Interstitial Nephritis

Introduction to interstitial nephritis Interstitial nephritis (interstitial nephritis), also known as tubulointerstitial nephritis, is a clinical pathological syndrome of tubulointerstitial acute and chronic damage caused by various causes. Clinically, it is often divided into acute interstitial nephritis and chronic interstitial nephritis. Acute interstitial nephritis is characterized by renal interstitial inflammatory cell infiltration, interstitial edema, renal tubular damage and renal insufficiency in a short period of time. The clinical manifestations can be light or severe, most cases are There are clear causes, removal of the cause, timely treatment, the disease can be cured or the condition can be reversed to varying degrees. The pathological manifestations of chronic interstitial nephritis nephritis are characterized by renal interstitial fibrosis, interstitial mononuclear cell infiltration and tubular atrophy. basic knowledge The proportion of illness: 0.03% Susceptible people: more common in middle-aged and elderly people Mode of infection: non-infectious Complications: renal diabetes, renal tubular acidosis, uremia, anemia, hypertension

Cause of interstitial nephritis

Common causes of acute interstitial nephritis

1 drugs: antibiotics, non-steroidal anti-inflammatory drugs, analgesics, anticonvulsants, diuretics, proton pump inhibitors and other drugs;

2 infection: bacteria, viruses, parasites and mycoplasma, chlamydia, etc.;

3 autoimmune diseases: systemic lupus erythematosus, sarcoidosis, mixed cryoglobulinemia, ANCA-associated vasculitis, etc.;

4 malignant tumors: lymphoma, leukemia, light chain deposition disease, multiple myeloma;

5 metabolic diseases: diabetes, hyperuricemia;

6 idiopathic acute interstitial nephritis.

Common causes of chronic interstitial nephritis

1 hereditary diseases: such as familial interstitial nephritis, polycystic kidney disease, medullary cystic lesions and hereditary nephritis;

2 drug-induced nephropathy: kidney damage caused by non-steroidal anti-inflammatory drugs, aristolochic acid drugs, cyclosporine and cisplatin;

3 urinary tract disease: obstructive nephropathy, reflux nephropathy; sputum nephritis;

5 heavy metal poisoning: such as lead, cadmium, lithium poisoning;

6 physical damage: such as radiation kidney disease;

7 systemic diseases: immune diseases (systemic lupus erythematosus, Sjogren's syndrome, cryoglobulinemia, chronic graft rejection), metabolic diseases (uric acid nephropathy, hypercalcemia nephropathy, hypokalemia nephropathy), Systemic diseases such as blood diseases (multiple myeloma, light chain deposition disease) can cause chronic interstitial nephritis.

Interstitial nephritis prevention

Most drug-related acute interstitial nephritis has a good prognosis, and renal function damage can be completely restored after removal of the cause. The factors affecting the prognosis of acute interstitial nephritis are as follows: 1 patients with previous chronic kidney disease have poor prognosis; 2 older onset, especially with hypertension, poor prognosis of patients with diabetes; 3 renal tubular epithelium Cell brush border detachment, renal tubular necrosis, poor prognosis; 4 renal interstitial cells diffuse invasive prognosis is poor; 5 onset of serum creatinine level and prognosis is not related, but renal failure lasts longer, prognosis Poor; 6 patients with severe renal interstitial fibrosis, poor prognosis. The above situation can leave varying degrees of renal dysfunction.

The prognosis of chronic interstitial nephritis is closely related to the etiology, renal interstitial lesions and the degree of impaired renal function. Thorough removal of the cause can delay the progression of chronic interstitial nephritis, Sjogren's syndrome, drug-induced interstitial nephritis has a good prognosis, but analgesic nephropathy and toxic nephropathy have a poor prognosis.

Interstitial nephritis complications Complications, renal glucosuria, renal tubular acidosis, uremia, anemia, hypertension

Chronic interstitial nephritis can be complicated by renal diabetes, and even fanconi syndrome; can be complicated by renal tubular acidosis until uremia; can also be complicated by renal anemia and hypertension, acute interstitial nephritis complicated with acute renal failure.

Interstitial nephritis symptoms common symptoms immunonephritis tubulointerstitial nephritis nausea weakness hyperoxia nocturia increased polyuria facial butterfly erythematous hematuria

Interstitial nephritis can occur at any age, and is more common in middle-aged and elderly people. Children are relatively rare. Chronic interstitial nephritis is more common in men, and the ratio of male to female is about 1.34:1.

Acute interstitial nephritis

Acute interstitial nephritis has different clinical manifestations and no specificity due to its different causes. Mainly characterized by oliguria or non-oliguric acute renal insufficiency, may be associated with fatigue, weakness, fever and joint pain and other non-specific manifestations. Loss of renal tubular function may occur with low specific gravity and low osmotic urinary pressure, renal tubular proteinuria, and water, electrolyte and acid-base balance disorders, and some patients present with Fanconi syndrome.

Drug-related acute interstitial nephritis often has a typical course of disease: renal function damage occurs after several days or weeks of use of the disease-causing drug, urine volume can be reduced or no change, urine test abnormalities, some with gross hematuria, no Bacterial leukocyte urine, low back pain, generally no hypertension and edema, often accompanied by systemic allergy symptoms such as fever, rash, eosinophilia triad, most patients with nausea, vomiting and other gastrointestinal symptoms. The clinical manifestations of acute interstitial nephritis caused by different drugs are not exactly the same. Some patients may develop acute interstitial nephritis if they are previously tolerant to a certain drug. A large amount of proteinuria can occur in acute interstitial nephritis caused by non-steroidal anti-inflammatory drugs.

Patients with infection-associated acute interstitial nephritis are often associated with signs of infection, such as fever, chills, headache, nausea, vomiting, and even sepsis, and may be associated with other organ system symptoms such as pneumonia, myocarditis, and liver damage. Among them, acute pyelonephritis complicated with renal parenchymal infection is the most common. Most renal parenchymal infections are secondary to bacterial infections in the urethra and bladder. The clinical manifestations vary from mild discomfort to sepsis: more acute onset, often chills, high fever, rib angle tenderness, Urinary tract irritation and other symptoms. Atypical cases showed fatigue, low back pain, weight loss, recurrent cystitis (dysuria, frequent urination, urgency, pain on the pubic arch). About one-third of elderly patients have no fever, and 20% of elderly patients have gastrointestinal symptoms or pulmonary symptoms. Urine examination showed white blood cell urine, pyuria and bacteriuria, and urine culture was positive.

For men, urinary tract obstruction caused by prostatitis and enlarged prostate is an important cause. Acute interstitial nephritis caused by blood-borne infections occurs in the elderly, diabetic patients, and patients who take long-term immunosuppressants or NSAIDs.

Idiopathic acute interstitial nephritis is more common in young women, clinical manifestations of fatigue, fever, rash, muscle pain, uveitis, some patients with lymphadenopathy, urine test showed mild to moderate proteinuria, tubular damage Obviously, non-oliguric renal insufficiency. About one-third of patients can have eye symptoms, and eye symptoms can occur several weeks before, during, or after months of kidney disease. 80% is mainly limited to the anterior pigmentation membrane, but there are also reports of posterior pigmentation. Clinically, there are no symptoms, but eye pain, photophobia, tearing, and visual impairment can also occur. Physical examination revealed ciliary congestion or mixed hyperemia, aqueous humor, post-corneal deposits, and iris adhesion. Complications such as post-iris adhesions and changes in intraocular pressure can occur in 20% of patients. Laboratory tests can have anemia, eosinophilia, rapid erythrocyte sedimentation rate, elevated CRP and globulin. This type of hormone treatment has obvious effects.

Other clinical manifestations of acute interstitial nephritis caused by systemic diseases may present clinical manifestations unique to the systemic diseases. For example, patients with systemic lupus erythematosus may have facial erythema, joint pain, photoallergies, hair loss, frequent oral ulcers, etc. Dry syndrome can occur in dry mouth, dry eyes, and multiple dental caries.

Chronic interstitial nephritis

Chronic interstitial nephritis is often occult, chronic or acute onset, due to chronic inflammation of the renal interstitial, mainly fibrotic tissue hyperplasia, tubular atrophy, it often has its common clinical manifestations.

1. Patients often show progressive polyuria or nocturia, accompanied by different degrees of abnormalities such as anorexia, fatigue, weight loss, etc., generally no edema, some cases without any clinical symptoms, only in physical examination or Other diseases found mild urinary changes, renal dysfunction, anemia, renal bone disease and suspected of the disease. Some patients may have a history of medication or physical and chemical factors in contact with the medical history. Some patients with systemic diseases may have primary disease manifestations.

2. Urine routine usually manifests as mild proteinuria (qualitative micro ~ +, quantitative <0.5g / d), urine protein is often a small molecule of renal tubular proteinuria. There may be a small amount of white blood cells in the urine sediment, generally no red blood cells and casts. Laboratory tests may show low specific gravity urine, diabetes, amino aciduria, phosphate urine, alkaline urine and hypophosphatemia, hypercalcemia, hyponatremia, hyperkalemia or hypokalemia, and renal tubular acidosis.

3. If accompanied by renal papillary necrosis, high fever, low back pain, gross hematuria and urinary tract irritation may occur during the course of the disease. Common causes are diabetes, pyelonephritis, analgesic nephropathy, urethral obstruction or vasculitis. Acute renal papillary necrosis can occur in acute renal failure. Necrotic tissue fragments can be found in urine sediment. Ring shadow or filling defects can be seen in pyelography. Calcification shadows in renal medulla and renal papilla are seen in chronic cases, and clinical urinary enrichment function is reduced.

4. Chronic interstitial nephritis can affect the glomerulus and blood vessels, resulting in impaired function, early endogenous creatinine clearance decreased, and serum creatinine can be increased. In the case of severe glomerular and vascular involvement, symptoms of chronic renal insufficiency, such as nausea, vomiting, anorexia, etc., are often severe, and the degree of renal dysfunction is not sufficient. About half of the patients develop high blood pressure, but the degree is often less severe than the high blood pressure caused by glomerulonephritis.

Interstitial nephritis

Urine check

Generally, it is a small amount of low molecular weight proteinuria. The urine protein is more than 0.5~1.5g/24h, and rarely >2g/24h. The urine sediment can have microscopic hematuria, white blood cells and tubular urine, and even eosinophils can be seen. Renal tubular dysfunction varies according to the location and extent of involvement of the tubules, including renal glucosuria, renal tubular acidosis, hypotonic urine, and Fanconi syndrome.

blood test

Some patients may have hypokalemia, hyponatremia, hypophosphatemia and high chloride metabolic acidosis. Blood uric acid is usually normal or slightly elevated. Chronic interstitial nephritis is associated with a high incidence of anemia and is often a positive cell positive anemia. The proportion of peripheral blood eosinophils in patients with acute interstitial nephritis is increased, which may be associated with elevated IgE. Idiopathic interstitial nephritis may have anemia, eosinophilia, rapid erythrocyte sedimentation rate, elevated CRP and globulin.

Film degree exam

Acute interstitial nephritis B-ultrasound can show that the kidney is normal size or volume, and the cortical echo is enhanced. Imaging studies such as B-ultrasound, radionuclide, and CT in chronic interstitial nephritis usually show a reduction in both kidneys and a poor kidney contour. Imaging studies can also help to determine certain specific causes, such as urinary tract obstruction, vesicoureteral reflux, and renal cystic disease. Intravenous urography (IVU) can show signs of renal papillary necrosis characteristic of analgesic nephropathy. Because the contrast agent has tubular toxicity, it should be used with caution when the renal tubule is damaged.

Renal biopsy pathology

Pathological examination is important for the diagnosis. In addition to infection-related 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, thus contributing to the prognosis of the treatment plan.

Acute interstitial nephritis tubulointerstitial lesions are characterized by interstitial diffuse inflammatory cell infiltration with interstitial edema. The infiltrating cells of acute interstitial nephritis caused by drugs often show flaky distribution. The disease is mainly located at the junction of the skin and the pulp. In severe acute interstitial nephritis, the infiltrating cells are diffusely distributed. Infiltrating cells are mainly T cells, monocytes, macrophages; may be associated with plasma cells, eosinophils and neutrophils. In some special cases, granulomatous lesions are seen around the interstitial or damaged tubules. The types of infiltrating cells of acute interstitial nephritis caused by different reasons were different. The acute interstitial nephritis associated with -lactam antibiotics was mainly CD4+ cells; the patients with cimetidine and NSAIDs had more CD8+ cells than CD4+ cells. More than 50% of the patients' macrophages in the kidney tissue are CD14+ cells, and the granuloma is mainly CD4+ cells and macrophages. Drug allergic interstitial nephritis with more eosinophilic infiltration, but also eosinophilic tubulitis. Infection-associated acute interstitial nephritis has more interstitial neutrophil infiltration. At this time, the infiltrating cells of tubulitis are mostly neutrophils.

The basic pathological manifestations of chronic interstitial nephritis are multifocal or large fibrosis of the interstitial tissue under light microscope, which may be accompanied by lymphocyte and mononuclear cell infiltration, tubular atrophy, degeneration, lumen enlargement, and tubular basement membrane. Hypertrophy, glomerular ischemic shrinkage or sclerosis, small intima and arteriolar intima may have different degrees of thickening, stenosis or atresia, but no vasculitis. Immunofluorescence was negative. Electron microscopy is of little value in the diagnosis of chronic interstitial nephritis by electron microscopy. Neonatal, basement membrane-like substances are visible in the regenerated tubulars under electron microscopy, leading to stratification of TBM. Chronic interstitial nephritis caused by immune diseases, dense deposits can be seen under electron microscope, and light chain deposition can be seen in TBM with clustered needle-like dense deposits.

Diagnosis and diagnosis of interstitial nephritis

diagnosis

History of infection or drug use, clinical presentation, some laboratory and imaging studies are helpful for diagnosis, but renal pathology remains the gold standard for the diagnosis of interstitial nephritis. Acute interstitial nephritis may be considered when clinically unexplained acute renal insufficiency occurs. Chronic interstitial nephritis should be considered for those with the following clinical features:

1 There are causes of chronic interstitial nephritis, such as long-term use of analgesics, chronic urinary tract obstruction, etc., or a family history of chronic interstitial nephritis;

2 clinical manifestations of tubule dysfunction, such as polydipsia, polyuria, nocturia, renal tubular acidosis, or renal insufficiency but no hypertension, no hyperuricemia;

3 urine examination showed severe damage to the tubule function. A small amount of small proteinuria (<2.0 g/24 h), urinary RBP, lysozyme, urinary 2-microglobulin, and NAG are elevated, and may have diabetes and amino aciduria. Chronic interstitial nephritis must further clarify the cause based on medical history and clinicopathological features.

Differential diagnosis

Acute interstitial nephritis is mainly distinguished from acute glomerulonephritis, acute glomerulonephritis, and other causes of acute renal failure. Special clinical manifestations, laboratory tests, and imaging studies of the corresponding disease may help to provide diagnostic clues, but renal biopsy should be considered promptly when identification is difficult.

Chronic interstitial nephritis should be considered in the identification of the disease, kidney puncture can be identified when it is difficult to identify.

1 Hypertensive renal damage: clinical manifestations similar to chronic interstitial nephritis, but a history of long-term hypertension, accompanied by target organs such as the heart and fundus to help identify;

2 chronic glomerulonephritis: often significant proteinuria, hematuria, edema and hypertension, glomerular dysfunction precedes the renal tubules.

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