Mesalazine-associated interstitial nephritis

BACKGROUND.: When used for oral treatment of inflammatory bowel disease,Asacol (a coated form of mesalazine = 5-aminosalicylic acid)can cause interstitial nephritis. The spectrum of severity,frequency of occurrence and the best renal function test todetect this complication are not known. The value of immunosuppressionin addition to drug withdrawal is similarly undetermined. METHODS.: Four cases of interstitial nephritis which occurred in associationwith oral Asacol treatment are presented and a further 12 caseswho received similar treatment are reviewed. Clinical trialspublished previously were scrutinized to assess the frequencyof impaired renal function. RESULTS.: The available evidence suggests that renal impairment of anyseverity may occur in up to 1 in 100 patients, but that clinicallysignificant interstitial nephritis occurs in less than 1 in500 patients. This is most reliably detected by an elevatedserum creatinine concentration. If the diagnosis of nephrotoxicityis delayed until 18 months after commencement of medication,restoration of renal function, which is seen on withdrawal ofmedication alone up to 10 months, does not occur and there isno evidence to date to indicate that addition of immunosuppressionconfers any significant advantage at this later stage. CONCLUSIONS.: It is suggested that serum creatinine concentration should bemeasured each month for the first 3 months of treatment, 3-monthlyfor the remainder of the first year and annually thereafter.The use of concurrent immunosuppressive therapy may necessitateextension to the period of intensive monitoring. Any elevationof serum creatinine which cannot be related to a relapse ofinflammatory bowel disease should prompt immediate withdrawalof Asacol and related medications and substitution of alternativetherapy. Neither the lack of urinary abnormalities on routinetesting nor the absence of clinical or laboratory features ofdrug allergy can be relied upon to rule out interstitial nephritisduring oral therapy with these drugs.     

Pantoprazole-induced acute interstitial nephritis

Pantoprazole is a proton-pump inhibitor (PPI) that is commonly prescribed for the treatment of gastroesophageal reflux-related disorders. There are many documented side effects of PPIs. Here we report a case of acute interstitial nephritis, which developed after 6 weeks of treatment with pantoprazole. A 23-year-old man presented with acute renal failure requiring renal replacement therapy. Acute interstitial nephritis was diagnosed by renal biopsy and was successfully treated with corticosteroids and withdrawal of pantoprazole. Drug-induced acute interstitial nephritis can occur with PPIs such as pantoprazole and vigilance needs to be maintained.     

Levofloxacin-induced granulomatous interstitial nephritis

The authors report the case of a 47-year-old woman in whom a systemic illness developed characterized by fever, malaise, abnormal liver function results, and acute renal failure after treatment for presumed urinary tract infection with levofloxacin. Because of suspicion of an allergic drug reaction, all medications were discontinued, but the patient remained febrile with renal failure for 18 days. Complete workup for presumed vasculitis, autoimmune illness, or infectious etiologies was negative, and the patient underwent both renal and liver biopsy. Liver biopsy results showed nonspecific changes. Renal biopsy disclosed extensive granulomatous interstitial nephritis with associated granulomatous vasculitis. The patient was begun on oral steroids with rapid defervescence of fever and progressive normalization of renal function. The authors discuss the association of granulomatous nephritis with drugs and review the known nephrotoxicity of fluoroquinolones. Am J Kidney Dis 41:E7.     

Antibiotic-induced recurring interstitial nephritis

Acute interstitial nephritis (AIN) is often induced by drug therapy and accounts for 1%–3% of adult cases of renal failure. A 13-year-old white female with cystic fibrosis developed two episodes of biopsy proven AIN following antibiotic use over a 5-year period. The first episode resolved with pulse steroid therapy and the second resolved without intervention. Steroid therapy may play a role in aborting subsequent AIN attacks. Received: 22 January 2001 / Revised: 19 June 2001 / Accepted: 19 June 2001     

Rabeprazole-induced acute interstitial nephritis

Acute interstitial nephritis is an uncommon but important cause of acute renal failure. Proton pump inhibitors are now thought to be the most common class of drugs implicated in drug-induced acute interstitial nephritis. This is the first reported case of rabeprazole-induced acute interstitial nephritis.     

Acute interstitial nephritis.

Acute allergic interstitial nephritis is manifested clinically by rash, fever, eosinophilia, hematuria, oliguria and azotemia. Histologically a monocytic inflammatory process in the renal interstitium is seen. The clinical course of a patient after excessive sodium cephalothin administration suggested allergic interstitial nephritis and implicates this drug as an etiologic agent.     

Captopril-associated acute interstitial nephritis

A 57-year-old male with mild impairment of renal function secondary to diabetic glomerulosclerosis developed acute renal failure (creatinine 32.4 mg/dl) associated with a generalized desquamative skin rash and peripheral eosinophilia shortly after initiation of antihypertensive therapy with captopril. An acute interstitial nephritis was demonstrated on renal biopsy, and improvement was temporally related to initiation of therapy with prednisone. A review of the literature revealed 5 similar cases in whom acute deterioration of renal function occurred following initiation of captopril and in whom there were features of a hypersensitivity reaction, including skin rash, fever, eosinophilia, azotemia, eosinophiluria, and a Coombs-positive hemolytic anemia. Renal biopsy, where available, revealed an acute interstitial nephritis. Observations from these cases suggest that, of the angiotensin-converting enzyme inhibitors, this syndrome appears to be specific for captopril, begins within the 1st month of therapy, is not dose-dependent, and generally resolves on cessation of therapy. Steroids may hasten recovery, but sufficient data are not available to confirm their efficacy.     

Drug-induced acute interstitial nephritis

Acute interstitial nephritis (AIN) due to the drugs is caused by allergic reaction and it is presented by acute renal failure, rush, eosinophilia and eosinophiluria. AIN due to NSAID in comparison with AIN caused by other drugs is presented with nephrotic syndrome and acute renal failure. Kidney biopsy is necessary for diagnosis of AIN. The most important and first step in the treatment is the discontinuation of the drug. In severe cases, the corticosteroids are indicated (1 mg/kg of body weight), or intravenous bolus of corticosteroids followed by high-oral dose administration for several weeks. Symptomatic therapy (diet, diuretics) is indicated for all patients, and hemodyalisis is indicated in patients with severe acute renal failure.     

Ciprofloxacin-induced acute interstitial nephritis.

Acute renal failure is a complication attributed to numerous medications. Few cases linked to the newer fluoroquinolones have been described. We report a case of acute interstitial nephritis confirmed by renal biopsy that developed in a patient within days of starting ciprofloxacin therapy. A review of the literature reveals common clinical manifestations of this rare adverse effect. Clinicians should be aware of this potential complication of ciprofloxacin use.     

Carbamazepine-induced acute granulomatous interstitial nephritis

A 79-year-old man, newly started on carbamazepine, presented with rash, eosinophilia and liver dysfunction progressing to acute renal failure despite discontinuation of the anti-epileptic agent. Percutaneous renal biopsy revealed acute granulomatous interstitial nephritis, which responded successfully to high-dose oral steroid therapy.