It is also known as intestinal nephritis because the clinical picture may in some cases of acute pyelonephritis include mesenteric lymphadenitis (mostly due to use of NSAIDs).

[1] In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney.

[1] There are a variety of known factors that can provoke the inflammatory process within the renal interstitium, including pharmacologic, environmental, infectious and systemic disease contributors.

The spectrum of disease presentation can range from an acute process to a chronic condition with progressive tubular cell damage and renal dysfunction.

[2] Other general symptoms that occur with variable frequency include nausea, vomiting, fatigue, lack of appetite, and weight loss.

In chronic tubulointerstitial nephritis the patient can experience symptoms such as nausea, vomiting, fatigue, and weight loss.

Pathologic examination will reveal the presence of interstitial edema and inflammatory infiltration with various white blood cells, including neutrophils, eosinophils, and lymphocytes.

Electron microscopy shows mitochondrial damage in the tubular epithelial cells, vacuoles in the cytoplasm, and enlarged endoplasmic reticulum.

One study showed that monocyte chemotactic protein-1 (chemokine CCL-2) and neutrophil gelatinase associated lipocalin (NGAL) were higher in patients with AIN than in controls (in this case healthy participants).

[citation needed] In most cases of acute tubulointerstitial nephritis, the function of the kidneys will return after the harmful drug is discontinued, or when the underlying disease is cured by treatment.