Diagnostic Considerations
When evaluating patients with suspected tubulointerstitial nephritis, other problems to be considered include the following:
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Tubular necrosis
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Gomerulonephritis
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Vasculitis
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Atheroembolic disease
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Radiation nephritis
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Toxic nephropathies.
Tubulointerstitial nephritis and uveitis syndrome (TINU) is a rare disorder characterized by the combination of tubulointerstitial nephritis with bilateral anterior uveitis of sudden onset. In approximately 65% of cases the nephritis precedes the uveitis; in 20% the uveitiis occurs first, and in 15% the two conditions occur simultaneously. Patients are typically younger than 20 years old; many are girls. [21] TINU is thought to be an autoimmune process. It may be precipitated by drugs or infections, but many cases are idiopathic. A human leukocyte antigen (HLA)–related genetic predisposition has been reported. [22, 23]
Differential Diagnoses
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Tubulointerstitial nephritis: Kidney biopsy reveals acute interstitial nephritis. The renal cortex shows a diffuse interstitial, predominantly mononuclear, inflammatory infiltrate with no changes to the glomerulus. Tubules in the center of the field are separated by inflammation and edema, as compared with the more normal architecture in the right lower area (periodic acid–Schiff, 40 X).
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Tubulointerstitial nephritis. On a kidney biopsy, the diagnosis of acute interstitial nephritis is based on the active inflammatory infiltrate on the right with unaffected glomeruli. Interstitial edema and fibrosis are present on the left side of the field, where some tubules show thickened basement membrane (hematoxylin and eosin, 20 X).
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Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The interstitium is expanded by mononuclear inflammatory infiltrate and edema. Acute tubular damage is present; some tubules are distended and contain granular casts (hematoxylin and eosin, 40 X).
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Tubulointerstitial nephritis. Kidney biopsy shows acute crescentic glomerulonephritis. The glomerular tuft is compressed by the proliferation of epithelial cells, forming a crescent. In addition, the interstitium shows mononuclear inflammatory infiltrate and edema (periodic acid–Schiff, 40 X).
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Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The mononuclear inflammatory infiltrate contains abundant eosinophils, suggesting an allergic etiology. Severe tubular damage is observed (hematoxylin and eosin, 40 X).
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Tubulointerstitial nephritis. Kidney biopsy shows acute interstitial nephritis. The inflammatory infiltrate forms an ill-defined granuloma, suggesting allergic or infectious etiologies. A partially destroyed tubule is present (periodic acid–Schiff, 40 X).
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Tubulointerstitial nephritis. Kidney biopsy shows chronic tubulointerstitial nephritis. The interstitium is expanded by fibrosis, with distortion of tubules and periglomerular fibrosis. Glomeruli do not show pathologic changes (hematoxylin and eosin, 20 X).
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Tubulointerstitial nephritis. Kidney biopsy in interstitial nephritis shows a cholesterol microembolism. The 2 arterioles in the center are occluded by elongated crystals (hematoxylin and eosin, 20 X).
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Tubulointerstitial nephritis. Kidney biopsy in interstitial nephritis shows a cholesterol microembolism. The arteriole in the center of the field has a thickened wall. The lumen is occluded by elongated spaces, corresponding to dissolved crystals surrounded by cellular reaction. The 2 glomeruli flanking the arteriole are sclerotic and hardly recognizable (hematoxylin and eosin, 40 X).
