Interstitial nephritis

Drugs such as antibiotics, non-steroidal anti-inflammatory drugs and proton pump inhibitors, infections and systemic diseases can trigger interstitial nephritis. The clinical outcome varies from asymptomatic progression to acute kidney injury. Interstitial nephritis often leads to characteristic and detectable partial tubular disorders such as tubular proteinuria (alpha(1)-microglobulin), phosphaturia with hypophosphatemia, aminoaciduria, diminished H+ secretion with metabolic acidosis with inadequate high urinary pH, glucosuria and salt loss. The main principle of treatment is avoidance of the inducing agent. In addition corticosteroids have been proven usable after exclusion of an infection so that a good prognosis can be expected for acute nephritis in the majority of cases. In chronic forms the interstitial nephritis involves the glomeruli as well as potentially resulting in end-stage renal failure in the long run. Supportive therapies are then required in the sense of chronic renal failure in order to prevent further functional loss up to end-stage renal disease.