Heroin kidney disease

Introduction to heroin kidney disease The most commonly used addictive drugs are diacetal morphine, and there are many complications of intravenous drug addiction, with kidney complications being the most common. Abuse of diclofenac-related kidney damage refers to kidney disease directly and/or indirectly caused by the abuse of diacetal morphine, including diacetal morphine-related nephropathy (HAN) caused by direct action of diacetal morphine, due to staphylococcal infection Post-infection glomerulonephritis, renal amyloidosis due to chronic suppurative skin infection, acute infectious tubulointerstitial nephritis due to sepsis, and/or acute drug-induced tubulointerstitial nephritis caused by antibiotics, Membranous glomerulonephritis caused by hepatitis B virus infection. basic knowledge Sickness ratio: 1%-5% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute renal failure, sepsis, amyloidosis

Causes of heroin kidney disease

(1) Causes of the disease

The etiology of diacetal morphine nephropathy remains unclear, and at least the following causes are thought to be involved in the development of diacetal morphine nephropathy:

1. Diacetal morphine itself has toxic effects on glomeruli

Morphine is an active metabolite of diacetal morphine. Animal models of morphine sulfate injection in rats have confirmed that morphine can cause inflammation of the renal interstitial, but does not cause glomerular lesions. Recent studies have shown that morphine can be used in a variety of ways. Induction of renal injury: induction of proliferation of mesangial cells, stimulation of mesangial cell matrix synthesis; reduction of mesangial cell metalloproteinase activity; promotion of accumulation of immune complexes in the mesangial area; reduction of mononuclear Phagocytic function of the phagocytic system; stimulation of superoxide formation in mesangial cells; induction of migration of mononuclear cells to the mesangial area. In addition, studies by Singhal et al. confirmed that morphine can regulate early growth-related genes at low concentrations (c- Expression of fos, c-jun, c-myc) mRNA promotes proliferation of renal fibroblasts, and induces apoptosis of renal fibroblasts by promoting p53 production at high concentrations; it also confirms that morphine promotes renal medullary stromal cells Proliferation promotes the accumulation of collagen I and collagen III, and the renal interstitial fibrosis process is completed by the above mechanism.

2. Renal toxicity of exogenous toxins

Exogenous toxins that enter the body with diacetal morphine can cause kidney damage. There are reports that 97% of the diacetyl morphine sold on the street is a dopant, and only 3% is a diacetin morphine component. In 12,366 parts of diacetate or cocaine, there are 11 ingredients in excess of 5%, including: mannitol, quinine, lactose procaine, caffeine, inositol, lidocaine, starch, methacetin, Sucrose, acetyl procaine and dextrose, it is likely that these dopants, rather than diacetal morphine, cause kidney damage.

3. Genetic susceptibility

Rao and other studies have shown that 90% of patients with diacetyl morphine nephropathy are black males, which may be determined by genetic differences. Haskell et al. compared patients with black dimorphine kidney disease and normal black people with primary focal small renal disease. The frequency of HLA-A, B, C and DR antigens in the hardened black patients showed that the frequency of HLA-BW53 in HAN patients was significantly higher than that in the control group, and it was considered that blacks had a tendency to develop diacetal morphine nephropathy.

(two) pathogenesis

The pathogenesis of diacetal morphine nephropathy is still unclear. Diquat morphine intravenous drug dependent patients often show a series of immunopathological reactions, such as elevated gamma immunoglobulin, false positive syphilis serum test, anti-self smooth muscle antibody positive, etc. There may be an immune mechanism involved in the development of diacetal morphine nephropathy. Immunofluorescence of renal biopsy specimens of diacetal morphine nephropathy shows immunoglobulin and complement deposition, suggesting that the immune mechanism may be the cause of diacetyl morphine nephropathy. However, what is the antigen that causes glomerular damage is still unclear, and some studies suggest that this may be a leaked non-specific serum protein, which can also be seen in other glomerular diseases such as diabetic nephropathy.

In the multisystemic damage syndrome caused by the abuse of diacetal morphine, the pathogen causing bacterial endocarditis mainly comes from the abuse of the skin, nose and throat of diacetyl morphine, rather than the contamination in diacetal morphine. In patients with glomerulonephritis, renal pathology is common for immunoglobulin and complement deposition, and the mechanism of glomerular damage in this disease is related to immune complexes. Bacterial cell wall antigens and corresponding antibodies may activate complement by bypass pathway. Glomerular injury, in a few cases, antibiotics used to treat bacterial endocarditis in this syndrome can lead to acute drug-induced tubulointerstitial nephritis. Therefore, renal failure caused by the abuse of addictive drugs is often multiple The combined result of kidney damage.

It has been suggested that diacetin or its contaminants may be associated with antigens that cause this syndrome. This syndrome is more common in black dimorphine addicts, so it is speculated that blacks may have genetic susceptibility to this syndrome.

It has been reported that patients with this syndrome with chronic suppurative skin infection develop amyloidosis in the kidneys, which are common in older drug-dependent patients who often switch to subcutaneous injections after finding a venous access to the drug.

Hepatitis B virus infection is common in patients with intravenous drug dependence, mainly related to the benign type of membranous or mesangial capillary glomerulonephritis, and children are more common in adults.

Heroin kidney disease prevention

Strengthening the attention of such patients and the understanding of diacetal morphine nephropathy is the key to improving the prevention and treatment of this disease. In the various kidney damages caused by the abuse of diacetal morphine, diacetyl morphine nephropathy is stopped. After the use of diacetal morphine, the kidney disease will gradually recover. Therefore, it is strictly forbidden to abuse the addictive drugs such as diacetal morphine. The drug addicts who have been exposed to drugs should be detoxified and treated symptomatically to prevent serious complications.

Heroin kidney disease complications Complications acute renal failure sepsis amyloidosis

1. In patients with bacterial endocarditis caused by the abuse of diacetal morphine, the endocardial site is mostly tricuspid, all complicated by acute renal failure.

2. Abuse of diacetal morphine can cause multiple systemic damage syndrome, and patients with secondary endocarditis appear clinically as symptoms of sepsis.

3. Patients with chronic suppurative skin infection may develop amyloidosis in the kidneys.

Heroin kidney disease symptoms common symptoms hypertension glomerular sclerosis renal failure coma hematuria kidney shrinkage pyuria sepsis drug dependence

The clinical manifestations and pathological types of this disease vary, mainly including three related kidney diseases:

1. Application of unsterilized syringes leads to bacterial endocarditis complicated by glomerulonephritis.

2. Proteinuria, nephrotic syndrome and progressive renal dysfunction occur after inhalation of diacetal morphine, which is most common with focal glomerular sclerosis.

3. Abuse of diacetal morphine caused by coma and acute renal failure caused by non-traumatic rhabdomyolysis, but most of the clinical manifestations of nephrotic syndrome, typical 6 to 48 months after the onset of end-stage renal disease, most patients There is renal dysfunction at the time of onset, manifested as diacetal morphine-related nephropathy of nephrotic syndrome, large amount of proteinuria in urine, hypoalbuminemia, hyperlipidemia and varying degrees of edema; some patients develop hypertension Late renal enlargement, azotemia, anemia, etc., progressive damage to renal function is a prominent feature of this type of patient, often progressing to ESRD within a few months to 2 to 3 years, hypertension may lead to renal function One of the pathophysiological mechanisms of sexual impairment, patients often end with ESRD due to uncontrollable hypertension. Some patients may have pyuria, or gross hematuria or microscopic hematuria, but no white blood cells or red blood cell casts.

Studies have shown that in patients with a history of diacetyl morphine dependence for more than 30 years, the incidence of chronic glomerulonephritis is usually high, due to staphylococcal infection caused by post-infection glomerulonephritis, clinical manifestations and acute streptococcal infection Glomerulonephritis is similar.

Patients with this disease take acetaminophen morphine generally after 7 years of edema, proteinuria, clinical exclusion of other kidney disease, renal pathological changes in line with diacetal morphine nephropathy can make a diagnosis, diagnosis basis: a history of diacetal morphine dependence, clinical appearance A large amount of proteinuria, hypoalbuminemia, hyperlipidemia, edema, progressive renal damage, and exclusion of hepatitis B virus glomerulonephritis, HIV-AN, renal amyloidosis, sepsis caused by bacteria Or kidney disease caused by infective endocarditis and other nephropathy associated with dimorphine drug dependence, can diagnose the disease, renal biopsy, immunopathology and electron microscopy are helpful for diagnosis, in HIV-positive patients, There are certain difficulties in identifying HIV-AN and HAN. About 50% of AIDS patients in New York do not get HIV through intravenous drug dependence, but through heterosexual, homosexual or bisexual infection. Identification of medical history, pathology, HIV-AN renal biopsy often shows collapse of global glomerular capillary plexus, renal tubular proliferative microcapsule formation and The degeneration of the tubules is more serious. Under the electron microscope, a large number of tubule reticular structures appear in the glomerular endothelial cells. The clinical course of HIV-AN is faster than that of HAN. The patients often have no hypertension, and the volume of the kidneys is not reduced or even increased. Large, HIV-AN often occurs in the final weeks or months of AIDS patients.

Examination of heroin kidney disease

1. Urine examination: 24h urine volume is basically normal, 24h urine protein quantitation (normal value 0.4g / 24h) is significantly increased, there may be a large amount of protein in the urine, in some cases even up to tens of grams per day; urine sediment red blood cell count Increased, polymorphic, visible white blood cell urine, increased urine C3 (normal value 2.76mg / L), increased urinary 2 macroglobulin, urine N-acetyl--aminotransferase increased (normal value 16.5U / g creatinine), 13h urinary osmotic pressure decreased, urine sugar was negative.

2. Blood examination: white blood cells, hemoglobin, platelets, peripheral blood lymphocytes are basically normal or elevated, blood albumin is reduced, blood lipids are elevated, and serum creatinine and urea nitrogen are progressively elevated.

3. Immunological examination: IgG, IgA, IgM, C3, C4, C-reactive protein (CRP) can have abnormal changes, anti-streptolysin, anti-nuclear antibody, anti-double-stranded DNA antibody, anti-extractable core The antigenic peptide antibody was negative, and the hepatitis B 5 examination showed that some patients were HBsAg positive.

Renal morphological changes in diacetal morphine nephropathy, including FSGS, membrane proliferative glomerulonephritis, patients who are often subcutaneously injected with diacetin, may also have renal amyloidosis, in addition to glomerular lesions in patients In addition, it can be accompanied by obvious interstitial inflammation.

4. Renal tissue biopsy: The type of glomerular damage in this syndrome is focal or diffuse. The type of glomerular damage determines the degree of clinical manifestations and renal failure. The common type of renal damage in patients is acute. Glomerulonephritis after staphylococcal infection, the lesion is diffuse.

(1) Light microscopy: light microscopy showed glomerular glomerular ablation, and fibrous exudate was seen in the discarded balloon. Individual glomeruli showed top lesions, and the lesions were twisted and collapsed, adjacent to the iliac crest. Endothelial cells are paired and foam cells, mononuclear cells, epithelial cells of the surrounding visceral layer are swollen and proliferated, large vacuoles are formed in the cytoplasm, epithelial cells of other squamous cells are also swollen, and mesangial areas are widened, mesangial cells, The matrix was slightly proliferated, the segment of the Bowman's wall was thickened, the PASM-Masson staining was negative, the tubulo-interstitial acute lesion was mild, the tubule epithelial edema was degenerated, more small vacuoles, the focal tubule epithelial cells brushed off, and the lumen was intraluminal. See protein tube type, no cystic dilatation of small tubules, reduced number of tubules in medullary area, atrophy of small focal tubules, thickening of basement membrane, slightly widened medullary interstitial area, fibrosis, small focal cell infiltration, small artery infiltration There may also be crescent formation, which is indistinguishable from other types of post-infection glomerulonephritis.

(2) Electron microscopy: Electron microscopy shows deposits in the subepithelial and basement membranes, usually in the form of immunoglobulin and complement granules, supporting the pathogenesis associated with immune complexes, and glomerulosclerosis in electron microscopy. The podocyte lesions are extensive, the cytoplasm is microvilli, the vacuoles are formed in the cytoplasm, the cytoplasm is weakened, the organelles are reduced, the foot processes are extensively fused, flattened, and the unfused foot gaps are narrowed. See the foot process peeling off the glomerular basement membrane.

(3) Immunofluorescence: IgG ( ), IgA ( ), IgM ( ), diffuse distribution, granular deposition in the mesangial area and vasospasm; C3, C4, C1q negative, secondary to other chronic infections and inflammatory diseases The same is true for amyloidosis. AA amyloid is found in the protein extract of the autopsy specimen of this syndrome.

Hepatitis B virus-associated membranous glomerular lesions in patients with this syndrome are similar to idiopathic membranous nephropathy. Electron microscopy and immunohistochemistry show deposits in the membrane and mesentery. Some researchers have found There are various hepatitis B antigens and antibodies in the kidney tissue or its eluate.

The biopsy pathology of HIV-AN nephropathy often shows that the glomerular capillary plexus collapses globally, the tubule proliferative microcapsule formation and tubule degeneration become more serious, and a large number of small tubes appear in the glomerular endothelial cells under electron microscope. grid.

5. B-ultrasound: Late B-ultrasound showed bilateral renal enlargement.

Diagnosis and diagnosis of heroin kidney disease

Should be identified with the following diseases: hepatitis B nephritis, AIDS nephropathy, renal amyloidosis, infective endocarditis and sepsis renal damage, identification of early HIV-AN and HAN is often very difficult, with hepatitis virus glomerulus The identification points of nephritis mainly include the sign of hepatitis virus infection in the blood of patients. The kidney biopsy has the mark of hepatitis virus antigen. The patients with renal amyloidosis often have long-term skin infection, history of ulcer, Congo red, thioiodene T, etc. Special staining is positive, infective endocarditis, and renal damage caused by sepsis often has clinical manifestations of primary disease.

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