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Heroin kidney disease

  Among the most commonly used addictive drugs, diacetylmorphine is the most common. Intravenous abuse of addictive drugs has many complications, among which kidney complications are relatively the most common. Renal damage related to diacetylmorphine abuse refers to kidney lesions caused directly and/or indirectly by diacetylmorphine abuse, including diacetylmorphine-related nephropathy (HAN) caused by direct action of diacetylmorphine, post-infectious glomerulonephritis caused by Staphylococcus aureus infection, renal amyloidosis caused by chronic suppurative skin infection, acute infectious tubulointerstitial nephritis and/or acute drug-induced tubulointerstitial nephritis caused by sepsis and/or antibiotics, and membranous glomerulonephritis caused by hepatitis B virus infection, etc.

 

Table of Contents

1. What are the causes of heroin kidney disease?
2. What complications are likely to be caused by heroin kidney disease?
3. What are the typical symptoms of heroin kidney disease?
4. How to prevent heroin kidney disease?
5. What laboratory tests are needed for heroin kidney disease?
6. Diet taboos for patients with heroin kidney disease
7. Conventional methods of Western medicine for the treatment of heroin kidney disease

1. What are the causes of heroin kidney disease?

  1. Etiology

  The etiology of diacetylmorphine kidney disease is still unclear. At least the following etiologies are considered to be involved in the occurrence of diacetylmorphine kidney disease:

  1. Does diacetylmorphine itself have a toxic effect on the glomerulus? Morphine is the active metabolite of diacetylmorphine. Previous animal models of rats injected with morphine sulfate have confirmed that morphine can cause interstitial inflammation of the kidney but will not cause glomerular lesions. Recent studies have shown that morphine can induce kidney injury through various pathways: induce the proliferation of glomerular mesangial cells, stimulate the synthesis of mesangial cell matrix; reduce the activity of mesangial cell metalloproteinases; promote the accumulation of immune complexes in the glomerular mesangial area; reduce the phagocytic function of the mononuclear phagocyte system; stimulate the formation of superoxides in mesangial cells; induce the migration of mononuclear cells to the mesangial area. In addition, the study by Singhal et al. confirmed that morphine can promote the proliferation of renal fibroblasts by regulating the expression of early growth-related gene mRNA (c-fos, c-jun, c-myc) at low concentrations, and induce the apoptosis of renal fibroblasts by promoting the production of p53 at high concentrations; it also confirmed that morphine promotes the proliferation of renal medullary interstitial cells, promotes the accumulation of collagen I and collagen III, and completes the HAN renal interstitial fibrosis process through the above mechanisms.

  2. The nephrotoxic effect of exogenous toxins entering the body with diacetylmorphine: Exogenous toxins entering the body with diacetylmorphine can cause kidney damage. There are reports that 97% of the diacetylmorphine sold on the streets is impurities, and only 3% is diacetylmorphine. The analysis of the U.S. Food and Drug Administration shows that in 12366 samples of diacetylmorphine or cocaine, there are 11 components exceeding 5%, including: mannitol, quinine, procaine lactate, caffeine, inositol, lidocaine, starch, meperidine, sucrose, acetylprocaine, and dextrose. Therefore, it is very likely that these impurities rather than diacetylmorphine cause kidney damage.

  3, Genetic susceptibility Studies by Rao et al. show that 90% of diacetylmorphine nephropathy patients are black males, which may be determined by genetic differences. Haskell et al. compared the frequencies of HLA-A, B, C, and DR antigens in black diacetylmorphine nephropathy patients, normal black people, and black people with primary focal glomerulosclerosis, and found that the frequency of HLA-BW53 in HAN patients was significantly higher than that in the control group, thus considering that blacks have a tendency to develop diacetylmorphine nephropathy.

  Second, pathogenesis

  1, The pathogenesis of diacetylmorphine nephropathy is not yet clear. Diacetylmorphine intravenous drug users often show a series of immune pathological reactions, such as elevated gamma immunoglobulin, false-positive syphilis serological test, positive anti-own smooth muscle antibody, etc., suggesting that there may be an immune mechanism involved in the occurrence of diacetylmorphine nephropathy. Immunofluorescence examination of renal biopsy specimens from diacetylmorphine nephropathy shows immunoglobulin and complement deposition, similarly suggesting that the immune mechanism may be the cause of diacetylmorphine nephropathy. However, what antigens cause glomerular damage is still unclear. Some studies also suggest that this may be non-specific serum proteins that leak out, which can also be seen in other glomerular diseases, such as diabetic nephropathy.

  2, In the multi-system damage syndrome caused by the abuse of diacetylmorphine, the pathogenic bacteria that cause bacterial endocarditis mainly come from the skin, nose, and throat of diacetylmorphine abusers, rather than from contamination in diacetylmorphine. In patients with this syndrome who have acute glomerulonephritis, renal pathological examination often shows immunoglobulin and complement deposition, supporting that the mechanism of glomerular damage in this disease is related to immune complexes, and bacterial cell wall antigens and corresponding antibodies may activate complement through the bypass pathway to cause glomerular damage. In a few cases, antibiotics used to treat bacterial endocarditis in this syndrome can also cause acute drug-induced tubulointerstitial nephritis. Therefore, renal failure caused by the abuse of addictive drugs is often a comprehensive result of multiple renal damage.

  (1) Some believe that diacetylmorphine or its contaminants may be related to the antigens that cause this syndrome. This syndrome is more common in black diacetylmorphine addicts. Therefore, some speculate that blacks may have a genetic predisposition to this syndrome.

  (2) Some reports have shown that patients with this syndrome who have developed chronic suppurative skin infections have amyloidosis in the kidneys, which is common in older drug addicts who often switch to subcutaneous injection after failing to find a venous access for injecting drugs.

  (3) Intravenous drug users often suffer from infection with the hepatitis B virus, mainly related to the benign type of membranous or mesangiocapillary glomerulonephritis, and it is more common in children than in adults.

 

2. What complications are easy to cause by heroin nephropathy

  1, Among patients with bacterial endocarditis caused by abuse of diacetylmorphine, the affected endocardial sites are mostly the tricuspid valve, and all have concurrent acute renal failure.

  2, Abuse of diacetylmorphine can cause multi-system damage syndrome, and patients with secondary endocarditis are clinically manifested as symptoms of sepsis.

  3. Starch-like degeneration of the kidneys may occur in patients with chronic suppurative skin infections.

3. What are the typical symptoms of heroin nephropathy?

  The clinical manifestations and pathological types of this disease are diverse, mainly involving three types of kidney diseases related to it:

  1. Bacterial endocarditis and glomerulonephritis occur due to the use of unsterilized syringes.

  2. Proteinuria, nephrotic syndrome, and progressive renal function decline occur after inhaling diacetylmorphine, and focal glomerulosclerosis is the most common finding.

  4. Acute renal failure caused by coma and non-traumatic rhabdomyolysis due to abuse of diacetylmorphine, but most clinical manifestations are nephrotic syndrome. The typical patient enters the end-stage renal disease within 6 to 48 months after an attack. Most patients show renal function impairment at the time of an attack, which is characterized by diacetylmorphine-related nephropathy with nephrotic syndrome, common with large amounts of proteinuria, hypoalbuminemia, hyperlipidemia, and varying degrees of edema; some patients may develop hypertension; in the late stage, there may be shrinkage of the kidneys, azotemia, anemia, etc., and progressive renal function impairment is a significant characteristic of this group of patients, often progressing to ESRD within several months to 2 to 3 years. Hypertension may be one of the pathophysiological mechanisms leading to progressive renal function impairment, and patients may ultimately develop ESRD due to uncontrollable hypertension. Some patients may have pyuria, gross hematuria, or microscopic hematuria, but without white or red cell casts.

  4. Studies have shown that in patients with more than 30 years of diacetylmorphine drug dependence, the incidence of chronic glomerulonephritis is usually high, and post-infectious glomerulonephritis caused by Staphylococcus infection has clinical manifestations similar to those of acute post-streptococcal glomerulonephritis.

  5. Patients with diacetylmorphine dependence generally develop edema and proteinuria 7 years after smoking, and a diagnosis can be made by excluding other kidney diseases and pathological changes in the kidneys that are consistent with diacetylmorphine nephropathy. The diagnostic criteria include a history of diacetylmorphine drug dependence, the appearance of large amounts of proteinuria, hypoalbuminemia, hyperlipidemia, edema, progressive renal function impairment, and the exclusion of other kidney diseases associated with diacetylmorphine drug dependence, such as hepatitis B virus glomerulonephritis, HIV-AN, renal amyloidosis, kidney damage caused by sepsis or infective endocarditis due to bacterial infection, etc. Renal biopsy, immunopathology, and electron microscopy can be helpful for diagnosis. In patients with HIV positivity, it is somewhat difficult to differentiate between HIV-AN and HAN. Among HIV-positive patients in New York, about 50% were not infected through intravenous drug use but through heterosexual, homosexual, or bisexual transmission. This group of patients can be distinguished based on their medical history. Pathologically, renal biopsy in HIV-AN often shows global collapse of glomerular capillary tufts, proliferative microcyst formation in renal tubules, and severe tubular degeneration. Under the electron microscope, a large number of reticulate structures appear in the endothelial cells of glomeruli. Clinically, HIV-AN has a more rapid course of disease progression than HAN, and patients often have no hypertension. The size of the kidneys does not shrink but may even increase, and HIV-AN often occurs in the final weeks or months of the course of AIDS.

4. How to prevent heroin nephropathy

  Enhancing the attention to and understanding of diacetylmorphine nephropathy in these patients is the key to improving the prevention and treatment level of the disease. Among the various renal lesions caused by clinical syndromes induced by diacetylmorphine abuse, diacetylmorphine nephropathy can gradually recover after the cessation of diacetylmorphine use, so the abuse of addictive drugs such as diacetylmorphine should be strictly prohibited. Narcotics addicts who have been exposed to toxins should be compulsorily戒毒 and treated symptomatically to prevent serious complications.

 

5. What laboratory tests are needed for heroin nephropathy

  1. Urine examination:24-hour urine volume is basically normal, and the 24-hour urine protein excretion (normal value ≤0.4g/24h) is significantly increased. There may be a large amount of protein in the urine, and in some cases, it may reach dozens of grams per day; the urine sediment red blood cell count is increased, showing polymorphism, and there may be leukocyte urine. Urinary complement C3 is increased (normal value ≤2.76mg/L), urinary α2-macroglobulin is increased, urinary N-acetyl-β-glucosaminidase is elevated (normal value ≤16.5U/g creatinine), urine osmolality decreases after 13 hours of water deprivation, and urine sugar is negative.

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

  3. Immunological examination:Abnormal changes may occur in IgG, IgA, IgM, C3, C4, and C-reactive protein (CRP). Increased levels of anti-streptolysin O, negative for antinuclear antibodies, double-stranded DNA antibodies, and extractable nuclear antigen peptide antibody. Some patients may have a positive HBsAg in the five-item hepatitis B test.

  The morphological changes in the kidney of diacetylmorphine nephropathy are diverse, including FSGS, membranous proliferative glomerulonephritis. In patients who are often given subcutaneous injections of diacetylmorphine, kidney amyloidosis may also occur. In addition to glomerular lesions, patients may also have marked interstitial inflammation.

  4. Renal tissue biopsy:The type of glomerular damage in this syndrome is focal and can also be diffuse. The type of glomerular damage determines the clinical manifestations and the degree of renal function failure. The common type of renal damage in patients is acute staphylococcal post-infectious glomerulonephritis, with diffuse lesions.

  (1) Microscopic examination: Light microscopy shows globular atrophy of renal glomeruli, with纤维素ous exudates still present in the atrophic cysts. Some glomeruli exhibit capsular lesions with twisted and shrunken segmental loops, adjacent to which there are paired endothelial cells and foamy cells, solitary nucleated cells, and swollen, proliferative parietal epithelial cells with large vacuoles in the cytoplasm. Other glomerular parietal epithelial cells are also swollen, with widened segmental mesangial areas, mesangial cell proliferation, slightly thickened Bowman's capsule walls, negative PASM-Masson staining, mild acute tubulointerstitial lesions, tubular epithelial edema and变性, with many small vacuoles, focal loss of brush border of tubular epithelial cells, protein casts in the lumen, no tubular cystic dilation, reduced tubular number in the medulla, focal tubular atrophy, thickened basement membranes, slightly widened interstitial area of the medulla, fibrosis, focal cellular infiltration, and渗出 in small arteries; crescent formation may also occur, which is difficult to distinguish from other types of post-infectious glomerulonephritis.

  (1) Electron microscopy examination: Under the electron microscope, deposits can be seen under the epithelium and within the basement membrane, usually with granular deposits of immunoglobulins and complements, supporting the pathogenesis related to immune complexes. In addition, electron microscopy also shows glomerulosclerosis, extensive podocyte lesions, obvious microvilli in the cytoplasm, formation of a large number of vacuoles in the cytoplasm, some cytoplasm becomes pale, organelles decrease, foot processes widely fuse, flatten, the gaps between unfused foot processes become narrow, and occasionally foot processes are shed from the glomerular basement membrane.

  (2) Electron microscopy: Under the electron microscope, deposits can be seen under the epithelium and within the basement membrane, usually with granular deposits of immunoglobulins and complements, supporting the pathogenesis related to immune complexes. In addition, electron microscopy also shows glomerulosclerosis, extensive podocyte lesions, obvious microvilli in the cytoplasm, formation of a large number of vacuoles in the cytoplasm, some cytoplasm becomes pale, organelles decrease, foot processes widely fuse, flatten, the gaps between unfused foot processes become narrow, and occasionally foot processes are shed from the glomerular basement membrane.

  (4) The damage caused by hepatitis B virus-related membranous glomerulonephritis in patients with this syndrome is similar to that of idiopathic membranous nephropathy. Electron microscopy and immunohistochemistry show deposits in the membrane and mesangium. Some researchers have found various hepatitis B antigens and antibodies in kidney tissue or its filtrate.

  (5) The pathological changes of HIV-AN kidney disease often show collapse of glomerular capillary plexus, proliferative microcyst formation in renal tubules, and severe tubular degeneration. Under the electron microscope, a large number of reticular structures appear in the glomerular endothelial cells.

  5. Ultrasound examination:Late B-ultrasound can show shrinkage of both kidneys.

6. Dietary taboos for heroin kidney disease patients

  First, the dietary therapy of heroin kidney disease

  1. Astragalus porridge

  30-60 grams of raw Astragalus, 60 grams of glutinous rice, 10 grams of dried tangerine peel powder. First, decoct Astragalus into a decoction and remove the dregs, then cook the glutinous rice into porridge, and add dried tangerine peel powder when the porridge is done.

  2. Euryale ferox and white fungus porridge

  30 grams of Euryale ferox, 10 grams of white fungus, 30 grams of glutinous rice. Shell the white fungus, and cook it with Euryale ferox and glutinous rice in a pot with water to make porridge.

  Second, other

  20 grams of Astragalus, 1 gram of black tea, Astragalus is decocted with 500 grams of water for 5 minutes, remove the dregs and take the juice, then add black tea.

  Corn silk tea: 100 grams of corn silk, 30 grams of Job's tears, 30 grams of bok choy, appropriate amount of rock sugar, add clear water to decoct into a decoction instead of tea.

  What is good for the body for heroin kidney disease patients to eat:

  1. It is advisable to eat more legume foods, such as mung beans, black soybeans, broad beans, and soybeans,

  2. It is advisable to eat more fresh fruits and vegetables, such as winter melon, lettuce, and yam,

  What is bad for the body for heroin kidney disease patients to eat:

  Avoid eating刺激性食物.

7. Conventional methods of Western medicine for the treatment of heroin kidney disease

  I. Treatment

  1. For diacetylmorphine kidney disease, there is currently no effective treatment method, and the efficacy of immunosuppressants is poor. Chronic diacetylmorphine abusers can progress to end-stage kidney disease years later. However, some patients experience relief of clinical symptoms, disappearance of proteinuria, normalization of serum albumin, and stable renal function after detoxification. The duration of remission is usually several years.

  2. In various renal damages caused by clinical syndromes induced by the abuse of diacetylmorphine, the treatment of acute infectious tubulointerstitial nephritis caused by sepsis and/or acute drug-induced tubulointerstitial nephritis caused by antibiotics is the same as that for tubulointerstitial kidney disease. For glomerulonephritis caused by acute staphylococcal infection, the main treatment is anti-infection and symptomatic supportive treatment, and oliguria in acute renal failure often requires temporary dialysis treatment. In patients with acute renal failure caused by sepsis and other factors, the oliguria period often lasts for about 4 weeks. When there is bacterial endocarditis, large doses of antibiotics sensitive to the pathogen should be used, and the course of treatment should follow the treatment plan for bacterial endocarditis. Vancomycin is often necessary, but it must be administered strictly according to the glomerular filtration rate, calculated according to the formula. For example, in acute renal failure, it is generally administered once every 7 days, 1.5 to 2g each time, and 0.5g is supplemented after each dialysis. For these patients, imported vancomycin (Stabizhin) is effective and relatively safe.

  (1) For chronic suppurative skin infections causing renal amyloidosis, strong treatment for skin infections can alleviate or even eliminate amyloid deposition.

  (2) For patients with severe valve damage, surgical treatment should be adopted under the application of strong and effective antibiotics, which can often save the lives of some patients.

  II. Prognosis

  The proteinuria of patients with this disease can completely disappear after detoxification, and the renal function will gradually return to normal. If diacetylmorphine is continued to be used, it often develops into end-stage renal failure. If FSGS is concurrent, the prognosis is poor. If HAN is not treated and diacetylmorphine use is not stopped, 25% to 40% of patients will progress to end-stage renal disease in 10 to 15 years, even after kidney transplantation, 20% to 30% of patients may still have FSGS in the transplanted kidney.

 

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