Renal papillary necrosis NSAIDs

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. 

Renal papillary necrosis and interstitial nephritis with the nephrotic syndrome have been documented (27,28). Other cases of the nephrotic syndrome, with or without renal insufficiency, which were apparently due to minimal-change nephropathy (which is relatively more common in NSAID users), have been reported (29,30). The unusual feature of diclofenac-associated renal interstitial mucinosis has been described (SEDA-17, 109). 

NSAIDs can produce a spectrum of renal diseases functional renal insufficiency, nephrotic syndrome with or without interstitial nephritis, renal papillary necrosis and... 

Renal papillary necrosis has been reported after longterm intake or abuse of aspirin and other NSAIDs (SEDA-11, 85) (SEDA-12, 79). 

NSAID-induced renal toxicity, comprising interstitial nephritis and renal papillary necrosis. The condition, named analgesic nephropathy, was not uncommon and was serious. In a number of cases malignancies in the urinary tract also occurred. 

Renal papillary necrosis Direct toxicity 4pg Massive NSAID ingestion Dehydration Discontinue NSAID Rehydrate... 

Long-term administration of NSAIDs can result in renal papillary necrosis and other renal injury. Diclofenac should be used with caution in patients at greatest risk, including the elderly, those with impaired renal function, heart failure, liver dysfunction, and those taking diuretics and ACE inhibitors. 

Renal papillary necrosis and other renal injury with long-term use. Most of the unwanted renal side effects of the class of NSAIDs are related to the inhibi-ton of prostanoid synthesis. The COX-2 enzyme has been implicated as a mediator of renal blood flow, renin release and sodium excretion. As a result, COX-2 inhibitors may lead to an alteration of renal homeostasis resulting in decreases in glomerular filtration rate, renal blood flow, sodium and water retention, and hyperkalemia [1]. 

These findings from special renal studies and the clinical trial data indicate that inhibition of Cox-2 does not eliminate the renal effects of NSAIDs because Cox-2-derived prostanoids are involved in normal renal function. However, the kidney contains considerably more Cox-1 than Cox-2, and the localization of the two isoforms is different It is not yet known whether the Cox-2 inhibitors will be safer in subgroups of patients prone to develop acute renal failure with NSAIDs, such as those patients with severe volume depletion, congestive heart failure, or hepatic cirrhosis with ascites (Bosch-Marce et al., 1999). Also, it is not known whether rare events, such as interstitial nephritis or papillary necrosis, will occur with long-term use of Cox-2 inhibitors, although studies in animals suggest that such events may be related to Cox-1 inhibition, since only Cox-1 is found in the papilla. Therefore, Cox-2 inhibitors may not produce these serious adverse effects (Khan etal., 1998). 

Acute deterioration of renal function Salt and water retention The concept of "renal sparing" NSAIDs Nephrotic syndrome with interstitial nephritis Chronic renal failure/papillary necrosis Other NSAID-induced renal syndromes Renal effects of COX-2 inhibitors 424 428 430 431 432 434 435... 

The NSAID-induced abnormahties of renal function, in descending order of chnical frequency, are (i) fluid and electrolyte disturbances (ii) destabilizahon of con-troUed hypertension (hi) decompensated congestive heart failure (iv) acute deterioration of renal function (v) nephrotic syndrome with interstitial nephritis and (Vi) chronic renal failure/papillary necrosis [1, 3-5]. 

Acute renal failure associated with NSAID falls into several categories (1) acute interstitial nephritis with glomerular abnormalities, (2) functional acute renal failure, probably haemodynamic in nature, (3) papillary necrosis, and (4) phenylbutazone anuria. 

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