NSAIDs renal

The arylpropionic acid derivatives are useful for the treatment of rheumatoid arthritis and osteoarthritis, for reduction of mild to moderate pain and fever, and for pain associated with dysmenorrhea. Side effects of the drugs are similar to but less severe than those described for the salicylates. Those who are sensitive to salicylates also may be sensitive to and have adverse reactions when taking ibuprofen and related drugs. Acute hypersensitivity to ibuprofen has been reported in patients with lupus. The hypersensitivity reaction to sulindac can be fatal. The use of sulindac has also been linked to cases of acute pancreatitis. The use of dimethylsulfoxide (DMSO) topically in combination with sulindac has been reported to induce severe neuropathies. The concurrent use of ibuprofen with aspirin reduces the antiinflammatory effects of both drugs. Ibuprofen is contraindicated in patients with aspirin sensitivity leading to bronchiolar constriction and in patients with an-gioedema. As with all NSAIDs, renal and liver function should be normal for adequate clearance of the drugs. 

Contraindications Active GI bleeding or ulcerations hypersensitivity to aspirin, indomethacin, or other NSAIDs renal impairment, thrombocytopenia... 

POTASSIUM-SPARING DIURETICS ANALGESICS-NSAIDs Risk of hyperkalaemia with NSAIDs Renal insufficiency caused by NSAIDs can exacerbate potassium retention by these diuretics Monitor renal function and potassium closely... 

Zafirovska KG, Bogdanovska SV, Marina N, GruevT, Lozance L Urinary excretion ofthree specific renal tubular enzymes in patients treated with nonsteroidal anti-inflammatory drugs (NSAID). Renal Failure 1993 15 51-54. 

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. 

The NSAIDs prolong bleeding time and increase the effects of anticoagulants, lithium, cyclosporine, and the hydantoins. These dru may decrease the effects of diuretics or antihypertensive drug >. Long-term use of the NSAIDs with acetaminophen may increase the risk of renal impairment. 

The most common adverse reactions seen with celecoxib include dyspepsia, abdominal pain, diarrhea, nausea, and headache Like other NSAIDs, celecoxib may compromise renal function. Elevation of aminotransferase levels also occurs. 

Before administering an NSAID, it is important for the nurse to determine if the patient has any history of allergy to aspirin or any otiier NSAID. The nurse determines if die patient has a history of gastrointestinal bleeding, hypertension, peptic ulceration, or impaired hepatic or renal function. If so, the nurse notifies the primary health care provider before administering an NSAID. 

NSAIDs are classified as non-selective (they inhibit COX-1 and COX-2) or selective (they inhibit only COX-2) based on degree of cyclooxygenase inhibition. COX-2 inhibition is responsible for anti-inflammatory effects, while COX-1 inhibition contributes to increased GI and renal toxicity associated with non-selective agents. Since the antiplatelet effect of non-selective NSAIDs is reversible, concurrent use may reduce the... 

NSAIDs Monitor patients for gastrointestinal distress, signs or symptoms of gastrointestinal bleeding, and hypertension and edema that may reflect renal dysfunction. Monitor CBC and serum creatinine as clinically indicated. 

NSAIDs are associated with gastrointestinal, renal, hepatic, and central nervous system toxicity and may increase blood pressure. NSAIDs that are selective for the cyclooxygenase-2 (COX-2) isozyme are less likely to cause gastrointestinal complications but may increase the risk of cardiovascular events. They are no more effective than nonselective NSAIDs. Selective agents should be reserved for patients at high risk of gastrointestinal complications and low risk for cardiovascular events. 

NSAIDs can cause renal insufficiency when administered to patients whose renal function depends on prostaglandins. Patients with chronic renal insufficiency or left ventricular dysfunction, the elderly, and those receiving diuretics or drugs that interfere with the renin-angiotensin system are particularly susceptible. Decreased glomerular filtration also may cause hyperkalemia. NSAIDs rarely cause tubulointerstitial nephropathy and renal papillary necrosis. 

The COX-2 enzyme is also produced normally in the kidney thus COX-2 inhibitors exert renal effects similar to those of conventional NSAIDs. Both drug classes may increase sodium reabsorption and fluid retention and can provoke renal insufficiency and hyperkalemia. COX-2 inhibitors should be used with caution in patients with heart failure or hypertension. 

Indomethacin was used traditionally, but its relative cyclooxygenase-1 (COX-1) selectivity theoretically increases its gastropathy risk. Thus other generic NSAIDs may be preferred. Adverse effects of NSAIDs include gastropathy (primarily peptic ulcers), renal dysfunction, and fluid retention. NSAIDs generally should be avoided in patients at risk for peptic ulcers, those taking warfarin, and those with renal insufficiency or uncontrolled hypertension or heart failure. 

FIGURE 56-2. Treatment algorithm for gout and hyperuricemia. Renal insufficiency is defined as an estimated creatinine clearance (CrCI) of less than 30 mL/minute. IA, Intraarticular NSAID, nonsteroidal anti-inflammatory drug. 

Systemic corticosteroids are a useful option in patients with contraindications to NSAIDs or colchicine (primarily renal impairment) or polyarticular attacks, especially in elderly patients. A single intramuscular injection of a long-acting corticosteroid such as triamcinolone hexacetonide may be used. Oral agents may be needed, especially for severe attacks. Prednisone 40 to 60 mg (or an equivalent dose of another agent) is given daily, with a gradual taper over 2 weeks. 

Although the risk of GI complications is relatively small with short-term therapy, coadministration with a proton pump inhibitor should be considered in elderly patients and others at increased GI risk. NSAIDs should be used with caution in individuals with a history of peptic ulcer disease, heart failure, uncontrolled hypertension, renal insufficiency, coronary artery disease, or if they are receiving anticoagulants concurrently. 

Acetaminophen is usually well tolerated, but potentially fatal hepatotoxicity with overdose is well documented. It should be used with caution in patients with liver disease and those who chronically abuse alcohol. Chronic alcohol users (three or more drinks daily) should be warned about an increased risk of liver damage or GI bleeding with acetaminophen. Other individuals do not appear to be at increased risk for GI bleeding. Renal toxicity occurs less frequently than with NSAIDs. 

They are particularly useful in patients who cannot take NSAIDs because of renal failure, or for patients in whom all other treatment options have failed and who are at high surgical risk, precluding joint arthroplasty. 

NSAIDs and Gl ulceration and bleeding, renal Blood in stool, black stool, dyspepsia. 

Potassium-sparing diuretics may cause hyperkalemia, especially in patients with chronic kidney disease or diabetes, and in patients receiving concurrent treatment with an ACE inhibitor, ARB, NSAID, or potassium supplement. Eplerenone has an increased risk for hyperkalemia and is contraindicated in patients with impaired renal function or type 2 diabetes with proteinuria. Spironolactone may cause gynecomastia in up to 10% of patients, but this effect occurs rarely with eplerenone. 

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