severe nausea, vomiting and diarrhoea, as well as compromised liver and kidney function. Side-effects are probably due to a transient asparaginase deficiency in various tissues. Under normal circumstances, dietary-derived plasma asparagine levels are sufficient to meet normal tissue demands, and the cellular... 

Rasburicase is a recombinant form of an enzyme, urate oxidase. This enzyme catalyses the conversion of uric acid to allantoin, a more soluble molecule, easily cleared by kidney. Monthly infusions of rasburicase appear to be a possible therapy for severe gout not treatable by other means. The most important adverse events are allergy and the development of antibodies which compromise rasburicase effectiveness. 

Concomitant use with sympathomimetic drugs, p-adrenoceptor antagonists, calcium channel-entry blockers and other cardioactive drugs may result in bradyarrhythmias, bigemini, or tachyarrhythmias. Cardiac rhythm should be closely monitored and drug dosages carefully adjusted. Digoxin is mainly excreted by the kidneys and plasma levels should be closely monitored in patients with acute renal failure and in those whose renal function is compromised. 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

People with exposure to anti-thyroid drugs (e.g., lithium), thyroid disease, or otherwise compromised thyroid function might have a more pronounced response to PBBs and PBDEs because of their underlying limitations in thyroid hormone production. Similarly, people with compromised function of other organs, such as those with liver or kidney diseases (e g., liver cirrhosis or hepatitis B), could be considered more susceptible to health effects of PBBs and PBDEs. 

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