Tubulointerstitial Nephritis Pathology Cases — Advanced

Acute interstitial nephritis is characterized by interstitial edema and inflammatory infiltrates, often with tubulitis. Eosinophils may be present but are neither required nor specific; the drug timeline and clinical context remain essential.

Chronic tubulointerstitial injury produces fibrosis, tubular atrophy, and chronic inflammatory infiltrates, with progressive loss of concentrating ability and eGFR. These lesions indicate chronicity and are less likely to reverse after removing a trigger.

Crystal nephropathy requires identification of the responsible exposure or metabolic abnormality. Stopping the culprit, restoring appropriate hydration, correcting urine chemistry when evidence supports it, and monitoring obstruction or AKI can prevent further injury.

Chronic analgesic exposure can cause papillary necrosis and chronic tubulointerstitial nephritis. The diagnosis requires exposure history and clinicopathologic correlation; hematuria, concentrating defects, sterile pyuria, or progressive CKD may occur.

Granulomatous interstitial nephritis can occur with sarcoidosis, drugs, infections, and other systemic conditions. Granulomas are not specific, so stains, cultures, exposure history, imaging, and systemic evaluation are required before attributing them to sarcoidosis.

Autoimmune tubulointerstitial disease, especially with Sjögren syndrome, can impair distal acid secretion and cause hypokalemic normal-anion-gap metabolic acidosis. Urine pH, potassium, bicarbonate, and other tubular findings help characterize the defect.

Acute pyelonephritis produces neutrophilic interstitial inflammation and tubulitis, often with clinical or microbiologic evidence of infection. Drug-associated AIN may have pyuria but usually requires a different exposure and exclusion of infection.

Light-chain cast nephropathy results from filtered monoclonal free light chains interacting with tubular proteins and obstructing or injuring distal nephron segments. Serum and urine monoclonal studies and rapid hematologic evaluation are important.

Proximal tubule injury can cause Fanconi-type losses of phosphate, glucose despite normal serum glucose, amino acids, bicarbonate, urate, and low-molecular-weight proteins. The pattern helps distinguish tubular from primarily glomerular disease.

Biopsy is useful when the diagnosis is uncertain, kidney function is worsening, an essential medication cannot be stopped, or corticosteroid treatment carries meaningful risk. It can separate active AIN from infection, tubular injury, obstruction, or chronic scarring.