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At least 289 records · Page 16Linked to original sources
PubMed2004

[Acute interstitial nephritis associated with omeprazole therapy].

From 1 to 3% of acute renal failures are due to acute interstitial nephritis (AIN). Most of them are due to drugs. Nonsteroidal antiinflammatory drugs, penicillins and sulfonamides are the most frequently reported. Clinical presentation of drug-induced AIN has changed over time and with the use of new drugs. In fact actually the classic triad of fever, rash and eosinophilia is uncommon. Omeprazole is a drug widely used in the treatment of gastroesophageal reflux disease and peptic ulcer disease. Serious side effects are rare with this drug, but despite of its safety we can see serious adverse effects such as acute renal failure. We describe two cases of acute interstitial nephritis after use of omeprazole and a review of all the cases published in the last years.

Acute Disease↗
PubMed2004

An unusual form of crystal-forming chronic interstitial nephritis following long-term exposure to tosufloxacin tosilate.

Fluoroquinolones are known to cause acute renal failure because of interstitial nephritis with or without epithelioid granulomas. We report the first case of slowly progressive renal failure caused by crystal-forming chronic interstitial nephritis with non-Langerhans' cell histiocytosis after long-term exposure to a fluoroquinolone, tosufloxacin tosilate. Lesions consisted of spindle- to cuboidal-shaped histiocytes with minimal collagenous matrix and low-level lymphocyte infiltration replacing normal tubulointerstitial structure of the kidney. Histiocytes were positive for CD68, but negative for S-100, suggesting they were derived from macrophages. There were numerous rhomboid- to needle-shaped crystal deposits in the cytoplasm of histiocytes, which showed bright birefringence under polarized light. No immunoglobulin deposits were seen in the kidney, and no evidence of paraproteinemia/lymphoproliferative diseases was identified in this patient. Despite a negative drug lymphocyte-stimulating test result using tosufloxacin tosilate, withdrawal of the drug and treatment with steroids gradually improved renal function. In this report, we describe the clinical course and histopathologic findings of this patient and discuss the possible pathogenesis.

Acute Kidney Injury↗
PubMed2002

Snakebite induced acute interstitial nephritis: report of a rare entity.

Snakebite induced acute renal failure continues to occur in many tropical areas of the world. Renal histological lesions other than acute tubular necrosis and acute cortical necrosis as the cause of acute renal failure are rare. Only 3 cases of acute interstitial nephritis in patients with snakebite induced acute renal failure have been previously reported. We report a patient with acute renal failure following viperine snakebite due to acute interstitial nephritis. After a prolonged oliguric phase, there was complete recovery of renal function without institution of steroids. Interstitial nephritis may result from a hypersensitivity reaction to some component of the snake venom.

Acute Disease↗
PubMedDate not supplied

Nabumetone-associated interstitial nephritis.

An 84-year-old woman was admitted to the hospital for progressive edema and decreased urine output. She had been taking nabumetone for 6 months, but had discontinued the agent 2 weeks before admission due to progressive edema. On admission she had 2-3+ pitting edema. Her serum electrolytes were sodium 122 mEq/L, potassium 5.9 mEq/L, chloride 93 mEq/L, and carbon dioxide 19 mEq/L. A urinalysis was significant for protein 3061 mg/dl, ketones 15 mg/dl, blood 2+, leukocytes 26-50/high-power field, and a protein:creatinine ratio 24.9. The serum creatinine and blood urea nitrogen concentrations were 2.7 mg/dl and 70 mg/dl, respectively. Throughout hospitalization the patient underwent aggressive diuresis. She developed congestive heart failure, and hemodialysis was initiated. A renal biopsy specimen on hospital day 9 showed tubular damage with minimal glomerular changes consistent with a diagnosis of nonsteroidal agent-induced nephropathy. On day 13, a 24-hour urine collection had a protein excretion of 3151 mg. Although the patient recovered from her renal failure (creatinine clearance 43 ml/min), the nephrotic syndrome persisted (13 g protein/day). The patient developed infectious complications and died on hospital day 32.

Aged↗
PubMed1976

An immunopathologic study of interstitial nephritis associated with experimental canine adenovirus infection.

The localisation of canine adenovirus in the renal tubules induces a marked cellular response in the interstitium. A number of mechanisms appear to be involved in the genesis of the lesions. Direct lytic damage to tubular epithelial cells by the virus is probably augmented by immunological factors. The production of local anti-viral antibody by plasma cells in the vicinity of virus-containing cells may result in the formation of toxic antigen-antibody complexes while the accumulation of large populations of macrophages suggests that cell-mediated hypersensitivity is also operative.

Adenoviridae Infections↗