Interstitial nephritis (or tubulo-interstitial nephritis) is a form of nephritis affecting the interstitium of the kidneys surrounding the tubules. This disease can be either acute, meaning it occurs suddenly, or chronic, meaning it is ongoing and eventually ends in kidney failure.
Common causes include infection, or reaction to medication (such as an analgesic or antibiotics such as Methicillin (Meticillin). Reaction to medications causes 71% to 92% of cases.
This disease is also caused by other diseases and toxins that damage the kidney. Both acute and chronic tubulointerstitial nephritis can be caused by a bacterial infection in the kidneys known as pyelonephritis, but the most common cause is by an adverse reaction to a drug. The drugs that are known to cause this sort of reaction are antibiotics such as penicillin and cephalexin, and nonsteroidal anti-inflammatory drugs (aspirin less frequently than others), as well as rifampicin, sulfa drugs, quinolones, diuretics, allopurinol, and phenytoin. The time between exposure to the drug and the development of acute tubulointerstitial nephritis can be anywhere from 5 days to 5 months (fenoprofen induced).
At times there are no symptoms of this disease, but when they do occur they are widely varied and can occur rapidly or gradually. When caused by an allergic reaction, the symptoms of acute tubulointerstitial nephritis are fever (27% of patients), rash (15% of patients), and enlarged kidneys. Some people experience dysuria, and lower back pain. In chronic tubulointerstitial nephritis the patient can experience symptoms such as nausea, vomiting, fatigue, and weight loss. Other conditions that may develop include hyperkalemia, metabolic acidosis, and kidney failure.
Eosinophiluria: Original studies with Methicillin-induced AIN showed sensitivity of 67% and specificity of 83%. The sensitivity is higher in patients with interstitial nephritis induced by methicillin or when the Hansel's stain is used. However, recent studies have called into question the accuracy of this test. A recent study showed that the sensitivity and specificity of urine eosinophil testing are 35.6% and 68% respectively. 
Remove the etiology such as an offending drug. Corticosteroids do not clearly help. Nutrition therapy consists of adequate fluid intake, which can require several liters of extra fluid.
The kidneys are the only body system that are directly affected by tubulointerstitial nephritis. Kidney function is usually reduced; the kidneys can be just slightly dysfunctional, or fail completely.
In chronic tubulointerstitial nephritis, the most serious long-term effect is kidney failure. When the proximal tubule is injured, sodium, potassium, bicarbonate, uric acid, and phosphate reabsorption may be reduced or changed, resulting in low bicarbonate, known as metabolic acidosis, low potassium, low uric acid known as hypouricemia, and low phosphate known as hypophosphatemia. Damage to the distal tubule may cause loss of urine-concentrating ability and polyuria.
In most cases of acute tubulointerstitial nephritis, the function of the kidneys will return after the harmful drug is not taken anymore, or when the underlying disease is cured by treatment. If the illness is caused by an allergic reaction, a corticosteroid may speed the recovery kidney function; however, this is often not the case.
Chronic tubulointerstitial nephritis has no cure. Some patients may require dialysis. Eventually, a kidney transplant may be needed.
^Buysen J, Houthoff H, Krediet R, Arisz L (1990). "Acute interstitial nephritis: a clinical and morphological study in 27 patients". Nephrol Dial Transplant5 (2): 94–9. doi:10.1093/ndt/5.2.94. PMID2113219.
^Schwarz A, Krause P, Kunzendorf U, Keller F, Distler A (2000). "The outcome of acute interstitial nephritis risk factors for the transition from acute to chronic interstitial nephritis". Clin Nephrol54 (3): 179–90. PMID11020015.
^Muriithi, A.K., S.H. Nasr, and N. Leung, Utility of urine eosinophils in the diagnosis of acute interstitial nephritis. Clinical Journal of The American Society of Nephrology: CJASN, 2013. 8(11): p. 1857-62.
^Perazella, M.A. and A.S. Bomback, Urinary eosinophils in AIN: farewell to an old biomarker? Clinical Journal of The American Society of Nephrology: CJASN, 2013. 8(11): p. 1841-3.
^Lins R, Verpooten G, De Clerck D, De Broe M (1986). "Urinary indices in acute interstitial nephritis". Clin Nephrol26 (3): 131–3. PMID3769228.
^Fogazzi, G.B., et al., Urinary sediment findings in acute interstitial nephritis. American Journal of Kidney Diseases, 2012. 60(2): p. 330-332
^Graham G, Lundy M, Moreno A (1983). "Failure of Gallium-67 scintigraphy to identify reliably noninfectious interstitial nephritis: concise communication". J Nucl Med24 (7): 568–70. PMID6864309.
^Linton A, Richmond J, Clark W, Lindsay R, Driedger A, Lamki L (1985). "Gallium67 scintigraphy in the diagnosis of acute renal disease". Clin Nephrol24 (2): 84–7. PMID3862487.
^Mahan KL, Escott-Stump S (2003). "39". In Alexopolos Y. Krause's Food, Nutrition, & Diet Therapy (11th ed.). Philadelphia Pennsylvania: Saunders. p. 968. ISBN0-7216-9784-4.