Overview
What is tubulointerstitial nephritis?
What is the pathophysiology of tubulointerstitial nephritis?
What causes tubulointerstitial nephritis?
What causes acute tubulointerstitial nephritis?
What causes chronic tubulointerstitial nephritis?
What is the role of lead in the etiology of tubulointerstitial nephritis?
What causes obstructive uropathy in tubulointerstitial nephritis?
What is the role of Sjögren syndrome in the etiology of tubulointerstitial nephritis?
What is the role of Balkan endemic nephropathy, in the etiology of tubulointerstitial nephritis?
What is the role of aristolochic acid in the etiology of tubulointerstitial nephritis?
What is the prevalence of tubulointerstitial nephritis?
What is the prognosis of tubulointerstitial nephritis?
Presentation
Which clinical history findings are characteristic of tubulointerstitial nephritis?
What are the signs and symptoms of acute tubulointerstitial nephritis?
Which drugs may induce acute tubulointerstitial nephritis?
What are the signs and symptoms of NSAID-related acute tubulointerstitial nephritis?
What are the signs and symptoms of antibiotic-induced acute tubulointerstitial nephritis?
What are the infectious causes of acute tubulointerstitial nephritis?
What are the signs and symptoms of chronic tubulointerstitial nephritis?
What is analgesic nephropathy?
What are cyclosporine- and tacrolimus-induced nephropathy?
What are the signs and symptoms of lead nephropathy in tubulointerstitial nephritis?
What are the signs and symptoms of obstructive uropathy in tubulointerstitial nephritis?
What are atherosclerotic kidney diseases in patients with tubulointerstitial nephritis?
What is cholesterol microembolic disease in tubulointerstitial nephritis?
Which metabolic disorders are associated with tubulointerstitial nephritis?
What is Balkan endemic nephropathy?
DDX
Which conditions should be included in the differential diagnoses of tubulointerstitial nephritis?
What are the differential diagnoses for Tubulointerstitial Nephritis?
Workup
How is tubulointerstitial nephritis diagnosed?
What is the role of a chemistry panel in the workup of tubulointerstitial nephritis?
What is the role of urine studies in the workup of tubulointerstitial nephritis?
What is the role of ultrasonography in the workup of tubulointerstitial nephritis?
What is the role of IV pyelography in the workup of tubulointerstitial nephritis?
What is the role of CT scanning in the workup of tubulointerstitial nephritis?
What is the role of an EDTA lead mobilization test in the workup of tubulointerstitial nephritis?
What is the role of kidney biopsy in the workup of tubulointerstitial nephritis?
Which histologic findings are characteristic of tubulointerstitial nephritis?
Treatment
How is tubulointerstitial nephritis treated?
How is acute tubulointerstitial nephritis treated?
How is chronic tubulointerstitial nephritis treated?
How is analgesic nephropathy treated in tubulointerstitial nephritis?
How is cyclosporine/tacrolimus–induced renal failure treated in tubulointerstitial nephritis?
How is lead nephropathy treated in tubulointerstitial nephritis?
Medications
What is the role of steroid therapy in the treatment of tubulointerstitial nephritis?
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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).