The disease begins about 15 days after exposure to the drug and is characterized by fever, eosinophilia (which may be transient), rash (in about 25% of individuals), and renal abnormalities. Urinary findings include hematuria, minimal or no proteinuria, and leukocyturia (sometimes including eosinophils). A rising serum creatinine or acute kidney injury with oliguria develops in about 50% of cases, particularly in older patients. Clinical recognition of drug-induced kidney injury is imperative, because withdrawal of the offending drug is followed by recovery, although it may take several months for renal function to return to normal.
Fig. 14.15 Drug-inducedinterstitialnephritis,withprominenteosinophilicandmononuclearinfiltrate.(Courtesy of Dr. H. Rennke, Department of Pathology, Brigham and Women’s Hospital, Boston, Massachusetts.)
TINconsistsofinflammatorydiseaseprimarilyinvolvingtherenaltubulesandinterstitium.
Acute pyelonephritis isabacterialinfectioncausedeitherbyascendinginfectionasaresultofreflux,obstruction,orotherabnormalityoftheurinarytract,ormuchlesscommonlybyhematogenousspreadofbacteria;itischaracterizedbyabscessformationinthekidneys,sometimeswithpapillarynecrosis.
Chronic pyelonephritis usuallyisassociatedwithurinaryobstructionorreflux;itresultsinscarringofthepelvicalycealsystemandtheinterstiumoftheinvolvedkidneyandgradualprogressionofchronickidneydisease.
Drug-induced interstitial nephritis isanIgE-orTcell–mediatedimmunereactiontoadrug;itischaracterizedbyinterstitialinflammation,oftenwithabundanteosinophils,andedema.
Acute tubular injury (ATI) is a clinicopathologic entity characterized by damage to tubular epithelial cells and an acute decline in renal function, often associated with shedding of granular casts and tubular cells into the urine. Clinicians use the term acute tubular necrosis, but frank necrosis is rarely observed in a kidney biopsy, so pathologists prefer the term acute tubular injury. The constellation of changes, broadly termed acute kidney injury, manifests clinically as decreased GFR with concurrent elevation of serum creatinine. ATI is the most common cause of acute kidney injury and may produce oliguria (defined as urine output of <400 mL/day).
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There are two forms of ATI that differ in the underlying causes.
Ischemic ATI is most often the result of a period of inadequate blood flow to all or some peripheral organs such as the kidney, sometimes in the setting of marked hypo-tension and shock. This can be caused by a variety of conditions, including severe trauma, blood loss, acute pancreatitis and septicemia. Ischemia to tubules may also result from reduced intrarenal blood flow, as in microscopic polyangiitis, malignant hypertension, and thrombotic microangiopathies. Mismatched blood transfusions and other hemolytic crises, as well as myoglobinuria, also produce a clinical picture resembling that of ischemic ATI.
Nephrotoxic ATI is caused by a variety of poisons, including heavy metals (e.g., mercury); organic solvents (e.g., carbon tetrachloride); and a multitude of drugs such as gentamicin and other antibiotics, and radiographic contrast agents.
Proximal tubular epithelial cells are particularly sensitive to hypoxemia and also are vulnerable to toxins (