Interstitial nephritis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. Associate Editor(s)-in-Chief: Mohsen Basiri M.D.
Two main diseases involve the renal tubules are: Acute tubular necrosis due to Ischemic or toxic injury .(for more about ATN click here), and tubulointerstitial nephritis with Inflammatory involvement of tubules and interstitium and its consequent reactions.
Since some cases of TIN are due to bacterial infection, and the renal pelvis is deeply involved, therefore pyelonephritis is term describes this condition; and In general, the term interstitial nephritis is used for TIN that is owing to nonbacterial causes of tubular injury such as drugs, viral infections,autoimmune systemic diseases, in which these condition mechanism of damage is due to inflammatory responses not direct damage.
In 1938, Councilman was the first to discover the association between systemic infections and the development of TIN; in autopsy kidneys of children dying of diphtheria and scarlet fever. He described the findings as: cellular and fluid exudation in the interstitial tissue of kidneys, before the era of antibiotics.
The widespread use of renal biopsy and histological examination in TIN revealed a cellular infiltration, which is dominantly composed of T cells, together with somemacrophages and plasma cells, and led to the discovery of similar findings in association with drug-related renal failure and the same conditions.
There is no established system for the classification of TIN, however according to clinical manifestations and the inflammatory process, TIN, in spite of the etiologic agent, can be divided into acute and chronic categories.
It is thought that acute interstitial nephritis is mediated by hypersensitivity reaction to endogenous or exogenous antigens expressed by tubular cells. Numerous drugs such as antibiotics, NSAIDS, sulfa-containing drugs, etc, as well as systemic diseases, and Infections may lead injury to renal cells. the cascade activation owing to cellular injury toward inflammatory cell infiltration, and activation of cytokines causes an immunologic reaction in acute or chronic process.
In acute interstitial nephritis, this cascade activation can cause renal tubular dysfunction, whereas in chronic interstitial nephritis an insidious interstitial fibrosis,scarring, , and tubular atrophy spreads gradually and causes progressive chronic renal insufficiency.
Common causes of interstitial nephritis include drug side effects, particularly analgesics and antibiotics. Other common causes include associated nephrologic conditions, as well as microbial infections.
Differentiating TIN from Other Diseases
Epidemiology and Demographics
Interstitial nephritis accounts for 10-15% of kidney disease worldwide. Analgesic-induced nephritis is 5-6 times more common in women. The elderly have more severe disease and increased risk of permanent damage. Children exposed to lead poisoning are more likely to develop nephritis as young adult.
There are no established risk factors for TIN; Whereas according to etiologic causative factors, consumption of culprit drugs in causing TIN,previous history of hypersensitivity reactions to specific drug, presence of autoimmune systemic disease or some neoplasia or genetic condition, occupational or environmental exposure to heavy metals, and infection etiologies in association with obstructive uropathy, play role in in the development of TIN.
There is insufficient evidence to recommend routine screening for TIN.
Natural History, Complications, and Prognosis
In the majority of patients with TIN, recovery of renal function has been observed, and improvement immediately occurs upon stopping the offensive agent, nevertheless, about 12% of patients may progress to develop ESRD and its complications; and thus require dialysis or transplantation.
However there is no definite prognostic indicators for TIN, but renal failure lasts for >3 weeks, elderly patients and presence of tubular atrophy and interstitial fibrosis in the renal biopsy are associated with worse prognosis.
Diagnostic Study of Choice
Renal biopsy is the gold standard and definitive test of establishing the diagnosis of TIN, however it is not needed in all patients and often considered to make a definitive diagnosis for patients who do not improve following withdrawal of offensive agent or in the presence of doubtful findings.
History and Symptoms
The majority of patients with interstitial nephritis are asymptomatic. However, nonspecific signs and symptoms may present depending upon underlying etiology and timing of presentation. Non specific symptoms include nausea, vomiting, malaise, and oliguria. Hematuria though not so common is also seen in some patients with tubulointerstitial nephritis. Other symptoms of interstitial nephritis include hypersensitivity reaction, such as rash, fever, and eosinophilia.
There are no physical examination findings specific to interstitial nephritis, and no characteristic findings exist. The presence of fever, rash in acute tubulointerstitial nephritis, livido reticularis, on physical examination may be suggestive of TIN, and provide clues to the diagnosis.
A variable combination of laboratory findings of TIN, such as rise in the plasma creatinine concentration, eosinophilia, eosinophiluria, changes of urine sediment, as well as evidences of tubulointerstitial damage based upon the culprit agent may present.
In some studies a variable amount of proteinuria among older patients and NSAID-induced AIN has been reported, although nephrotic-range proteinuria among patients with TIN is rare.
There are no ECG findings associated with TIN, however electrolyte imbalances due to complications of TIN may cause changes in ECG.
There are no x-ray findings associated with TIN.
Echocardiography and Ultrasound
There are no echocardiography/ultrasound findings associated with TIN.
There are no CT scan findings associated with TIN.
There are no MRI findings associated with TIN.
Other Imaging Findings
Other Diagnostic Studies
The mainstay of treatment for tubulointerstitial nephritis is discontinuation of potentially offending agen. The majority of patients due to drug-induced interstitial nephritis, improve spontaneously, however, renal function may not return to previous condition. No additional measures is needed among patients with minimal rise in the serum creatinine or those who demonstrate betterment after discontinuation of offending agent; otherwise if renal failure persists after removing the culprit drug, obtaining a renal biopsy and attempt glucocorticoids therapy for patients with biopsy-confirmed AIN must be considered.
There are no established measures for the primary prevention of tubulointerstitial nephritis.
The mainstay preventive action is to stay away from re-exposure to the offensive agents of the acute episode. Among patients with chronic inflammatory diseases such as Sjogren's syndrome, sarcoidosis, or SLE, proper control of the underlying condition alongside with consideration of offensive agent is important and should be kept in mind.