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Chronic interstitial nephritis (CIN) is by definition tubulointerstitial nephritis that has failed to resolve on its own or has been resistant to whatever treatment was rendered after several months or years. However, it can also arise de novo as a consequence of chronic, low-grade, or injurious exposures of the tubulointerstitium to the culprit agent, ie, medication, physical factor, infectious agents, etc. Such exposures may be intermittent or persistent. Histopathologically, it is characterized by the presence of interstitial chronic inflammation, interstitial fibrosis, and tubular atrophy (Figure 37–1).

Figure 37–1.

Chronic tubulointerstitial nephritis with interstitial fibrosis, fibroblasts, and scattered mononuclear inflammatory cells. There is extensive tubular atrophy and loss. Glomeruli are spared. Hematoxylin and eosin (×200). (Courtesy of Dr. Shane Meehan, Department of Pathology, University of Chicago.)

Depending on the culprit agent, the disease may have a particular predilection for either the proximal tubules, the distal tubules, or both. The functional abnormalities usually depend on the tubular site of involvement, ie, distal tubule dysfunction may be characterized by acidosis and hyperkalemia, as seen in obstructive uropathies, whereas injury involving the renal medulla is characterized by an impaired ability to concentrate urine as seen in sickle cell nephropathy (Table 37–1).

Table 37–1. Clinical Features of Chronic Tubulointerstitial Nephritis.

As CIN progresses, there may be concomitant glomerular abnormalities, probably secondary to maladaptive alterations in the glomeruli or a result of the tubulointerstitial processes. At that time, patients may present with nephrotic-range proteinuria, which can cloud the primary underlying disease process.

The various causes of CIN can be classified into several categories (Table 37–2).

Table 37–2. Causes of Chronic Tubulointerstitial Nephritis.1

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