Acute tubulointerstitial nephritis

Introduction

Primary interstitial nephropathies is a group of disorders associated with interstitial inflammation and subsequent damage of the tubular cells and the development of fibrosis. We share traditionally into acute and chronic tubulointerstitial nephritis (TIN), on the basis of clinical course and morphology. Acute tubulointerstitial nephritis is characterized by acute inflammation interstitial inflammation and edema with subsequent rapid decline in GFR. Vascular and glomerular structures are spared here, and the prognosis is good if the patient receives adequate treatment. Acute TIN is found to be the cause of ca. 10-15% of reported acute renal failure.

Causes

Acute TIN is usually a result of immunologic reaction to external influences such as drugs and infectious agents. The list of drugs that can give TIN is long and in principle, all drugs cause hypersensitivity reactions with acute TIN. The reaction is dose-dependent and typically occurs on repeated exposure to the same or related drugs. Systemic immunological diseases can also cause acute TIN. In a significant proportion of cases can not be sure cause exists and termed idiopathic. Acute TIN occur in all age groups, but the incidence appears to increase with increasing age. Direct inflammatory responses (ascending UTI) or hypersensitivity reactions initiates local inflammation with edema formation and leukocyte infiltration.

Table of common causes of acute tubulointerstitial nephritis

Causes Examples
Medications NSAIDs
Antibiotic
Diuretics
Infections Systemic (viral, bacterial and others)
Infections pyelonephritis
Immune-mediated causes SLE
Sjøgren
Sarcoidosis
Idiopathic

Causes	Examples
Medications	NSAIDs
	Antibiotic
	Diuretics
Infections	Systemic (viral, bacterial and others)
	Infections pyelonephritis
Immune-mediated causes	SLE
	Sjøgren
	Sarcoidosis
Idiopathic

Clinical presentation

By ascending urinary tract infections (acute pyelonephritis), the patient could present with systemic symptoms of infection with fever and positive SIRS criteria together with pyuria and bank tenderness over the kidney lodges. Drug-associated acute TIN can also present itself at systemic symptoms of hypersensitivity reaction with rash, arthralgias and fever. Renal acute TIN will present with an acute decline in GFR and thus as an acute renal failure. Mild proteinuria is often seen, rarely more than 1 g / day. Tubular dysfunctions can occur out of which parts of the nephrons that are mainly affected. UL kidneys will display normally large or edematous enlarged kidneys. NSAIDs can sometimes cause acute TIN with nephrotic proteinuria. Glomeruli will then be affected and histological patients will have changes with minimal change nephropathy in addition to acute tubulo-interstitial changes. Immunological cross-reactivity against glomerular structures can therefore be present in acute TIN triggered by NSAIDs.

Urinary Findings

Web microscope with descriptions of the items.
erythrocytes
white, eosinophils and white cell cylinders
Pyuria

Histopathology

It is seen interstitial edema and leukocyte infiltration

Course and treatment

The spectrum of acute TIN goes from mild self-limiting illness to acute renal failure oligurisk being requiring dialysis. Acute TIN is potentially reversible and forecasts an overall good. Treatment is aimed at detecting and removing precipitating cause. Steroid treatment to curb ongoing inflammation is debated and reserved for the severe cases to prevent or shorten the time in dialysis needs. Perhaps future studies will document the effect of immunosuppressive therapy in more then irreversible interstitial fibrosis has been shown to act as early as 10-14 days out in the course of acute TIN, but this is not yet an established treatment.