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Go back to clinical information and images Diagnosis: Acute Tubulointerstitial nephritis Due to the findings in the renal biopsy, the patient was questioned again and said he had taken NSAIDs for the ankle trauma. One week after biopsy, serum cretinine decreased and patient was discharged. One month later creatinine clearance was normal. In the biopsy there was not chronic changes (i.e. fibrosis or atrophy), so, from the point of view of pathology, this tubulointerstitial disease was acute. Tubulointerstitial diseases involve tubules and/or the interstitium of the kidney and spare the glomeruli. Although primary glomerular diseases are often associated with prominent tubulointerstitial changes, the clinical presentation is dominated by the consequences of glomerular injury. Tubulointerstitial nephritis encompass diverse etiologies and pathophysiologic processes, and the patient can present with acute or chronic conditions. Many forms of tubulointerstitial nephritis involve exposure to drugs or other nephrotoxic agents and infection. By far the most common form of tubulointerstitial inflammation is immunologic. In acute interstitial nephritis, the tubular damage leads to renal tubular dysfunction, with or without renal failure. Regardless of the severity of the damage to the tubular epithelium, the renal dysfunction is generally reversible, possibly reflecting the regenerative capacity of tubules with preserved basement membrane. Conversely, chronic tubulointerstitial nephritis is characterized by interstitial scarring, fibrosis, and tubule atrophy, resulting in progressive chronic renal insufficiency. The principal mechanism in acute tubulointerstitial nephritis is hypersensitivity reaction to drugs such as penicillins, NSAIDs, and sulfa drugs. Another mechanism is acute cellular injury caused by infection, viral or bacterial, often associated with obstruction or reflux. See the chapter Tubulinerstitial Diseases of our Tutorial. Go back to clinical information and images Bibliography
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