Andrew Idoko

Group 332
Variant 14
Discuss the pathogenesis and clinical manifestations of
tubulointerstitial
diseases and discuss how their pathogenesis relates to
treatment and outcomes.

The term tubulointerstitial is used to broadly refer to kidney diseases that

involve structures in the kidney outside the glomerulus. These diseases
generally involve tubules and/or the interstitium of the kidney and spare the
glomeruli
Tubulointerstitial nephritis involves the immune-mediated infiltration of the
kidney interstitium by inflammatory cells. Lethal or sublethal injury to renal
cells leads to expression of new local antigens, inflammatory cell infiltration,
and activation of proinflammatory and chemoattractant cytokines.
The most common cause of acute tubulointerstitial nephritis is an allergic
reaction to a drug. Antibiotics such as penicillin and the sulfonamides,
diuretics, and nonsteroidal anti-inflammatory drugs (NSAIDs)—including
aspirin—may trigger an allergic reaction. The interval between the exposure to
the allergen that caused the reaction and the development of acute
tubulointerstitial nephritis varies usually from 3 days to 5 weeks.

Drugs can also cause tubulointerstitial nephritis through nonallergic

mechanisms. For example, NSAIDs can directly damage the kidney, taking up to
18 months to cause chronic tubulointerstitial nephritis.

Infection of the kidneys (pyelonephritis) can also cause acute or chronic

tubulointerstitial nephritis. Kidney failure is unlikely unless inflammation
causes a blockage in the urinary tract or pyelonephritis occurs in both kidneys.

Tubulointerstitial nephritis may be caused by immunologic disorders that

primarily affect the kidney such as anti-tubular basement membrane (anti-
TBM) antibody-associated interstitial nephritis.

Tubulointerstitial nephritis (TIN) is a frequent cause of acute kidney injury (AKI)

that can lead to chronic kidney disease (CKD). TIN is associated with an
immune-mediated infiltration of the kidney interstitium by inflammatory cells,
which may progress to fibrosis.

Symptoms

Blood in the urine.

Fever.
Increased or decreased urine output.
Mental status changes (drowsiness, confusion, coma)
Nausea, vomiting.
Rash.
Swelling of any area of body.
Weight gain (from retaining fluid)

Flulike symptoms, flank pain, hypertension, and oliguric acute renal failure are
common. In some patients, circulating antirifampin antibodies and
immunoglobulin G (IgG) deposits along the tubular basement membranes have
been reported

Treatment of chronic tubulointerstitial nephritis depends on the etiology and

generally consists of supportive measures, such as adequate blood pressure
control and management of anemia.
Analgesic nephropathy.
Cyclosporine/tacrolimus–induced renal failure.
Lead nephropathy.

Treatment for interstitial nephritis depends on the cause. When AIN is caused
by a drug allergy, the only treatment needed may be drug removal. Other
cases of AIN can be treated with anti-inflammatory medications. Quick
treatment often leads to a full recovery.

In most cases, interstitial nephritis is a short-term problem. Treatment of the

underlying problem cures the condition. Rarely it can lead to long-term or
permanent kidney damage, such as chronic kidney failure. This is more likely to
happen in older adults