Kidney drug adverse effects/toxicity

Gastrointestinal complaints (eg, nausea, diarrhea, vomiting, flatulence) are the most common adverse effects but rarely require discontinuation of therapy. Other potential adverse effects include headache and asthenia. Tenofbvir-associated proximal renal tubulopathy causes excessive renal phosphate and calcium losses and 1-hydroxylation defects of vitamin D, and preclinical studies in several animal species have demonstrated bone toxicity (eg, osteomalacia). Monitoring of bone mineral density should be considered with long-term use in those with risk factors for or with known osteoporosis, as well as in children. Reduction of renal function over time, as well as cases of acute renal failure and Fanconi s syndrome, have been reported in patients receiving tenofovir alone or in combination with emtricitabine. For this reason, tenofovir should be used with caution in patients at risk for renal dysfunction. Tenofovir may compete with other drugs that are actively secreted by the kidneys, such as cidofovir, acyclovir, and ganciclovir. 

Adverse effect Hypoglycemia due to sulfonylureas Dose-relation toxic effect Time-course time-independent Susceptibility factors disease (impaired liver or kidney function, alcoholism) drug interactions reduced food intake exercise... 

Aminoglycoside use is limited somewhat by problems with toxicity.66 Nephrotoxicity, as indicated by bloody urine, acute renal tubular necrosis, and so on, is one of the more common and serious adverse effects.49,66 Ototoxicity, as indicated by dizziness and ringing or fullness in the ears, may also occur. This effect can be irreversible in severe cases.67 Toxicity may occur more frequently in certain individuals, such as patients with liver or kidney failure, or in elderly patients. To reduce the risk of toxicity, drug levels in the bloodstream must be periodically monitored so dosages can be adjusted for individual patients. Other adverse effects include hypersensitivity (e.g., skin rashes, itching) in susceptible individuals. 

Adverse Effects. The primary adverse effect of systemic pentamidine administration is renal toxicity. Renal function may be markedly impaired in some patients, but kidney function usually returns to normal when the drug is withdrawn. Other adverse effects include hypotension, hypoglycemia, gastrointestinal distress, blood dyscrasias (leukopenia, thrombocytopenia), and local pain and tenderness at the site of injection. Adverse effects are reduced substantially when the drug is given by inhalation, and this method of administration is desirable when pentamidine is used to prevent pneumocystis pneumonia in patients with human immunodeficiency virus (HIV) disease. 

This chapter addresses immunosuppressive drugs, or immunosuppressants, that are currently available to prevent the rejection of transplants or to treat specific diseases caused by an autoimmune response. Clearly, these drugs must be used very cautiously because too much suppression of the immune system will increase a patient s susceptibility to infection from foreign pathogens. Likewise, these drugs are rather toxic and often cause a number of adverse effects to the kidneys, lungs, musculoskeletal system, and other tissues. Nonetheless, immunosuppressive agents are often life-... 

Aspirin, paracetamol, and hydrocortisone are used to control febrile reactions of amphotericin. Patients with a history of adverse effects with amphotericin should be prophylactically treated with antipyretics and hydrocortisone. Antiemetics and pethidine also are used for the treatment of adverse effects of amphotericin. With sodium supplements and hydration therapy, damage to the kidney can be reduced. If conventional amphotericin is not well tolerated by the patient, colloidal carriers can be used as alternative options. Administration of amphotericin with a nephrotoxic drug, such as cyclosporin, may further increase toxicity. Diuretics and anticancer drugs should be avoided with amphotericin. 

Nitroprusside [nye troe PRUSS ide] is administered intravenously, and causes prompt vasodilation, with reflex tachycardia. It is capable of reducing blood pressure in all patients, regardless of the cause of hypertension. The drug has little effect outside the vascular system, acting equally on arterial and venous smooth muscle. [Note Because nitroprusside also acts on the veins, it can reduce cardiac preload.] Nitroprusside is metabolized rapidly (t1/2 of minutes) and requires continuous infusion to maintain its hypotensive action. Sodium nitroprusside exerts few adverse effects except for those of hypotension caused by overdose. Nitroprusside metabolism results in cyanide ion production, although cyanide toxicity is rare and can be effectively treated with an infusion of sodium thiosulfate to produce thiocyanate, which is less toxic and is eliminated by the kidneys (Figure 19.14). [Note Nitroprusside is poisonous if given orally because of its hydrolysis to cyanide.]... 

Since acute radiation toxicity responses become apparent shortly after exposme, history is an important criterion in determining whether the radiation is related to the cause of a particular complication or adverse effect. As with any attempt to specify a dose-response relationship, the dose is an important component. In contrast, late radiation toxicity in organs such as the kidneys, fiver, or central nervous system (CNS) will not be seen until months or perhaps even years after radiation exposure (Center for Drug Evaluation, 2005). The integrated response is often to the radiation response and attempts to heal any radiation damage that has been caused. 

Ind avenous cidofovir is well tolerated. The major deatment-limidng toxicity of this drug is irreversible nephrotoxicity (Plosker and Noble, 1999). Ind avenous pre-hydradon with normal saline and aclminisdadon of oral probenecid must be used with each cidofovir infusion to lessen the effects on the kidney. Serum creadnine and urine protein must be monitored with each infusion and adjusted accordingly. Other adverse effects associated with its use are neudopenia and peripheral neuropathy (Plosker and Noble, 1999). 

The renal toxicity of ciclosporin has been described as being an adverse effect of the drug on the compensatory mechanisms of the kidney, without effects on proximal tubular function (urea and sodium reabsorption) (91). A rise in serum creatinine concentration may be adequate to identify acute-onset ciclosporin nephrotoxicity, but it is not suitable for identification of chronic, late-onset ciclosporin nephrotoxicity (92). 

Emetine, once the drug of choice for the treatment of amebiasis, despite marked cardiotoxicity, has largely been replaced by metronidazole and related compounds for this indication. Large doses of emetine can damage the heart, hver, kidneys, intestinal tract, and skeletal muscle. Allergic reactions and tumor-inducing effects have not been described. Dehydroemetine is a httle less toxic but also less effective than emetine its adverse effects are similar (SED-11, 594). 

Of the clinically established platinum compounds, cisplatin has the most toxic effects on organs like the nervous system, the organ of Corti, and the kidneys in a dose-dependent fashion. The dose per cycle has therefore usually been limited to 100-120 mg/m intravenously, in order to avoid drug-induced irreversible organ dysfunction (12,13). The complete spectrum of late or long-term adverse effects of cisplatin in survivors of testicular cancer has been reviewed (32). 

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