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Interstitial nephritis
From Wikipedia, the free encyclopedia
| ICD-10 | N10.-N12. |
|---|---|
| ICD-9 | 580.89, 581.89, 582.89, 583.89 |
| DiseasesDB | 6854 |
| MedlinePlus | 000464 |
| eMedicine | med/1596 |
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, which means it occurs suddenly or chronic, meaning it is ongoing and eventually ending in kidney failure.
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Common causes include infection, or reaction to medication (such as an analgesic or antibiotics). 71%[1] to 92%[2] of cases are reported to be caused by drugs. This disease is also caused by other diseases and toxins that do damage to the kidney. Both acute and chronic tubulointerstitial nephritis can be caused by a bacterial infection in the kidneys, known as pyelonephritis. The most common cause is by an allergic reaction to a drug. The drugs that are known to cause this sort of reaction are antibiotics such as penicillin, and nonsteroidal anti-inflammatory drugs, such as aspirin. The time between exposure to the drug and the development of acute tubulointerstitial nephritis can be anywhere from 5 days to 5 weeks.
At times there are no symptoms of this disease, but when they do occur they are widely varied and can occur rapidly or gradually[3][1][4][5][6]. When caused by an allergic reaction, the symptoms of acute tubulointerstitial nephritis are fever (27% of patients)[1], rash (15% of patients)[1], 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.
About 23% of patients have eosinophilia[1].
Urinary findings include:
- Eosinophiluria: sensitivity is 67% and specificity is 83% [3][7]. The sensitivity is higher in patients with interstitial nephritis induced by methicillin or when the Hansel's stain is used.
- Isosthenuria [8]
The sensitivity of an abnormal gallium scan has been reported to range from 60%[9] to 100%[10].
Remove the etiology such as an offending drug. Corticosteroids do not clearly help [2]. Nutrition therapy consists of adequate fluid intake, which can require several liters of extra fluid. "39", in Alexopolos Y: Krause's Food, Nutrition, & Diet Therapy, 11th (in English), Philadelphia Pennsylvania: Saunders, 968. ISBN 0-7216-9784-4.
The kidneys are the only body system that is 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 tube is injured sodium, potassium, bicarbonate, uric acid, and phosphate intake 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.
- ^ a b c d e Baker R, Pusey C (2004). "The changing profile of acute tubulointerstitial nephritis". Nephrol Dial Transplant 19 (1): 8-11. PMID 14671029.
- ^ a b Clarkson M, Giblin L, O'Connell F, O'Kelly P, Walshe J, Conlon P, O'Meara Y, Dormon A, Campbell E, Donohoe J (2004). "Acute interstitial nephritis: clinical features and response to corticosteroid therapy". Nephrol Dial Transplant 19 (11): 2778-83. PMID 15340098.
- ^ a b Rossert J (2001). "Drug-induced acute interstitial nephritis". Kidney Int 60 (2): 804-17. doi:10.1046/j.1523-1755.2001.060002804.x. PMID 11473672.
- ^ Pusey C, Saltissi D, Bloodworth L, Rainford D, Christie J (1983). "Drug associated acute interstitial nephritis: clinical and pathological features and the response to high dose steroid therapy". Q J Med 52 (206): 194-211. PMID 6604293.
- ^ Handa S (1986). "Drug-induced acute interstitial nephritis: report of 10 cases". CMAJ 135 (11): 1278-81. PMID 3779558.
- ^ Buysen J, Houthoff H, Krediet R, Arisz L (1990). "Acute interstitial nephritis: a clinical and morphological study in 27 patients". Nephrol Dial Transplant 5 (2): 94-9. PMID 2113219.
- ^ 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 Nephrol 54 (3): 179-90. PMID 11020015.
- ^ Lins R, Verpooten G, De Clerck D, De Broe M (1986). "Urinary indices in acute interstitial nephritis". Clin Nephrol 26 (3): 131-3. PMID 3769228.
- ^ Graham G, Lundy M, Moreno A (1983). "Failure of Gallium-67 scintigraphy to identify reliably noninfectious interstitial nephritis: concise communication". J Nucl Med 24 (7): 568-70. PMID 6864309.
- ^ Linton A, Richmond J, Clark W, Lindsay R, Driedger A, Lamki L (1985). "Gallium67 scintigraphy in the diagnosis of acute renal disease". Clin Nephrol 24 (2): 84-7. PMID 3862487.