Antibacterial toxic nephropathy

Introduction to antibacterial toxic nephropathy Nephropathyduetopoisoning ofantibiotic refers to kidney disease caused by the application of antibiotics that are nephrotoxic or susceptible to kidney damage. Kidney damage caused by antibiotics is a group of more common drug-induced diseases. Many antibiotics in clinical practice. Its metabolites are excreted by the kidneys, some of which have obvious nephrotoxicity or allergic reactions. The damage of antibiotics to the kidneys is mainly caused by acute allergic interstitial nephritis and acute tubular necrosis. In severe cases, acute kidneys can be caused. Functional failure. basic knowledge The proportion of the disease: the incidence rate is about 0.001%, mostly caused by taking antifungal drugs Susceptible people: no specific population Mode of infection: non-infectious Complications: ataxia

Antimicrobial toxic nephropathy

(1) Causes of the disease

1. The occurrence of toxic nephropathy may be related to the following factors

(1) Antibiotics for kidney toxicity: such as amphotericin B, neomycin, cephalosporin II, etc. have direct nephrotoxic effects, while penicillin G, cephalosporin (IV, VI), etc. may cause kidney due to allergies. damage.

(2) Age and renal function status: In elderly patients and original kidney patients, the incidence of nephrotoxicity is significantly higher and more serious.

(3) Changes in effective blood volume and renal blood flow: When the blood volume decreases and the renal blood flow decreases, the renal toxicity of the antibiotic is more likely to occur.

(4) The degree of infectious diseases and electrolyte imbalance: When the patient's infection is severe or even toxic shock or electrolyte imbalance, the antibiotic nephrotoxicity increases.

(5) Liver function status of the patient: Some antibiotics can be detoxified by the liver and then excreted by the kidney. When the liver function declines, the burden on the kidney is aggravated, and nephrotoxicity occurs.

There are many antibiotics that are most common in clinically causing acute allergic interstitial nephritis, among which -lactam antibiotics are the most obvious.

In China, penicillin and sulfa drugs were commonly used in clinical practice in the 1950s and 1960s, and they were also the main drugs causing acute allergic interstitial nephritis. Most of the reports in the 1960s and 1970s were due to the partial synthesis of penicillin. Especially after the wide application of new penicillins, the incidence rate has increased significantly, becoming the main drug causing acute allergic interstitial nephritis; since the 1980s and 1990s, the types of drugs causing this disease are more diverse and mixed. The results of medication, especially the widespread use of cephalosporins, have led to an increasing incidence of acute interstitial nephritis. In some cases, clinical cases are sometimes combined with drug allergy and drug nephrotoxicity, causing acute interstitial nephritis. And acute tubular necrosis, resulting in acute renal failure, according to the European Dialysis Association, 398 cases of acute renal failure caused by a variety of drugs in acute interstitial nephritis 176 cases, accounting for 44.2%, in drug-induced ATN, The number of people caused by antibiotics was the highest, reaching 43.7%.

2. Antibiotics that often cause ATN include the following categories

(1) Aminoglycoside antibiotics: These antibiotics have high nephrotoxicity and are most likely to cause ATN, including kanamycin, gentamicin, amikacin, tobramycin, neomycin and streptomycin.

(2) -lactam antibiotics: penicillins have no obvious nephrotoxicity and do not cause ATN. The first generation of cephalosporins has different degrees of nephrotoxicity, especially cefotaxime, followed by cefotaxime and cefazolin. .

(3) Sulfonamides: such as sulfathiazole and sulfadiazine can cause: 1 crystal nephropathy, especially in oliguria or urine pH <5.5, its crystal blockage of renal tubules can cause ATN, 2 hemoglobinuria: can make G6PD Intravascular hemolysis occurs in children with defects, resulting in hemoglobinuria.

(4) Other antibiotics: such as amphotericin B, polymyxin, vancomycin, etc. also have obvious nephrotoxicity, can cause ATN.

(two) pathogenesis

1. The pathogenesis of acute drug-induced interstitial nephritis is the immune mechanism. The drug acts as an antigen to activate the immune response and affects the kidney. It is not a drug that directly causes toxic damage to the kidney. The immune mechanism includes humoral immunity and cellular immunity.

(1) Cellular immune mechanism: In recent years, experimental results have shown that cellular immunity plays a major role in the pathogenesis of acute allergic interstitial nephritis. In most cases, including anti-tubular basement membrane disease, mononuclear cells are present in the renal interstitial. Infiltration is the main function of the immune-mediated mechanism. It is confirmed by monoclonal antibody technology that infiltrating monocytes are mainly lymphocytes, and cell-mediated damage leads to delayed type hypersensitivity and T cell-mediated toxicity. effect.

(2) humoral immune mechanism: anti-tubular basement membrane (TBM) antibody can be found in 70% of glomerular basement membrane (GBM) disease, such patients with tubulointerstitial inflammatory lesions Compared with patients with anti-GBM alone, some patients with acute allergic interstitial nephritis may have anti-TBM antibodies in the blood circulation or on TBM, such as acute allergic interstitial nephritis caused by new penicillin I. Anti-TBM antibodies were detected in the blood circulation. IgG was deposited linearly on TBM. The drug hapten was bound to TBM (carrier) when it was excreted from the proximal tubule, which resulted in the appearance of immune-induced antibodies, resulting in tubule damage and secondary. Interstitial inflammation, but most of the acute allergic interstitial nephritis caused by new penicillin I and other drugs, does not appear in this antibody.

The drug acts as an antigen and enters the body to produce antibodies. Antigen antibodies form immune complexes that deposit in the kidneys, causing kidney damage.

In some patients with acute allergic interstitial nephritis, elevated serum IgE levels, basophilic, eosinophils and plasma cells containing IgE in renal interstitial infiltrating cells suggest IgE-mediated rapid hypersensitivity The reaction is involved in the disease.

Certain quinolones have immunomodulatory effects, prevent the production of immunoglobulins, and increase the production of growth factor type I interleukins, which are considered to be potential causes of clinical toxicity.

2. The pathogenesis of antibiotic acute tubular necrosis

Acute tubular necrosis is most easily caused by aminoglycoside antibiotics. Aminoglycosides are not absorbed orally. The renal cortex concentration is higher than plasma concentration after injection. These drugs have strong antibacterial effect and low price, so they are widely used in clinical applications. 98% to 99% of the drug is filtered from the glomerulus and is excreted from the urine in the original form, so it has nephrotoxicity and can damage the auditory nerve.

Aminoglycosides are divided into three groups: kanamycin, gentamicin and neomycin. Its antibacterial principle is to block the synthesis of bacterial proteins, aminoglycans and 30 subunits of bacterial ribosome. The combination leads to the inefficient synthesis of the protein, and thus the growth of the bacteria is stopped. Some people think that it also affects the permeability of the membrane, making the drug easier to enter the cytoplasm and enhancing the effect, causing a vicious circle, membrane permeability destruction, and essential components of the bacteria. Out of the family and died, these three families, due to serious toxicity of the neomycin group, are no longer systemic application; kanamycin has been used less in pediatrics, normal pediatric medication 1.0 ~ 1.5g / d, 5 ~ 7 days It can cause kidney damage; gentamicin is still a commonly used drug. It is reported that 6% to 18% of acute renal failure is caused by gentamicin and should be paid attention to. The following is an example of gentamicin as an example. Antibiotic-induced ATN risk factors, pathology, mechanism of action, early diagnosis, clinical manifestations.

(1) High-risk factors: In patients with normal renal function, ATN is rarely used in conventional doses and administration methods, but when patients have significant dehydration, hypotension, renal impairment or the elderly, aminoglycoside antibiotics cause The opportunities for ATN will increase significantly, so these high-risk factors should be considered:

1 elderly patient;

2 diabetes;

3 dehydration, low blood pressure;

4 sodium, calcium deficiency; acidosis;

5 recently used aminoglycoside antibiotics;

6 combined with cephalosporin, diuretic, especially loop diuretics;

7 combined with anesthesia, amphotericin, non-steroidal anti-inflammatory drugs;

The blood concentration of 8 aminoglycosides is constant compared with the peak, the difference is toxic, the aminoglycoside antibiotics have a good effect of one dose per day, the toxicity is small, the cost is saved, but it is also considered that the elderly may produce a peak concentration per day. Increased the risk of nephrotoxicity. In addition, it is closely related to the degree of virulence of the drug. The virulence of aminoglycosides is related to the number of free amino groups contained in the molecule. It has been observed that the number of free amino groups in the chemical structure of aminoglycosides is increased. The greater the damage to the kidney, the only two free amino groups of streptomycin, the least nephrotoxic effect; kanamycin, amikacin, gentamicin have four free amino groups, which is more toxic; The neomycin of 6 free amino groups has the greatest nephrotoxic effect.

(2) Pathogenesis: At present, the pathogenesis of aminoglycoside nephropathy is still unknown. The lysosomal enzyme theory is accepted by most people. The concentration of aminoglycoside in lysosomes of renal tubular epithelial cells is much higher than that in other organelles or plasma. The concentration is even as high as 10 to 200 times the concentration of extracellular fluid. Gentamicin causes direct nephrotoxicity to renal tubular necrosis, which is mainly related to the following factors:

1 Gentamicin is mostly free in the body, and it is filtered from the glomerulus without metabolism. It is reabsorbed in the renal tubules by 10% to 30%, and then secreted and excreted by the renal tubules.

2 In the kidney mainly in the renal cortex, the concentration in the cortex is 10 to 20 times the blood concentration, so it is easy to cause renal disease.

3 Gentamicin with strong cation has a strong affinity with the acidic phospholipid with anion on the brush border of the proximal tubular epithelial cells, and enters into the cell through the pinocytosis to bind to the primary lysosome, making it a secondary Lysosomal.

4 gentamicin can inhibit the action of lysosomes, resulting in the accumulation of phospholipids, forming myeloid bodies, leading to secondary lysosomal storage diseases.

5 Gentamicin can destroy lysosomes, release lysosomal enzymes, and inhibit mitochondrial function and damage mitochondria, causing autolysis, necrosis, and even cell death.

6 Gentamicin can produce oxygen free radicals such as O2-, H2O2 and OH- which are toxic to cells, and cause abnormalities in cell RNA synthesis, transport and transcription, resulting in cell death.

Antibacterial toxic nephropathy prevention

1. Strictly control the indications for medication, drug dosage and course of treatment: generally according to the usual dose, such as gentamicin dose of 8 to 160,000 U / d, the course of treatment is 5 to 6 days is appropriate, generally can not exceed 10 days, And to avoid repeated medication.

2. Avoid using this kind of medicine in the case of insufficient blood volume. If you want to use it, it is best to correct the water and electrolyte imbalance before taking the medicine to avoid the increase of nephrotoxicity.

3. For the elderly, diabetics and patients with chronic kidney disease, especially those with chronic renal insufficiency, try to avoid and use this drug as much as possible, although it is common for the elderly to use aminoglycoside antibiotics to develop nephrotoxicity, but such as treatment Less than 1 week can effectively reduce nephrotoxicity.

4. The problem of combined use should be prohibited from being combined with other nephrotoxic drugs, such as first- or second-generation cephalosporins and other nephrotoxic drugs such as non-steroidal anti-inflammatory drugs.

5. During the medication, we should pay close attention to the strict monitoring of urine routine, urine enzymes, and renal function, so as to detect the nephrotoxicity in the early stage and stop the drug in time.

6. Avoid use when acidosis.

7. According to the patient's creatinine clearance rate adjustment dose and administration interval, a small dose is given, the course of treatment is not more than 1 week, when the creatinine clearance rate is <50ml/min, the blood concentration of the drug should be closely monitored. The valley value is the initial stage. The most toxic indicator, for patients with renal failure, should be treated according to acute renal failure.

8. According to the renal function adjustment dose and interval time.

Antibiotic toxic nephropathy complications Complications, ataxia

Can be complicated by hearing loss, tinnitus, ataxia, etc., some patients can progress to permanent renal failure.

Antimicrobial toxic nephropathy symptoms Common symptoms Weak urine routine abnormal appetite loss tinnitus hearing loss kidney damage pus vaginal dizziness leukocyte urinary ataxia

1. The clinical manifestations of acute drug-induced interstitial nephritis are diversified, but not specific; can occur at any age, urine volume and blood pressure are normal, no or a small amount of proteinuria, if not highly alert, easy to miss diagnosis, patients often have whole body Sexual allergic reaction, regardless of drug dose.

(1) Fever: Most of the acute allergic interstitial nephritis has fever in the early stage. It usually appears 3 to 5 days after administration. It is reported that 87% to 100% of patients have fever. Recently, it has been reported that fever is generally 50% to 64.3%. Occurred in the patient, usually the second individual temperature peak appeared after the application of antibiotics and infection was controlled.

(2) Drug eruption: 25% to 50% of patients with drug eruption after medication, pleomorphic, red pruritus or polymorphous erythema or peeling rash.

(3) joint pain: highly allergic people may also have allergic arthritis, joint pain, low back pain, lymphadenopathy or liver function damage (ALT, AST increased), etc., patients may also be due to renal interstitial edema, kidney enlargement The kidney capsule is pulled to make it feel bilateral or unilateral low back pain.

(4) hematuria: hematuria is often the first clinical manifestation of this disease, accounting for 95%, gross hematuria accounted for 1/3, and often appear proteinuria or even nephrotic syndrome, acute renal failure, hematuria is common in oxacillin allergy, in recent years Quinolones have an increasing tendency to cause hematuria.

(5) oliguria, edema, serous effusion: 40% to 50% of patients with oliguria, edema, serous effusion, may be related to renal failure and hypoproteinemia, some patients may not have the above body Allergic reactions, typical triads are fever, rash, joint pain is generally less than 1/3, indicating that there is variability in the diagnostic characteristics, due to drug-induced interstitial nephritis often manifested as sudden deterioration of renal function, rapid oliguria Acute renal failure (ARF), in addition to glomerular dysfunction (serum creatinine and urea nitrogen increased rapidly), renal tubular dysfunction is often very obvious, resulting in renal glucosuria and low osmotic pressure and other abnormalities, so Unexplained acute renal failure should be suspected of acute drug-induced interstitial nephritis, and should be diagnosed with early renal biopsy to prevent missed diagnosis.

2. Acute tubular necrosis caused by aminoglycoside antibiotics, no obvious symptoms in the early stage, especially those with non-oliguric type, often ignored by doctors, patients often have fatigue, dizziness, general malaise, loss of appetite, nausea and vomiting. Hearing loss, tinnitus, ataxia, etc., animal experiments show that the urinary enzyme increased on the 4th day of gentamicin injection (including lysozyme, -glutamyltranspeptidase, N-acetyl-) -Glucosidase, etc.), the increase in urinary enzymes is the response after administration, not the indication for withdrawal. On the 5th to 6th day, abnormal urine, hematuria, leukocyteuria, proteinuria, diabetes, and a large number of necrotic kidneys may occur. Epithelial cells and cell casts, suggesting that the renal tubular damage is serious, blood urea nitrogen and creatinine are significantly increased after the seventh day, the nephrotoxicity of gentamicin is related to the dose, time, when clinical appearance of proteinuria, hematuria, Pyuria, tubular urine, oliguria or non-oliguric acute renal failure, blood urea nitrogen, creatinine increased significantly, is not only an indication of clinical withdrawal, non-oliguric refers to no oliguria or anuria Acute tubular necrosis, The average daily urine volume exceeds 1000ml. In most patients, the renal function begins to improve within a few days after stopping the drug. However, some patients still continue to rise in serum creatin 10 days after stopping the drug, and the average can return to normal or near normal after 42 days after the onset. Some patients progress to permanent renal failure, although the clinical manifestations of non-oliguric patients are less urinary, the incidence of complications is low, and the mortality rate is low, but still 26%, should be given attention to the elderly Infirm, the non-oliguric type of the original kidney disease should be dialyzed as soon as possible, which can improve the survival rate and reduce the mortality rate.

Examination of antibacterial toxic nephropathy

Blood routine

Eosinophils in the blood increased significantly, reaching 80%, but lasted only 1 to 2 days; red blood cells and hemoglobin, platelets are often normal, sometimes mild anemia, which may be caused by interstitial tubule damage affecting erythropoiesis and Renal failure toxic substance retention; elevated blood IgE and positive TBM antibodies.

2. Urine routine

2/3 patients had microscopic hematuria; leukocyte urine, aseptic pyuria, and urine sediment examination. About 30% of white blood cells were eosinophils in the early stage of Reiter staining. Some people had statistics of urinary eosinophils in acute interstitial nephritis. The detection rate is more than 66%, and urine eosinophils account for 20% of the white blood cells in the urine. It can be used as a standard for diagnosing this disease. It can have white blood cell cast or red blood cell cast, and urine osmotic pressure is often higher than blood osmotic pressure and urine. Sodium is reduced, proteinuria is mostly mild, moderate, and a large amount of proteinuria can be seen in ampicillin. Norfloxacin is allergic to nephrotic syndrome, and other antibiotics are rare.

3. Renal tubular function index

It can detect blood, urine 2M, 1M, TH protein (Tamm-Horsfall protein, THP), blood, urine osmotic pressure and urinary retinol binding protein (RBP), which is a new indicator for the diagnosis of proximal renal tubular function at home and abroad. The renal tubular function damage of this disease is generally prominent, the urinary sodium excretion score is >2; can be expressed in Fanconis syndrome, that is, proximal tubular dysfunction, diabetes, amino aciduria, phosphate urine and high chloride metabolic acid Poisoning; can also be distal renal tubular dysfunction, uric acid dysfunction, isotonic urine, loss of sodium nephropathy and potassium disorders, these are often important clues for the diagnosis of drug-induced interstitial nephritis.

4. Glomerular function index

It is generally believed that drug-induced interstitial nephritis rarely affects glomeruli. In recent years, this disease can be associated with glomerular lesions, such as membranous nephropathy, crescentic nephritis, clinical manifestations of nephrotic syndrome, so blood BUN can be detected. , Scr and blood, urine IgG, Alb and GFR.

5. Decreased glomerular filtration rate

Common reasons are generally considered to be:

(1) Renal interstitial edema, increased pressure causes a decrease in glomerular filtration rate.

(2) The glomerular filtrate leaks into the interstitial through the damaged renal tubule, and further reduces the glomerular filtration rate.

(3) Renal tubular damage reduces sodium and water reabsorption, and the glomerular filtration rate is also reduced by the feedback of the bulb.

(4) The renal interstitial infiltrating cells locally produce vasoconstrictor-induced renal ischemia, causing a decrease in glomerular filtration rate.

1. Imaging examination

B-ultrasound, CT and other examinations can be found that the size of the kidneys is normal or increased.

2. Renal biopsy histopathological examination

Renal damage caused by antibiotics is often caused by acute interstitial, renal tubular inflammation, normal glomerular or only mild mesangial cells. Renal biopsy is a means of confirming the disease. Different drugs can cause similar kidneys. Histopathological changes, the lesions were bilateral diffuse distribution.

(1) Light microscopy and immunofluorescence have the following characteristics:

1 renal interstitial edema.

2 diffuse lymphocytes and monocytes infiltration and varying amounts of eosinophils 3 renal tubular epithelial cells were degenerative degeneration, severe cases of focal necrosis, lumen expansion.

4 glomerular and renal blood vessels are normal.

5 Immunofluorescence was mostly negative, but benzocilillin was sometimes found to have IgG along the basement membrane of the renal tubule, C3 deposition (line-like), and TBM antibody in the blood circulation.

Some of the acute interstitial nephritis with glomerular damage, the pathological changes of small lesions, can also occur small ball sclerosis.

(2) Under electron microscope, the basement membrane of the small tube is discontinuous, and partial thickening and stratification of the basement membrane are visible, and the glomerulus is normal or the lesion is light.

The commonly used gentamicin-caused lesions are mainly in the proximal tubules. The pathological changes are necrosis of the tubule brush margin microvilli, secondary lysosomes and "myeloid bodies", renal tubules Epithelial cell degeneration, necrosis, general basement membrane integrity, non-broken lesions, cell debris visible in the lumen of the renal tubule, focal inflammatory cells (lymphocytes, mononuclear macrophages, etc.) infiltrated in the interstitial, proximal kidney Tubulous lesions are severe and extensive, and may involve distal tubules, necrotic or degenerative epithelial cells shedding, tubular formation may block renal tubules, severe lesions may also involve glomeruli, and endothelial pores may become smaller under electron microscope. Epithelial cells Foot process fusion, deformation.

Diagnostic and differential diagnosis of toxic nephropathy

Diagnostic criteria

1. The clinical diagnosis of acute allergic interstitial nephritis has no uniform standards. If there are gross hematuria and acute allergic reactions such as fever, rash and joint pain, and acute renal failure with unexplained causes, acute allergies should be considered. The possibility of sexual interstitial nephritis.

In 1980, Laberke et al proposed that acute allergic interstitial nephritis syndrome should have systemic manifestations of fever, rash, eosinophilia, hematuria, decreased renal function, anemia, etc.; based on comprehensive analysis of relevant literature, drug allergic interstitial The clinical diagnosis of nephritis is usually:

1 has a history of use of allergic drugs;

2 systemic allergic reaction, often drug eruption, drug fever and peripheral blood eosinophilia;

3 abnormal urine test: aseptic leukocyte urine (including eosinophilic urine) may be associated with leukocyte cast, microscopic hematuria or gross hematuria, mild to severe proteinuria (often mild proteinuria); 4 in the short term Progressive renal dysfunction; partial and/or distal renal tubular functional damage and glomerular dysfunction, renal glucosuria and low osmotic pressure;

5 related antibodies, such as anti-diphenylmethoxypenicillin hapten antibodies, are detected in the blood circulation of the patient;

6 re-exposure to this class of drugs again;

7 along the TBM visible complement C3 sedimentation;

8B shows that the size of the kidneys is normal or increased. Anyone with the above 12 and 3 and/or 4 or 5 may not be diagnosed with a clinical diagnosis of renal biopsy.

However, clinical practice has found that many cases of allergic interstitial nephritis (AIN) lack the most critical systemic allergic reaction, which makes it difficult for clinical diagnosis, and occurs in suspicious cases with recent medication history. Unexplained ARF, especially with renal diabetes and low urine protein, should be suspected, and renal biopsy should be performed in time to understand the type and extent of interstitial damage, help to develop treatment plans and determine prognosis, atypical Case diagnosis must rely on renal biopsy pathological examination, and the diagnosis can only be established if the pathological manifestation is consistent with drug allergic AIN.

The drug-specific lymphocyte transformation test helps to identify the pathogenic drugs. This test is a safe and reliable test for blood collection in vitro. It is based on the application of specific antigens in vitro to stimulate sensitization in patients. Lymphocytes cause transformation, depending on the level of lymphocyte response to drug antigens, to identify whether it is allergic to this drug, with high specificity, rare false positives, but negative results can not rule out the possibility of drug allergy.

2. The diagnosis of nephrotoxicity of aminoglycoside antibiotics should be closely observed after drug administration, so as to detect nephrotoxic damage early, the sooner it is discovered, the sooner the drug is stopped, the faster the kidney damage recovers, the better, the following Early diagnosis:

(1) Observing changes in urine volume, early detection of oliguria, oliguria, and no urine.

(2) Closely monitor the urine routine (red blood cells, white blood cells, proteins, etc.), and check the cell type of urine sediment.

(3) Monitoring lysozyme, alkaline phosphatase, -glutamyltranspeptidase, N-acetyl--glucosaminidase and isoenzyme, blood, urine 2 microglobulin, etc. It is necessary to stop the observation.

(4) The urine GGT/Cr ratio is measured, and if the ratio is three times larger than the base value, it is valuable.

(5) Follow-up observation of changes in renal function, such as unexplained blood urea nitrogen, elevated creatinine, it is necessary to consider drug-induced renal damage.

(6) Digital imaging analysis method can detect the nephrotoxicity of aminoglycoside antibiotics earlier than azotemia.

(7) In animal experiments, the excessive expression of "Heat shock protein 47" (HSP47) was found to be an important marker of gentamicin nephrotoxicity in renal tissue immunohistochemistry. Detection of HSP47 protein helps early diagnosis of kidney damage.

Differential diagnosis

Acute renal failure

Acute glomerulonephritis, rapid glomerulonephritis, primary nephrotic syndrome, lupus nephritis and acute renal failure caused by acute tubular necrosis have common manifestations of acute renal failure and special characteristics of their primary disease Performance, but no systemic allergic reaction; elevated IgE in the blood; urinary eosinophils account for more than 1/3 of nucleated cells; anti-TBM antibodies, which can help identify, some scholars reported 167Ga scanning examination, in acute interstitial nephritis The renal uptake density increases, while acute tubular necrosis does not take up, which may also help differential diagnosis.

2. Renal failure occurs in chronic glomerular lesions

When there is unexplained acute renal failure or progressive renal failure, the possibility of acute interstitial nephritis should be considered. Systemic allergic reactions, elevated blood IgE and aseptic eosinophilic urine are helpful in diagnosis. A renal biopsy is performed to confirm the diagnosis.

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