INTERSTITIAL NEPHRITIS

Essentials of Diagnosis

Fever.

Transient maculopapular rash.

Acute renal insufficiency.

Pyuria (including eosinophiluria), white blood cell casts, and hematuria.

General Considerations
Acute interstitial nephritis accounts for 10–15% of cases of intrinsic renal failure. An interstitial inflammatory response with edema and possible tubular cell damage is the typical pathologic finding. Cell-mediated immune reactions prevail over humoral responses. T lymphocytes can cause direct cytotoxicity or release lymphokines that recruit monocytes and inflammatory cells.
Although drugs account for over 70% of cases, acute interstitial nephritis also occurs in infectious diseases, immunologic disorders, or as an idiopathic condition. The most common drugs are penicillins and cephalosporins, sulfonamides and sulfonamide-containing diuretics, NSAIDs, rifampin, phenytoin, and allopurinol. More recently, proton-pump inhibitors have also been recognized as a cause of acute interstitial nephritis. Infectious causes include streptococcal infections, leptospirosis, cytomegalovirus, histoplasmosis, and Rocky Mountain spotted fever. Immunologic entities are more commonly associated with glomerulonephritis, but systemic lupus erythematosus, Sjögren’s syndrome, sarcoidosis, and cryoglobulinemia can cause interstitial nephritis.
Clinical Findings
Clinical features can include fever (> 80%), rash (25–50%), arthralgias, and peripheral blood eosinophilia (80%). The urine often contains red cells (95%), white cells, and white cell casts. Proteinuria can be a feature, particularly in NSAID-induced interstitial nephritis but is usually modest. Eosinophiluria can be detected by Wright’s or Hansel’s stain.
Treatment & Prognosis
Acute interstitial nephritis often carries a good prognosis. Recovery occurs over weeks to months, but acute dialytic therapy may be necessary in up to one-third of all patients before resolution. Patients rarely progress to ESRD. Those with prolonged courses of oliguric failure and advanced age have a worse prognosis. Treatment consists of supportive measures and removal of the inciting agent. If renal failure persists after these steps, a short course of corticosteroids can be given. Short-term, high-dose methylprednisolone (0.5–1 g/d for 1–4 days) or prednisone (60 mg/d for 1–2 weeks) followed by a prednisone taper can be used in these more severe cases of drug-induced interstitial nephritis.