nsaid and acute tubulointerstitial nephritis

We describe a case of a 40-year-old lady diabetic and hypertensive, who presented with increasing fatigue and decreased physical endurance attributable to deterioration in renal function. The renal biopsy revealed drug-induced acute tubulointerstitial nephritis and the chronology of the events suggested the aetiology to be a recent intake of aceclofenac for knee pain. The patient improved with oral corticosteroids and the renal functions returned to baseline in 3 weeks. We did not come across a case of aceclofenac-induced acute tubulointerstitial nephritis on extensive electronic search of literature...

BACKGROUND: Acute tubulointerstitial nephritis, a cause of acute kidney injury, is seen occasionally following treatment with medications such as antibiotics and non-steroidal anti-inflammatory drugs. To date, the development of biopsy-proven acute tubulointerstitial nephritis after treatment with exenatide has not been reported. CASE REPORT: A 58-year-old man was prescribed exenatide for poorly controlled Type 2 diabetes mellitus. He subsequently developed deterioration in kidney function, with the estimated glomerular filtration rate declining from 59 to 39 ml min(-1) 1...

A 37-year-old lady presented with hypercalcemia and acute renal impairment. She had no previous medical problems apart from the use of non steroidal anti-inflammatory drugs for nonspecific body pains. Her abdominal ultrasound scan as well as urine studies were nonspecific. Further workup for hypercalcemia (skeletal survey, high resolution computed tomography (CT) of the chest and abdomen, purified protein derivative (PPD) test, serum protein electrophoresis, tumor markers, immunology screening, and Bence Jones proteinuria) was negative...

Acute tubulointerstitial nephritis (TIN) is a frequent cause of acute renal failure, characterised by the presence of inflammatory cell infiltrate in the interstitium of the kidney. Immuno-allergic reaction to certain medications, mainly non-steroidal anti-inflammatory drugs and antibiotics are by far the most important etiology for TIN today, but other situations such as infections, toxins, and vasculitis are known to induce TIN. Incidence of TIN is increasing, probably due to prescription habits and NSAID overuse, representing 3-7% of acute kidney injury in biopsies in children...

INTRODUCTION: Drug-induced tubulointerstitial nephritis and acute tubular necrosis are common, and are often caused by drugs especially antibiotics or non-steroidal anti-inflammatory drugs. Drug-induced liver dysfunction and renal failure after subcutaneous injection of phosphatidylcholine was not reported so far. 3-sn-Phosphatidylcholine has been described as a cell lysis reaction-inducing drug. Its in vitro data indicated a relevant toxicity potential. In particular human cell types such as fibroblast-like preadipocytes, vascular and skeletal muscle cells, or renal epithelial cells react more sensitive than other human cell types...

Injury to the interstitium of the kidney is regarded as a common pathway leading to end-stage renal insufficiency, regardless of etiology. Tubular interstitial nephritis is characterized histologically by inflammatory changes in the tubulointerstitial compartment, such as interstitial edema, leukocyte infiltration, accumulation of extracellular matrix proteins, tubular dilation and atrophy. Acute interstitial nephritis is often associated with use of drugs, such as β-lactam antibiotics and non-steroidal anti-inflammatory drugs, and is likely mediated through allergic mechanisms...

A number of therapeutic agents can adversely affect the kidney, resulting in tubulointerstitial, glomerular or vascular disease. Drug-induced tubulointerstitial nephritis and acute tubular necrosis are common, and are often cause by antibiotics or non-steroidal anti-inflammatory drugs. Drug-induced glomerular and vascular disease is relatively rare. This review describes the morphological patterns of drug-induced disease in the kidney. The histopathological changes are often similar to disease that is idiopathic or due to other causes, so that awareness and clinical correlation are most helpful to arrive at the aetiology...

The nephrotoxic potential of anti-inflammatory drugs alone and in compound preparations has been known for over fifty years. Nephrotoxicity associated with selective cyclooxygenase 2 (COX-2) inhibitor use is reported in adult patients but not in children. We present here the first report of reversible acute renal failure associated with the COX-2 inhibitor rofecoxib (Vioxx) in three children. Patient 1, an 18 month old girl with neonatal Bartter syndrome, developed acute renal failure with a peak creatinine of 1...

The nephrotoxic effect of nonselective nonsteroidal anti-inflamatory drugs (NSAIDS) has been widely described. The main benefit of the Cox-2 inhibitors in relation to the NSAIDS is the production of a very similar analgesic effect, but with fewer gastrointestinal side effects. However, their effects on renal function are little known as yet and their long-term safety is still pending definition. The use of selective Cox-2 inhibitors as anti-inflamatory analgesic is becoming more and more common in our environment...

This review summarizes drug induced nephrotic syndrome. Major drugs which induce drug related nephrotoxicity are antibiotics, NSAID, radiocontrast media, anticancer drug and antirheumatic drug. Drug induced nephropathy can show various forms of renal diseases. The nephropathy consists of acute tubular necrosis, acute tubulointerstitial nephritis, pre-renal type renal failure, obstructive renal failure, chronic tubulointerstitial nephritis and glomerular damage. Major drugs which induce nephrotic syndrome and glomerular damage are gold, penicillamine, bucillamine and NSAID...

AIMS: To study the mechanisms behind NSAID-associated nephropathy. METHODS: Analysis of published case reports satisfying strict criteria for NSAID nephropathy. RESULTS: Ninety-seven cases with acute nephritis (AN; 19 patients), minimal change nephropathy (MC; 38 patients), membranous glomerulonephritis (MGN; 19 patients), focal sclerosis (FS; 13 patients) and other glomerulonephritis subgroups (8 patients) were identified. Hypersensitivity reactions were seen in all groups, most often in AN...

While the relative incidence of serious nephrotoxicities in the population consuming nonsteroidal anti-inflammatory drugs (NSAIDs) is very low, the frequency of adverse events in patients at risk has considerably increased due to the rising popularity of the use of the drugs in recent years. Under normal conditions, NSAIDs have relatively little effect on the kidney because of low renal production of prostaglandins. However, in the presence of renal hypoperfusion in which local synthesis of vasodilator prostaglandins is increased to protect the glomerular hemodynamics and to maintain appropriate renal tubular transport of fluid and electrolytes, inhibition of prostaglandin synthesis by NSAIDs can lead to vasoconstrictive acute renal failure as well as fluid and electrolyte disorders such as sodium retention and resistance to diuretics, hyponatremia and hyperkalemia...

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a common cause of acute renal failure. The clinical presentation differs from that of interstitial nephritis due to antibiotic use: proteinuria is much more common in NSAID-induced nephritis, while eosinophilia, eosinophiluria, fever and rash are more common in antibiotic-related nephritis. Tubulointerstitial disease associated with NSAID use is more common in women than in men and is more frequently seen in the elderly. Because no prospective study of treatment for NSAID-induced acute tubulointerstitial nephritis has been performed, the efficacy of steroid therapy remains uncertain...