Acute tubulointerstitial nephritis

Tubulointerstitial nephritis is not very common, but this disease is often undiagnosed due to the relative non-specificity of the clinical symptoms of acute renal failure.

[1], [2], [3],

Causes of the acute tubulointerstitial nephritis

Acute tubulointerstitial nephritis is characterized by pronounced inflammatory changes in the structures of renal interstitium with infiltration predominantly by lymphocytes (up to 80% of all cells) and polymorphonuclear leukocytes, and granulomas are less often found. In the epithelium of the tubules, edema, dystrophy of cells, foci of necrosis are determined. When immunohistochemical study of deposits of immunoglobulins in the interstitium, as a rule, do not find.

A detailed familiarity with the anamnesis allows us to establish the cause of acute tubulointerstitial nephritis. More than 60% of patients develop the disease due to medication. The contribution of infectious agents to the development of acute tubulointerstitial nephritis is currently decreasing.

Group	Common causes
Medicinal products	Antibacterial drugs Penicillin derivatives, cephalosporins, sulfonamides, rifampicin, ciprofloxacin, erythromycin, vancomycin Nonsteroidal anti-inflammatory drugs Diuretics Thiazides, furosemide, triamterene Acyclovir, allopurinol, captopril, clofibrate, fenofibrate, H 2 -blockers, omeprazole, interferon alfa, phenothiazine derivatives, warfarin Other
Infections	Bacterial: streptococcal, brucellosis, legionellosis, mycoplasmal, syphilis, tuberculosis, rickettsiosis Viral: caused by cytomegalovirus, Epstein-Barr virus,  hantaviruses, parvovirus B19, HIV Parasitic infestations: toxoplasmosis, leishmaniasis
Systemic diseases	Sarcoidosis, systemic lupus erythematosus, Sjogren's disease and syndrome
Various	Idiopathic Associated with one- or bilateral uveitis

Acute tubulointerstitial nephritis develops in response to most of the currently used drugs, but many cases can be attributed to a difficult-to-forecast individual intolerance. Some classes of medicinal substances (antibacterial drugs, NSAIDs) cause acute tubulointerstitial nephritis especially often.

Acute tubulointerstitial nephritis, caused by the intake of NSAIDs, usually develops years after the constant intake of these drugs. Risk groups are primarily elderly patients. The mechanisms of the development of proteinuria, which often reach the nephrotic level, have not been fully studied; among the most likely are direct damage to the structures of the glomerulus.

Infections and parasitic infestations, the main cause of acute tubulointerstitial nephritis in childhood, play a significantly smaller role in adults. The development of infectious acute tubulointerstitial nephritis occurs in septic states, sometimes micro-abscesses are formed in the interstitium. The risk group for the development of acute infectious tubulointerstitial nephritis is HIV-infected, elderly, sick with diabetes mellitus, and also receiving cytostatics or immunosuppressors.

Acute tubulointerstitial nephritis is observed in systemic diseases: Sjogren's disease and syndrome, systemic lupus erythematosus, especially in sarcoidosis.

A special variant of acute tubulointerstitial nephritis, sometimes with extremely rapid impairment of renal function, is characteristic of embolism of the intrarenal arteries with cholesterol crystals separated from the detritus of the lipid core of an atherosclerotic plaque localized in the abdominal aorta or renal arteries. The release of cholesterol crystals into the bloodstream occurs when the integrity of the fibrous plaque of the atherosclerotic plaque is violated during endovascular interventions, including angiographic, as well as in traumas and an overdose of anticoagulants.

In cases where the cause of acute osteopathy-interstitial nephritis is not established, it is said about the idiopathic form of the disease. A special variant of idiopathic tubulointerstitial nephritis is described in combination with acute uveitis (one- or two-sided). The disease often develops in adolescent girls, as well as young women.

[4], [5], [6], [7], [8],

Symptoms of the acute tubulointerstitial nephritis

Symptoms of acute tubulointerstitial nephritis are represented by signs of acute renal failure (primarily oligo and anuria) and nonspecific symptoms - fever.

Medicinal acute tubulointerstitial nephritis

To diagnose the drug etiology of acute tubulointerstitial nephritis, it is very important to detect the so-called allergic triad:

• fevers;
• maculopapular rash;
• arthralgia.

Symptoms of acute tubulointerstitial nephritis induced by drugs depend on the drug that caused kidney damage.

Acute tubulointerstitial nephritis, associated with the use of beta-lactam antibiotics (especially methicillin, which is currently practically not used), is characterized by a combination of a drug allergic triad with signs of rapidly worsening kidney function. About 1/3 of patients need hemodialysis.

The medicinal etiology of acute tubulointerstitial nephritis, especially when acute renal failure has already developed, confirms the fact of taking medications, often long, just before the onset of the disease and excluding other causes of kidney damage.

[9], [10], [11], [12], [13]

Acute tubulointerstitial nephritis in systemic diseases

In patients with  sarcoidosis  , the development of acute renal failure is described in the presence of a large number of sarcoid granules in renal tubulointerstitium. This variant of kidney damage, as a rule, is observed with the expressed clinical activity of the disease.

Cholesterol embolism of the intrarenal arteries is considered as a special variant of ischemic kidney disease. In addition to pronounced violations of intrarenal hemodynamics, cholesterol emboli cause the development of acute tubulointerstitial nephritis, a feature of which is the predominance of eosinophils in the inflammatory infiltrate. Characteristic oligo- and anuria, a marked rise in blood pressure,  pain in the lumbar region. Simultaneously with the renal arteries, the target of the cholesterol emboli is often arteries of the lower limbs (typical ischemic pains), arteries of the intestine and pancreas (symptoms of the "abdominal toad" and acute pancreatitis, respectively), as well as skin. Cholesterol embolism of the arteries of the skin is accompanied by a reticular livedo and the formation of trophic ulcers. Renal failure, which occurs with massive embolism with cholesterol crystals, is almost irreversible in most cases.

The most characteristic clinical sign of the defeat of renal tubulointerstitium associated with the use of Chinese herbs containing aristocholic acid is renal failure of varying severity.

[14], [15], [16], [17]

Idiopathic acute tubulointerstitial nephritis

The clinical picture is represented by thirst, polyuria, gradually joining signs of impaired renal function, as well as fever, weight loss. Anterior uveitis precedes the appearance of signs of kidney damage or occurs simultaneously.

Diagnostics of the acute tubulointerstitial nephritis

Laboratory diagnosis of acute tubulointerstitial nephritis

Mark proteinuria; its value, as a rule, does not exceed 1-2 g / day. Proteinuria of the nephrotic level indicates the connection of acute tubulointerstitial nephritis with the intake of NSAIDs. Acute tubulointerstitial nephritis is characterized by hypercreatininemia, hyperkalemia, an increase in the concentration of C-reactive protein, and sometimes an increase in ESR.

For medicinal tubulointerstitial nephritis, as well as for embolism of the intrarenal arteries, cholesterol crystals are characterized by eosinophilia of the blood and eosinophiluria. In urine, leukocyte cylinders are often found. With embolism, an increase in ESR and concentration of C-reactive protein in the blood is also noted.

A typical sign of acute drug tubulointerstitial nephritis, induced by beta-lactam antibiotics, is hematuria, which is extremely rare for this form of kidney damage of another etiology. In addition, an increase in the serum activity of liver enzymes is found; often marked eosinophilia.

Idiopathic acute tubulointerstitial nephritis is characterized by an increase in ESR, hypergammaglobulinemia and eosinophilia of the blood.

[18], [19], [20]

Instrumental diagnosis of acute tubulointerstitial nephritis

With ultrasound, the kidneys are normal or enlarged. An increase in the intensity of the ultrasonic signal from the cortical substance of the kidneys indicates the severity of interstitial inflammation. Computed tomography of the abdominal cavity is of little informative.

A skin biopsy can confirm the diagnosis of embolism with cholesterol crystals.

Treatment of the acute tubulointerstitial nephritis

Treatment of acute tubulointerstitial nephritis consists primarily of influencing the cause that caused it, - the abolition of the drug or in the treatment of infection. The expediency of prescribing glucocorticosteroids in acute drug tubulointerstitial nephritis has not been proven. Their appointment is considered justified in cases where renal failure persists for more than 7 days after the drug was discontinued. Short courses of prednisolone in high doses are preferred.

To prevent acute tubulointerstitial nephritis is possible only with regard to its drug variant. It is necessary to prescribe medications that can cause its development in risk groups (especially in the elderly) with caution. Long-term use of these drugs, especially in high doses, patients elderly and senile age is undesirable.