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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2012  |  Volume : 23  |  Issue : 6  |  Page : 1294-1296
Nimesulide-induced acute renal failure


1 Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Sion, Mumbai, India
2 Department of Obstetrics and Gynaecology, J.J.M. Medical College, Davangere, Karnataka, India
3 Department of Oral Pathology, Bhartiya Vidyapeeth Dental College, Mumbai, India

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Date of Web Publication17-Nov-2012
 

How to cite this article:
Zaki SA, Nilofer AR, Taqi SA. Nimesulide-induced acute renal failure. Saudi J Kidney Dis Transpl 2012;23:1294-6

How to cite this URL:
Zaki SA, Nilofer AR, Taqi SA. Nimesulide-induced acute renal failure. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2020 Nov 26];23:1294-6. Available from: https://www.sjkdt.org/text.asp?2012/23/6/1294/103581
To the Editor,

Non-steroidal anti-inflammatory drugs (NSAIDs) are the most widely prescribed drugs in the treatment of pain and inflammation. [1] The two main adverse drug reactions associated with NSAIDs relate to gastro­intestinal effects and adverse renal effects of the agents. Nimesulide is a new-generation NSAID that differs from conventional NSAID in its structure and pharmacological profile, claiming fewer side-effects and at least being equally efficacious. [2],[3] We describe a patient presenting with acute renal failure (ARF) following the administration of nimesulide.

A 6-year-old boy presented with complaints of fever and vomiting for 2 days and anuria for 1 day. Vomiting was non-bilious and non-projectile, containing ingested food particles. Fever was high grade and continuous, and was not associated with chills. There was no history of loose motions, cough, breathlessness or bleeding manifestation. His birth history, past history and family history were all normal. There was no history of urinary complaints or hospitalization in the past. Initially, the patient was shown to a private practitioner for fever and was started on a NSAID preparation containing nimesulide. On the second day of fever, he developed anuria. On examination, he was afebrile, with a heart rate of 98/min, respiratory rate of 23/min and blood pressure of 96/62 mmHg. His height and weight were normal for his age. There was no evidence of pallor, petechiae or rash. His investigations on the second day of illness revealed: hemoglobin 12.6 gm/dL, total leucocyte count 8600/mm 3 (neutrophils 56%, lymphocytes 44%), platelet count 3.6 lac/mm 3 , serum sodium 139 mEq/L and serum potassium 6.8 mEq/L. His arterial blood gas study was normal. His blood urea nitrogen was 34 and serum creatinine was 2.1 mg/dL. Urine culture was negative and urine microscopy revealed 1+ proteinuria, 4 RBC/ high-power field and 2 pus cells/high-power field. Ultrasonography revealed normal kidneys and bladder. The patient's relatives refused hospitalization for personal reasons and were followed-up on an outdoor basis. Nimesulide was stopped on the second day of illness when the child presented to us. On the third day, the patient started passing urine. His investigations done serially are shown in [Table 1]. His renal parameters and serum potassium became normal on the fifth day. A diagnosis of nimesulide-induced acute renal failure was made in this case considering the event as possible adverse drug reaction as per the Naranjo causality scale assessment for adverse drug reaction. The patient is remaining well on follow-up without any urinary complaints after six months.
Table 1: Investigations done serially in the patient.

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Analgesic nephropathy was first described in 1950. [4],[5] Phenacetin was subsequently identified as the chief culprit, and was withdrawn from the market. [5] Since the early 1980s, several case control studies have reported association between renal failure and use of various analgesics including acetaminophen and aspirin. [1],[5],[6],[7] Renal adverse effects are mainly due to inhibition of prostaglandin synthesis, and include acute reversible "vasomotor" renal failure and disorders of water, sodium and potassium balance. [1],[3],[7] Hemodynamically mediated ARF develops almost exclusively in predisposed patients, like those with impairment of renal, cardiac and hepatic function as well as in elderly individuals. [1] NSAIDs can provoke ARF in such conditions where an increased action of vasodilating prostaglandins is required to maintain a sufficient renal perfusion. Fortunately, it is not associated with structural damage, and is usually reversible. [1],[8],[9] Acute tubular, interstitial or tubulointerstitial nephritis, chronic interstitial nephritis with papillary necrosis, nephrotic syndrome, acute tubular necrosis, papillary necrosis, acute glomerulitis or vasculitis and chronic renal injury are other renal complications of these drugs. [1],[7],[8],[10]

First-generation NSAIDs are non-specific inhibitors of both COX-1 and COX-2 forms of cyclo-oxygenase enzyme. [3] New-generation NSAIDs are supposed to have fewer side-effects due to the specificity for the COX-2 enzyme. [3] However, recent studies in humans have detected COX-2 in the macula densa and medullary interstitial cells. [6],[11] COX-2 is induced by pro-inflammatory cytokines, and is responsible for the increased production of prostaglandins in inflammatory tissues. [11] Nimesulide, a selective COX-2 inhibitor, is claimed to have few renal side-effects compared with the non-selective NSAIDS. [2],[3] However, recent studies have found that after repeated doses of nimesulide, there is an increase of urinary Tamm-Horsfall glycoprotein and beta-N-acetyl glucosamindase. [12] This suggests that nimesulide is potentially nephrotoxic. Nimesulide has also been found to induce an acute transient fall of renal blood flow in healthy men when furesemide is concomitantly given. When the glomerular filtration rate becomes dependent on prostaglandins, the administration of nimesulide may attenuate the diuretic, kaliuretic and natriuretic effects of furosemide. [13]

Management of NSAID nephropathy is to discontinue treatment with the offending drug. Supportive treatment in the form of fluid and electrolyte balance and dialysis should be initiated when required. A search of the literature found very few cases of nimesulide-induced renal failure being reported. [1],[3] To the best of our knowledge, this is the first case of nimesulide-induced renal failure reported in the pediatric age group. We did not perform a renal biopsy as the patient had improved and it would not have changed the management of the disease. In conclusion, we wish to highlight that nimesulide can provoke acute renal failure and a history of NSAID use should be sought in all patients presenting with unexplained renal failure.

 
   References Top

1.Apostolou T, Sotsiou F, Yfanti G, et al. Acute renal failure induced by nimesulide in a patient suffering from temporal arteritis. Nephrol Dial Transplant 1997;12:1493-6.  Back to cited text no. 1
[PUBMED]    
2.Davis R, Brogden RN. Nimesulide, an update of its pharmacodynamic and pharmacokinetic properties, and therapeutic efficacy. Drugs 1994;48:431-54.  Back to cited text no. 2
[PUBMED]    
3.Van der Niepen P, Janssen van Doorn K, Van den Houte K, Verbeelen D. Nimesulide and acute renal failure caused by oxalate precipitation. Nephrol Dial Transplant 2002;17:315-62.  Back to cited text no. 3
[PUBMED]    
4.Spuhler O, Zollinger HU. Die chronischinterstitielle nephritis. Z Klin Med 1953;151:1-50.  Back to cited text no. 4
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5.Perneger TV, Whelton PK, Klag MJ. Risk of kidney failure associated with the use of acetaminophen, aspirin and nonsteroidal anti-inflammatory drugs. N Engl J Med 1994;331: 1675-9.  Back to cited text no. 5
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6.Breyer MD, Harris RC. Cyclooxygeanse 2 and the kidney. Curr Opin Nephrol Hypertens 2001;10:89-98.  Back to cited text no. 6
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7.Ravnskov U. Glomerular, tubular and interstitial nephritis associated with non-steroidal anti-inflammatory drugs. Evidence of a common mechanism. Br J Clin Pharmacol 1998; 47:203-10.  Back to cited text no. 7
    
8.Schlondor D. Renal complications of NSAIDs. Kidney Intern 1993;44:643-53.  Back to cited text no. 8
    
9.Dubose Jr, Molony DA. Grand round. Nephrotoxicity of NSAIDs. Lancet 1994;344:515-8.  Back to cited text no. 9
    
10.Pirson Y, van Ypersele de Strihou C. Renal side effects of nonsteroidal anti-inflammatory drugs: Clinical relevance. Am J Kidney Dis 1986;8:338-44.  Back to cited text no. 10
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11.Venturini CM, Isakson P, Needleman Ph. Non-steroidal anti-inflammatory drug induced renal failure: A brief review of the role of cyclooxygenase isoforms. Curr Opin Nephrol Hypertens 1998;7:79-82.  Back to cited text no. 11
    
12.Warrington SJ, Ravic M, Dawnay A. Renal and general tolerability of repeated doses of nimesulide in normal subjects. Drugs 1993;46: S263-9.  Back to cited text no. 12
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13.Steinhauslin F, Munafo A, Buelin T, Macciocchi A, Biollaz J. Renal effects of nimesulide in furisemide treated subjects. Drugs 1993;46: S257-62.  Back to cited text no. 13
    

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Correspondence Address:
Syed Ahmed Zaki
Department of Pediatrics, Lokmanya Tilak Municipal General Hospital, Sion, Mumbai
India
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DOI: 10.4103/1319-2442.103581

PMID: 23168870

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