As a rule, diseases of the kidney primarily affect the glomeruli, vasculature, or remainder of the renal parenchyma that consists of the tubules and interstitium. Although the interstitium and the tubules represent separate functional and structural compartments, they are intimately related. Injury initially involving either one of them inevitably results in damage to the other. Hence the term tubulointerstitial diseases is used. Because inflammatory cellular infiltrates of variable severity are a constant feature of this entity, the terms tubulointerstitial diseases and tubulointerstitial nephritis have come to be used interchangeably. The clinicopathologic syndrome that results from these lesions, commonly termed tubulointerstitial nephropathy, may pursue an acute or chronic course. The chronic course is discussed here. The abbreviation TIN is used to refer synonymously to chronic tubulointer-stitial nephritis and tubulointerstitial nephropathy.
TIN may be classified as primary or secondary in origin. Primary TIN is defined as primary tubulointerstitial injury without significant involvement of the glomeruli or vasculature, at least in the early stages of the disease. Secondary TIN is defined as secondary tubulointerstitial injury, which is consequent to lesions initially involving either the glomeruli or renal vasculature. The presence of secondary TIN is especially important because the magnitude of impairment in renal function and the rate of its progression to renal failure correlate better with the extent of TIN than with that of glomerular or vascular damage.
Renal insufficiency is a common feature of chronic TIN, and its diagnosis must be considered in any patient who exhibits renal insufficiency. In most cases, however, chronic TIN is insidious in onset, renal insufficiency is slow to develop, and earliest manifestations of the disease are those of tubular dysfunction. As such, it is important to maintain a high index of suspicion of this entity whenever any evidence of tubular dysfunction is detected clinically. At this early stage, removal of a toxic cause of injury or correction of the underlying systemic or renal disease can result in preservation of residual renal function. Of special relevance in patients who exhibit renal insufficiency caused by primary TIN is the absence or modest degree of the two principal hallmarks of glomerular and vascular diseases of the kidney: salt retention, manifested by edema and hypertension; and proteinuria, which usually is modest and less than 1 to 2 g/d in TIN. These clinical considerations notwithstanding, a definite diagnosis of TIN can be established only by morphologic examination of kidney tissue.
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