What Is Interstitial Nephritis?

Interstitial nephritis, also known as tubulointerstitial nephritis, is a clinical pathological syndrome of acute and chronic tubular interstitial damage caused by various reasons. Clinical is often divided into acute interstitial nephritis and chronic interstitial nephritis. Acute interstitial nephritis is characterized by multiple causes of renal interstitial inflammatory cell infiltration, interstitial edema, renal tubule damage to varying degrees with renal insufficiency. The clinical manifestations can be mild or severe. Have a clear cause, remove the cause, and timely treatment, the disease can be cured or the disease can be reversed to varying degrees. The pathological manifestations of chronic interstitial nephritis are characterized by renal interstitial fibrosis, interstitial mononuclear cell infiltration, and renal tubular atrophy.

Basic Information

nickname

Tubulointerstitial nephritis

English name

interstitial nephritis

Visiting department

Nephrology

Common locations

kidney

Common causes

Pathogenic microbial infections, systemic lupus erythematosus, dryness syndrome, antibiotics, heavy metals, etc.

Common symptoms

Polyuria, thirst, nausea, nocturia, gross hematuria, muscle weakness, soft palsy, joint pain, etc.

Causes of Interstitial Nephritis

Infection

Pathogenic infections can include pathogenic microbial infections such as bacteria, fungi, and viruses, including Staphylococcus aureus sepsis, severe streptococcal infections, diphtheria, red fever, mycoplasma pneumonia, syphilis, brucellosis, legionellosis, hepatitis B virus Antigenemia, cytomegalovirus infection, typhoid fever, measles, pyelonephritis and so on.

Systemic disease

Such as systemic lupus erythematosus, Sjogren's syndrome, sarcoidosis, and primary cryoglobulinemia. Hematological diseases, such as multiple myeloma, paroxysmal hemoglobinuria, lymphoproliferative disease, sickle cell disease, etc.

3. Drugs cause disease

May be related to long-term application of cyclosporine, aminoglycoside antibiotics, amphotericin B, analgesics, non-steroidal anti-inflammatory drugs, and cisplatin.

4. Heavy metal salts

May be related to long-term exposure to cadmium, lithium, aluminum, gold, beryllium, etc.

5. Chemical poison or biological toxin

Such as carbon tetrachloride, tetrachloroethylene, methanol, ethylene glycol, phenol, nitrosourea or snake venom, fish gall venom, bee venom, mycotoxin and other poisoning history.

6. Metabolic diseases

Such as cystine disease, hypokalemia nephropathy, uric acid nephropathy, diabetic nephropathy and a history of amyloid nephropathy.

Clinical manifestations of interstitial nephritis

Generally have polyuria, thirst, nausea, nocturia, gross hematuria, muscle weakness, soft palsy, joint pain and other manifestations.

Acute interstitial nephritis

Acute interstitial nephritis has different clinical manifestations and no specificity due to its different etiology. The main prominent manifestations are oliguria or non-oliguria acute renal insufficiency, which may be accompanied by nonspecific manifestations such as fatigue, weakness, fever and joint pain. Loss of renal tubular function can occur with low specific gravity and low osmotic urine, tubular proteinuria, and water, electrolyte, and acid-base disorders. Some patients present with Fanconi syndrome.

2. Chronic interstitial nephritis

Chronic interstitial nephritis is usually occult, chronic, or acute. Due to chronic inflammation of the renal interstitial changes, fibrotic tissue hyperplasia and renal tubular atrophy are common clinical manifestations.

Interstitial nephritis test

Urine test

Generally small amount of small molecule proteinuria, urine protein quantification is mostly 0.5 ~ 1.5 g / 24 hours, rarely> 2.0 g / 24 hours; urine sediment examination can be microscopic hematuria, white blood cells and cast urine, occasionally eosinophils . Renal tubule dysfunction varies according to the location and degree of involvement of the tubules, and may include renal diabetes, renal tubular acidosis, hypotonic urine, Fanconi syndrome, and so on.

Blood test

Some patients may have symptoms such as hypokalemia, hyponatremia, hypophosphatemia, and hyperchloric metabolic acidosis. Blood uric acid is usually normal or slightly elevated. Chronic interstitial nephritis anemia has a high incidence and severity, and it is usually positive cell positive pigment anemia. Patients with acute interstitial nephritis have an increased percentage of eosinophils in the peripheral blood, which may be accompanied by an increase in IgE. Idiopathic interstitial nephritis may have anemia, increased eosinophils, rapid erythrocyte sedimentation, and elevated CRP and globulin.

3. Imaging examination

B ultrasound of acute interstitial nephritis can show that the kidney is normal in size or volume, and the cortical echo is enhanced. Imaging examinations of chronic interstitial nephritis such as ultrasound, radionuclide, and CT usually show that both kidneys are shrinking and the outline of the kidneys is not smooth. Imaging studies can also help determine some specific causes, such as urinary tract obstruction, bladder ureteral reflux, and kidney cystic disease. Intravenous urography (IVU) can show signs of renal papillary necrosis characteristic of analgesic nephropathy. Because the contrast agent has renal tubular toxicity, it should be used with caution in renal tubular injury.

4. Kidney biopsy pathology

Pathological examination is of great significance for the diagnosis. Except for infection-associated acute interstitial nephritis, other types of renal puncture should be actively performed to distinguish the type of renal interstitial infiltrating cells and the degree of fibrosis, thereby helping to determine the prognosis of the treatment plan.

Interstitial nephritis diagnosis

A history of infection or drug use, clinical manifestations, some laboratory and imaging studies can help diagnose, but kidney pathology is still the gold standard for the diagnosis of interstitial nephritis.

The possibility of acute interstitial nephritis should be considered when clinically unknown acute renal insufficiency occurs. Those with the following clinical characteristics should consider chronic interstitial nephritis: there are inducements leading to chronic interstitial nephritis, such as long-term analgesics, chronic urinary tract obstruction, etc., or a family history of chronic interstitial nephritis; clinical manifestations are Tubules dysfunction, such as thirst, polyuria, increased nocturia, renal tubular acidosis, etc., or renal insufficiency without hypertension, hyperuricemia, etc .; Urine examination showed severe tubule dysfunction. A small amount of small molecule proteinuria (<2.0 g / 24 hours), urine RBP, lysozyme, urine ₂ -microglobulin, NAG increased, and there may be diabetic and amino acid urine. The etiology of chronic interstitial nephritis must be further clarified based on medical history and clinicopathological characteristics.

Interstitial nephritis treatment

General treatment

Removing the cause, controlling infection, stopping allergenic drugs in time, and treating the primary disease are the first steps in the treatment of interstitial nephritis.

2. Symptomatic supportive treatment

Correct the renal anemia, electrolytes, acid-base and volume imbalances, blood creatinine significantly increased or combined with hyperkalemia, heart failure, pulmonary edema and other indications for blood purification, blood purification treatment should be performed in a timely manner, acute interstitial nephritis Optional continuous blood purification treatment. For those who enter the uremia stage, if conditions permit, kidney transplantation is feasible.

(1) Promote the regeneration of renal tubules Cordyceps sinensis can promote the growth of renal tubular epithelial cells, improve the stability of cell membranes, enhance the tolerance of renal tubular epithelial cells to hypoxia, and has a certain treatment for tubulointerstitial nephritis.

(2) Immunosuppressants Interstitial nephritis mediated by immune factors such as autoimmune diseases and drug allergies can be treated with hormones and immunosuppressants.