Acute tubulointerstitial nephritis

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

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Causes acute tubulointerstitial nephritis.

Acute tubulointerstitial nephritis is characterized by pronounced inflammatory changes in the structures of the renal interstitium with infiltration mainly by lymphocytes (up to 80% of all cells), as well as polymorphonuclear leukocytes, and granulomas are found less frequently. Edema, cell dystrophy, and foci of necrosis are determined in the epithelium of the tubules. Immunohistochemical studies usually do not reveal immunoglobulin deposits in the interstitium.

A detailed history allows us to establish the cause of acute tubulointerstitial nephritis. In more than 60% of patients, the development of the disease is due to the use of drugs. The contribution of infectious agents to the development of acute tubulointerstitial nephritis is currently decreasing.

Group	The most common reasons
Medicines	Antibacterial drugs Penicillin derivatives, cephalosporins, sulfonamides, rifampicin, ciprofloxacin, erythromycin, vancomycin Nonsteroidal anti-inflammatory drugs Diuretics Thiazides, furosemide, triamterene Acyclovir, allopurinol, captopril, clofibrate, fenofibrate, H2 - blockers, omeprazole, interferon alpha, phenothiazine derivatives, warfarin Other
Infections	Bacterial: streptococcal, brucellosis, legionellosis, mycoplasma, 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 unilateral or bilateral uveitis

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

Acute tubulointerstitial nephritis due to NSAIDs usually develops years after continuous use of these drugs. The risk group primarily consists of elderly patients. The mechanisms of development of proteinuria, often reaching nephrotic levels, are not fully understood; direct damage to glomerular structures is considered to be the most probable.

Infections and parasitic invasions, which are 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 conditions, sometimes microabscesses form in the interstitium. The risk group for the development of acute infectious tubulointerstitial nephritis is HIV-infected people, the elderly, patients with diabetes mellitus, as well as those receiving cytostatics or immunosuppressants.

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

A special variant of acute tubulointerstitial nephritis, sometimes with extremely rapid deterioration of renal function, is characteristic of embolism of intrarenal arteries by 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 cap of an atherosclerotic plaque is compromised during endovascular interventions, including angiographic ones, as well as in trauma and overdose of anticoagulants.

In cases where the cause of acute tubulointerstitial nephritis is not established, the disease is called idiopathic. A special variant of idiopathic tubulointerstitial nephritis is described in combination with acute uveitis (unilateral or bilateral). The disease most often develops in adolescent girls and young women.

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Symptoms acute tubulointerstitial nephritis.

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

Drug-induced acute tubulointerstitial nephritis

For the diagnosis of drug-induced etiology of acute tubulointerstitial nephritis, the detection of the so-called allergic triad is of great importance:

• fevers;
• maculopapular rash;
• arthralgia.

Symptoms of drug-induced acute tubulointerstitial nephritis depend on the drug causing the kidney damage.

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

The drug etiology of acute tubulointerstitial nephritis, especially in cases of already developed acute renal failure, is confirmed by the fact of taking medications, often for a long time, immediately before the onset of the disease and the exclusion of other causes of kidney damage.

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Acute tubulointerstitial nephritis in systemic diseases

In patients with sarcoidosis, the development of acute renal failure has been described in the presence of a large number of sarcoid granulomas in the renal tubulointerstitium. This variant of kidney damage is usually observed with pronounced clinical activity of the disease.

Cholesterol embolism of the intrarenal arteries is considered a special variant of ischemic kidney disease. In addition to significant intrarenal hemodynamic disturbances, cholesterol emboli cause the development of acute tubulointerstitial nephritis, the peculiarity of which is the predominance of eosinophils in the inflammatory infiltrate. Oligo- and anuria, a marked increase in blood pressure, and pain in the lumbar region are characteristic. Along with the renal arteries, the arteries of the lower extremities (typical ischemic pains are characteristic), the arteries of the intestine and pancreas (symptoms of "abdominal toad" and acute pancreatitis, respectively), and the skin often act as targets for cholesterol emboli. Cholesterol embolism of the arteries of the skin is accompanied by reticular livedo and the formation of trophic ulcers. Renal failure that occurs with massive embolism of cholesterol crystals is practically irreversible in most cases.

The most characteristic clinical sign of renal tubulointerstitial damage associated with the use of Chinese herbs containing aristolochic acid is renal failure of varying degrees of severity.

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Idiopathic acute tubulointerstitial nephritis

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

Diagnostics acute tubulointerstitial nephritis.

Laboratory diagnostics of acute tubulointerstitial nephritis

Proteinuria is noted; its value, as a rule, does not exceed 1-2 g/day. Proteinuria of nephrotic level indicates a connection between acute tubulointerstitial nephritis and NSAID intake. Acute tubulointerstitial nephritis is characterized by hypercreatininemia, hyperkalemia, increased concentration of C-reactive protein, and sometimes increased ESR.

For drug-induced tubulointerstitial nephritis, as well as with embolism of intrarenal arteries by cholesterol crystals, blood eosinophilia and eosinophiluria are characteristic. Leukocyte casts are often found in the urine. With embolism, an increase in ESR and the concentration of C-reactive protein in the blood is also noted.

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

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

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Instrumental diagnostics of acute tubulointerstitial nephritis

Ultrasound examination reveals normal or enlarged kidney sizes. Increased ultrasound signal intensity from the renal cortex indicates the severity of interstitial inflammation. Abdominal computed tomography is uninformative.

A skin biopsy can confirm the diagnosis of cholesterol crystal embolism.

Treatment acute tubulointerstitial nephritis.

Treatment of acute tubulointerstitial nephritis consists primarily of addressing the underlying cause, such as discontinuing the drug or treating the infection. The advisability of prescribing glucocorticosteroids for acute drug-induced tubulointerstitial nephritis has not been proven. Their use is considered justified in cases where renal failure persists for more than 7 days after discontinuing the drug. Short courses of high-dose prednisolone are preferred.

Preventing acute tubulointerstitial nephritis is possible only with respect to its drug variant. Prescribing drugs that can cause its development in risk groups (especially in the elderly) should be done with caution. Long-term use of these drugs, especially in high doses, by elderly and senile patients is undesirable.