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Interstitial nephritis,tubulointerstitial nephritis
- 2. INTRODUCTION Interstitial nephritis, also known as tubulointerstitial nephritis, is inflammation of the area of the kidney known as the interstitium, which consists of a collection of cells, extracellular matrix, and fluid surrounding the renal tubules.In addition to providing a scaffolding support for the tubular architecture, the interstitium has been shown to participate in the fluid and electrolyte exchange as well as endocrine functions of the kidney. There are a variety of known factors that can provoke the inflammatory process within the renal interstitium, including pharmacologic, environmental, infectious and systemic disease contributors. The spectrum of disease presentation can range from an acute process to a chronic condition with progressive tubular cell damage and renal dysfunction.
- 3. SIGN AND SYMPTOMS Signs and symptoms Interstitial nephritis may present with a variety of signs and symptoms, many of these nonspecific. Fever is the most common, occurring in 30- 50% of patients, particularly those with drug-induced interstitial nephritis.Other general symptoms that occur with variable frequency include nausea, vomiting, fatigue, lack of appetite, and weight loss. More specific symptoms, such as flank pain, pain with urination, and visible blood in the urine, as well as signs like hypertension can be helpful in increasing suspicion for the diagnosis.The "classic" triad of symptoms reported in early documented cases consisted of rash, joint pain, and increased eosinophils in the blood; however, more recent epidemiology suggests that this grouping of symptoms only occurs in a small minority (5-10%) of patients. However, with modern drugs causing between 70-90% of current cases, it is not surprising that the earliest documented cases and a minority of today's may present different symptoms.
- 5. CAUSES 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.
- 9. Examples of Drugs Associated With Interstitial Nephritis
- 10. 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 medication. The medications that are known to cause this sort of reaction are β-lactam antibiotics such as penicillin and cephalexin, and nonsteroidal anti-inflammatory drugs (aspirin less frequently than others), as well as proton-pump inhibitors, rifampicin, sulfa medications, fluoroquinolones, diuretics, allopurinol, mesala mine, 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).
- 11. DIAGNOSIS 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 a high concentration of potassium in the blood, metabolic acidosis, and kidney failure.
- 12. Blood tests About 23% of patients have a high level of eosinophils in the blood. Urinary findings Urinary findings include: 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, a 2013 study showed that the sensitivity and specificity of urine eosinophil testing are 35.6% and 68% respectively. Isosthenuria Blood in the urine and occasional RBC casts Sterile pyuria: white blood cells and no bacteria Nephrotic-range amount of protein in the urine may be seen with NSAID- associated AIN
- 13. Pathology While non-invasive patient evaluation (physical examination, blood and urine testing, imaging studies) can be suggestive, the only way to definitively diagnosis interstitial nephritis is with a tissue diagnosis obtained by kidney biopsy. Pathologic examination will reveal the presence of interstitial edema and inflammatory infiltration with various while blood cells, including neutrophils, eosinophils, and lymphocytes. Generally, blood vessels and glomeruli are not affected. Electron microscopy shows mitochondrial damage in the tubular epithelial cells, vacuoles in the cytoplasm, and enlarged endoplasmic reticulum. Gallium scan The sensitivity of an abnormal gallium scan has been reported to range from 60% to 100%.
- 14. TREATMENT Corticosteroids have been a mainstay of therapy for tubulointerstitial nephritis, but mycophenolate mofetil may also have a role. Ultimately, however, treatment depends on the underlying etiology. Treatment consists of addressing the cause, such as by removing an offending drug. There is no clear evidence that corticosteroids help. Nutrition therapy consists of adequate fluid intake, which can require several liters of extra fluid.