Infectious acute tubulointerstitial nephritis

Introduction to infectious acute tubulointerstitial nephritis Infectious acute tubulointerstitial nephritis (acute infectious tubulo-interstitial nephritis) is an acute tubulointerstitial nephritis caused by direct infection of renal interstitial. Acute interstitial nephritis (acuteinterstitial nephritis) is caused by a variety of different causes, sudden occurrence of renal interstitial edema and inflammatory cell infiltration as the main pathological changes within a few days, with acute tubulointerstitial damage as the main manifestation Pathological syndrome. basic knowledge The proportion of illness: 0.0030% Susceptible people: no specific population Mode of infection: non-infectious complication:

Causes of infectious acute tubulointerstitial nephritis

(1) Causes of the disease

Infectious ATIN is mainly found in acute pyelonephritis and can also be caused by blood-borne infections. The most common causes are bacterial, fungal, viral and protozoal infections, recent infections caused by drug use and drug abuse in male reproductive organs. Sexual tubulointerstitial nephritis is also gradually increasing, the main causes of infectious ATIN are:

1. Bacillus Escherichia coli, Escherichia coli, Proteus, Mycobacterium, Staphylococcus, Klebsiella, Aerobacteria, Alcaligenes, Pseudomonas aeruginosa, Streptococcus faecalis.

2. Spirochete.

3. Fungal tissue cytoplasmic bacteria.

4. Rickettsia.

5. Viral cytomegalovirus, Hantaan virus, adenovirus, enterovirus.

(two) pathogenesis

Acute interstitial nephritis caused by systemic infection may not be caused by direct invasion of the renal interstitial bacteria, but by immunological damage of the kidney or stroma by bacteria or its toxins. Another possibility is that the infectious agents directly invade the kidneys. Qualitative, interstitial edema and neutrophil inflammatory infiltration, mainly in the renal medulla, and cortical inflammation is a characteristic of reactive tubulointerstitial nephritis, infective ATIN caused by acute pyelonephritis, and its interstitial damage Focal, inflammatory lesions are radially distributed, which is significantly different from the pathological changes of reactive tubulointerstitial nephritis caused by systemic streptococcal infection. In the latter, the infiltration is surrounded by blood vessels, mainly concentrated in the cortex and cortex. Junction area, acute pyelonephritis is an acute suppurative inflammation caused by bacteria directly invading the renal interstitial, also known as acute suppurative interstitial nephritis. The common pathogen is Escherichia coli, followed by Escherichia coli, Proteus and Pseudomonas aeruginosa, the factors that cause infection are urinary tract obstruction or other urinary tract abnormalities, pregnancy, advanced age, low immunity, urinary tract dysfunction.

Infectious acute tubulointerstitial nephritis prevention

Prevention: It is mainly for the active symptomatic treatment of infections and systemic diseases caused by various causes to prevent the occurrence of interstitial nephritis. More attention should be paid to the imbalance of liquid and electrolytes for this disease. Appropriately strengthen nutritional support therapy to prevent fatal complications such as acute renal failure, and take various measures to avoid factors that aggravate infection and promote gastrointestinal bleeding.

Complications of infectious acute tubulointerstitial nephritis Complication

Severe cases can be complicated by renal parenchymal hemorrhagic necrotic acute renal failure syndrome.

Infectious acute tubulointerstitial neuritis symptoms Common symptoms Hyperthermia chills Leukocytosis Leukocyte urinary chills Urine pain Kidney area tenderness Tube type protein Urine pyuria Urinary shiver

The main clinical manifestations are chills, high fever, increased white blood cells, left ventricular shift and other systemic infectious symptoms, as well as renal tubular damage, microscopic hematuria, white blood cell urine, tubular urine, urine specific gravity and urine osmotic pressure. In severe cases, acute renal failure syndrome may occur. 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, generally in the infection. In the first few days, symptoms occasionally appear 10 to 12 days after infection.

The clinical manifestations of infective ATIN caused by acute pyelonephritis are 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.

Acute bacterial pyelonephritis generally does not cause renal function decline, unless accompanied or complicated by diabetes or urinary tract obstruction, when acute pyelonephritis causes ATIN, the common clinical manifestations are mild tubular dysfunction, may have urine concentration and acidification function Loss, generally reversible, the condition can be restored after infection control, acute renal decline can be seen in hemorrhagic fever kidney syndrome, leptospirosis, brucellosis and candidiasis caused by infectious ATIN, in backward areas ATIN caused by acute bacterial pyelonephritis may cause renal failure due to extensive renal hemorrhagic necrosis due to treatment, but it is rare.

The proteinuria of infectious ATIN is mostly ~, 24h urine protein is generally less than 2g, proteinuria in the range of nephropathy is not common.

Infectious acute tubulointerstitial nephritis

The diagnosis method is the same as that of urinary tract infection. The key is the identification of upper and lower urinary tract infections.

1. Urine examination in the acute pyelonephritis urine antibody test positive, visible leukocyte urine and / or pyuria, urine culture positive; other infectious ATIN urine can be seen white blood cells, red blood cell cast, and renal tubular proteinuria, Microscopic hematuria, urine specific gravity and urine osmotic pressure decreased significantly, urine culture was usually negative, urine NAG enzyme increased, and urine 2-m increased.

2. Blood tests for increased white blood cells, left ventricular shift and other systemic infectious symptoms, Tamm-Horsfall antibody positive, elevated IgG, acute renal dysfunction may have azotemia and elevated serum creatinine, the most common serum Electrolyte disorders are hyperkalemia, hyperchloremia and low bicarbonate. High potassium and high chloride metabolic acidosis often occurs before GFR is severely reduced (less than 20 ml/min) and can occur when concentration is reduced. High sodium, if the proximal tubules are not fully functional, there may be normal metabolic acidosis of hypokalemia, hypophosphatemia and hypouricemia.

3. Renal biopsy is of great significance for the diagnosis and treatment of acute interstitial nephritis. Pathologically, the renal interstitial can be seen with focal or diffuse inflammation, monocytes, plasma cells or polymorphonuclear cells infiltrating, renal tubular epithelium. Cell degeneration, and deposition of immune substances is sometimes seen in the renal interstitium.

4. Special examination B ultrasound, KUB, IVP examination of the kidney without morphological changes.

Diagnosis and diagnosis of infectious acute tubulointerstitial nephritis

Diagnostic criteria

Diagnosis is based on the above clinical manifestations to determine urinary tract infections or systemic infections, such as chills, high fever, increased white blood cells, nuclear left shift and other systemic infectious symptoms, as well as renal tubular proteinuria, microscopic hematuria, white blood cell urine, Tube-type urine, urine specific gravity and urine osmotic pressure decreased significantly, such as renal damage, severe acute renal failure syndrome, laboratory tests support upper urinary tract infection, B-ultrasound, KUB, ICP examination of kidney no morphological changes, Renal interstitial renal interstitial can be seen in focal or diffuse inflammation, mononuclear cells, plasma cells or polymorphonuclear cell infiltration, renal tubular epithelial cell degeneration, and sometimes visible immune deposition, etc., can consider the diagnosis of this disease.

Differential diagnosis

Infectious acute interstitial nephritis in acute renal failure should be associated with renal vasculitis, acute tubular necrosis, rapid glomerulonephritis, atherosclerotic embolism nephropathy and acute streptococcal infection after nephritis.

Renal failure can occur in these diseases, but should have the clinical features of the primary disease, acute tubular necrosis, oliguria or auria for a long time, urinary filtration sodium score >1, urine sodium concentration>40, renal failure index>2 Urinary osmotic pressure <250mOsm/L, acute glomerulonephritis usually occurs 1 to 3 weeks after infection, hematuria and hypertension are seen in more than 90% of cases, nephritis edema, transient hypocomplementemia, rapidity Nephritis usually occurs in subacute onset, and the lesions are progressively aggravated. When there is difficulty in identification, renal biopsy can clarify the diagnosis. More than half of the acute glomerulonephritis has a crescent formation. In recent years, some scholars have reported 167Ga scanning examination, acute interstitial Osteoinflammation has a high density of shadows, while acute tubular necrosis can not be taken, which is helpful for differential diagnosis.

In addition, it should be differentiated from renal tuberculosis. There may be pulmonary or extrapulmonary tuberculosis in the kidney; tubercle bacilli can be found in the urine; tuberculosis can be found in the urine culture; IPP has special tuberculosis imaging changes.

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