genitourinary disorders
Tubulointerstitial Nephritis
Diagnosis of Tubulointerstitial Nephritis
Risk factors In acute tubulointerstitial nephritis (ATIN), active urinary sediment with sterile pyuria Sometimes renal biopsy Usually imaging to exclude other causes Few clinical and routine laboratory findings are specific for tubulointerstitial nephritis. Thus, suspicion should be high when the following are present: Typical symptoms or signs Risk factors, particularly a temporal relationship between onset and use of a potentially causative medication Characteristic urinalysis findings, particularly sterile pyuria Modest proteinuria, usually<1 g/day (except with use of nonsteroidal anti-inflammatory drugs [NSAIDs], which may cause nephrotic-range proteinuria, 3.5 g/day) Evidence of tubular dysfunction (eg, Renal Tubular Acidosis , Concentrating defect out of proportion to the degree of renal failure Eosinophiluria cannot be relied upon to make or exclude the diagnosis. Other tests (eg, imaging) are usually necessary to differentiate ATIN or chronic tubulointerstitial nephritis (CTIN) from other disorders. A presumptive clinical diagnosis of ATIN is often made based on the specific findings mentioned above, but Renal biopsy is necessary to establish a definitive diagnosis. Urinalysisthat shows signs of active kidney inflammation (active urinary sediment), including red blood cells (RBCs), white blood cells (WBCs), and WBC casts, and absence of bacteria on culture (sterile pyuria) is typical; marked hematuria and dysmorphic RBCs are uncommon. Eosinophiluria has traditionally been thought to suggest ATIN; however, the presence or absence of urinary eosinophils is not particularly useful diagnostically. Proteinuria is usually minimal but may reach nephrotic range with combined ATIN-glomerular disease induced by NSAIDs,ampicillin,rifampin, interferon alfa, orranitidine. Blood test findings of tubular dysfunction include Hypokalemia (caused by a defect in potassium reabsorption) and a nonanion gap radionuclide scanning, or both may be needed to differentiate acute tubulointerstitial nephritis from other causes of Acute Kidney Injury (AKI) when kidney biopsy is not possible. In ATIN, ultrasonography may show kidneys that are greatly enlarged and echogenic because of interstitial inflammatory cells and edema. Radionuclide scans may show kidneys avidly taking up radioactive gallium-67 or radionuclide-labeled white blood cells (WBCs). Positive scans strongly suggest ATIN (and indicate that acute tubular necrosis is less likely), but a negative scan does not exclude ATIN. Renal biopsy None An uncertain diagnosis Progressive renal injury No improvement after potential causative medications are stopped Findings suggesting early disease Medication-induced ATIN for which corticosteroid therapy is under consideration In acute tubulointerstitial nephritis, glomeruli are usually normal. The earliest finding is interstitial edema, typically followed by interstitial infiltration with lymphocytes, plasma cells, eosinophils, and a few polymorphonuclear leukocytes. In severe cases, inflammatory cells can be seen invading the space between the cells lining the tubular basement membrane (tubulitis); in other specimens, granulomatous reactions resulting from exposure to beta-lactam antibiotics, sulfonamides, mycobacteria, or fungi may be seen. The presence of noncaseating granulomas suggests sarcoidosis. A lymphoplasmacytic infiltration of the kidney interstitium with storiform fibrosis suggests Tubulointerstitial Nephritis . Immunofluorescence or electron microscopy seldom reveals any pathognomonic changes. Findings of CTIN are generally similar to those of ATIN, although urinary RBCs and WBCs are uncommon. Because CTIN is insidious in onset and interstitial fibrosis is common, imaging tests may show small kidneys with evidence of scarring and asymmetry. In chronic tubulointerstitial nephritis, renal biopsy is not often done for diagnostic purposes. However, if there is concern for alternative diagnoses, it could be pursued. Glomeruli vary from normal to completely destroyed. Tubules may be absent or atrophied. Tubular lumina vary in diameter but may show marked dilation, with homogeneous casts. The interstitium contains varying degrees of inflammatory cells and fibrosis. Nonscarred areas appear almost normal. Grossly, the kidneys are small and atrophic. 