tubulointerstitial nephritis
Introduction
Introduction Tubulointerstitial nephritis can be divided into chronic tubulointerstitial nephritis and acute tubulointerstitial nephritis, infectious acute tubulointerstitial nephritis.
Cause
Cause
Cause:
1. Acute tubulointerstitial nephritis: is an allergic toxicity to medical treatment. Only a small number of drugs (in more than 80 related drugs) are associated with most cases. The identification of drug-related causes is important because severe kidney damage can often be prevented or reversed. Sarcoidosis, legionellosis, leptospirosis, streptococcus, viral infections and certain Chinese herbal medicines may also be associated.
2. Infectious acute tubulointerstitial nephritis: Infectious ATIN is mainly found in acute pyelonephritis, and can also be caused by blood-borne infection. The most common causes are bacterial, fungal, viral and protozoal infections. Infectious acute tubulointerstitial nephritis caused by recent HIV infection due to drug use and drug abuse in the male reproductive organs has also gradually increased. The main causes of infectious ATIN are:
1. Bacteria: Escherichia coli, E. coli, Proteus, Mycobacterium, Staphylococcus, Klebsiella, Aerobacter, Alcaligenes, Pseudomonas aeruginosa, Streptococcus faecalis.
2. Spiral: Leptospira.
3. Fungi: Tissue cytoplasmic bacteria.
4. Rickettsia.
5. Virus: cytomegalovirus, Hantan virus, adenovirus, enterovirus.
Examine
an examination
1. Examination of interstitial nephritis The patient undergoes routine urine examination 3 times after admission, and then 2 to 3 times per week. Pay attention to weekly check of urine protein quantitation, disk electrophoresis urine, 2-microglobulin, lysozyme, TH-protein, retinol binding protein, morning urine osmotic pressure, urine pH, 24h urinary potassium, sodium, chlorine, calcium, magnesium, phosphorus, uric acid, blood test, blood sugar, uric acid, potassium, sodium, chlorine, calcium, magnesium , phosphorus, creatinine, urea nitrogen, carbon dioxide binding, erythrocyte sedimentation rate, anti-"O", anti-nuclear antibodies, ds-DNA, SM antibodies, blood or urine eosinophils and endogenous creatinine clearance.
2, other examination of interstitial nephritis routine double-B-ultrasound examination, as appropriate for CT examination, intravenous pyelography or retrograde urography, if necessary, renal nucleus scanning, bone marrow puncture and renal biopsy.
3, typical cases of interstitial nephritis often: recent medication history, systemic allergy, urine test abnormalities, renal tubular and renal dysfunction.
The general diagnosis is that if there is the first two of the above performances, plus any of the latter two, clinical acute interstitial nephritis can be diagnosed. However, there is often no second item in atypical cases, which must be confirmed by renal biopsy. Kidney biopsy is the only way to confirm the diagnosis. Indications include a diagnosis that is not certain or a progression of renal failure.
Diagnosis
Differential diagnosis
Differential diagnosis of tubulointerstitial nephritis:
1. Acute tubulointerstitial nephritis: varies in performance, but is typically associated with acute renal failure associated with medication or infection with or without oliguria. In most cases, fever can occur with a urticaria rash. White blood cells, red blood cells and white blood cell casts often appear in urine sediment, but sometimes there is no abnormality. >75% of cases can present eosinophils in both blood and urine (using Hansel staining). Proteinuria is usually small. Non-steroidal anti-inflammatory drugs are typically devoid of fever, rash and eosinophilia. However, it is often seen that the nephropathy range of proteinuria with glomerular microscopic lesions (also seen in ampicillin, rifampicin, interferon or ranitidine).
Many patients have signs of tubular dysfunction, such as polyuria (concentration defects), reduced volume (Na preservation defects), hyperkalemia (K-excretion defects), and metabolic acidosis (acid excretion defects). Because interstitial edema is usually larger and excessively absorbed by radioactive gallium or radionuclide-labeled white blood cells. However, a negative scan of the 67 gallium radionuclide does not rule out the diagnosis.
2. Infectious acute tubulointerstitial nephritis: clinically mainly systolic symptoms such as chills, hyperthermia, elevated white blood cells, left nucleus, and renal tubular proteinuria, microscopic hematuria, leukocyteuria, tubular urine, urine The expression of renal damage such as specific gravity and urinary osmotic pressure is significantly reduced, and severe renal failure syndrome can occur in severe cases. The renal damage of glomerulonephritis after acute infection occurs in 2 to 3 weeks after the infection of the pathogenic microorganism. The onset time of infectious ATIN is earlier, usually in the first few days of infection, occasionally after 10-12 days of infection. symptom. The clinical manifestations of infective ATIN caused by acute pyelonephritis are the most characteristic. Patients can have fever, chills, pain and tenderness in the kidney area, dysuria, white blood cell urine, pyuria and bacteriuria, urinary tube type, urine culture. Often positive.
3, acute bacterial pyelonephritis: generally does not cause a decline in renal function, unless accompanied or complicated by diabetes or urinary tract obstruction. When acute pyelonephritis causes ATIN, the common clinical manifestations are mild tubular dysfunction, which may have impaired urine concentration and acidification, generally reversible, and the condition can be restored after infection control. Acute renal decline can be seen in infective ATIN caused by hemorrhagic fever with renal syndrome, leptospirosis, brucellosis, and candidiasis. In the backward areas, acute bacterial pyelonephritis caused by ATIN may not cause timely renal hemorrhagic necrosis due to treatment, leading to renal failure, but less common.
1. Interstitial nephritis examination: After the patient is admitted to the hospital, the urine routine examination is performed 3 times, and then 2 to 3 times per week. Pay attention to the weekly urine protein quantitation, disc electrophoresis urine, 2-microglobulin, lysozyme. , TH-protein, retinol binding protein, morning urine osmotic pressure, urine pH, 24h urinary potassium, sodium, chlorine, calcium, magnesium, phosphorus, uric acid, blood tests for blood sugar, uric acid, potassium, sodium, chlorine, calcium, Magnesium, phosphorus, creatinine, urea nitrogen, carbon dioxide binding, erythrocyte sedimentation rate, anti-"O", anti-nuclear antibody, ds-DNA, SM antibody, blood or urine eosinophils and endogenous creatinine clearance.
2. Other examination of interstitial nephritis: routine double-B-ultrasound examination, CT examination, intravenous pyelography or retrograde urography, as appropriate, renal nuclear scan, bone marrow biopsy and renal biopsy.
3, typical cases of interstitial nephritis often: recent medication history, systemic allergy, urine test abnormalities, renal tubular and renal dysfunction.
The general diagnosis is that if there is the first two of the above performances, plus any of the latter two, clinical acute interstitial nephritis can be diagnosed. However, there is often no second item in atypical cases, which must be confirmed by renal biopsy. Kidney biopsy is the only way to confirm the diagnosis. Indications include a diagnosis that is not certain or a progression of renal failure.
