OVERVIEW
With the gradual increase in the number of drug users, heroin nephropathy is also on the rise. Heroin can be ingested by snorting, smoking and eating, or by subcutaneous or intravenous injection, and is often injected with cocaine. Heroin has a half-life of 3 minutes and is rapidly metabolized to have pharmacological effects, and morphine is excreted in the urine in either free or unbound form. The average age of patients with this disease is less than 30 years, 90% are male, and the duration of drug use prior to the onset of the disease ranges from 6 months to 30 years (average 6 years).
Etiology
1. Application of unsterilized syringes leads to bacterial endocarditis complicated by glomerulonephritis.
2. Proteinuria, nephrotic syndrome and progressive renal decompensation occur after heroin inhalation, with focal glomerulosclerosis being the most common.
3. Acute renal failure due to non-traumatic rhabdomyolysis complicated by coma caused by heroin abuse.
Symptoms
Clinical most patients for nephrotic syndrome, typical of the attack after 6 to 48 months into the end-stage renal disease, the majority of patients with episodes of renal decompensation, manifested as a nephrotic syndrome of heroin nephropathy, commonly a large number of microalbuminuria, hypoalbuminemia, hyperlipidemia and varying degrees of edema; some patients occur hypertension; late stage of the emergence of shrinking kidneys, azotemia, anemia, and so on. Progressive impairment of renal function is a distinctive feature of this group of patients, often progressing to ESRD within a few months to 2-3 years.Hypertension may be one of the causes of progressive impairment of renal function. ESRD often occurs as a result of uncontrollable hypertension.Some patients may have pyuria, or hematuria or microscopic hematuria without leukocytes or erythrocyte tubular pattern.
Studies have shown that the incidence of chronic glomerulonephritis is usually high in patients with a history of heroin drug dependence of more than 30 years.
Tests
1. Gold standard urine rapid test
The urine test (morning urine is the best) can produce accurate results in 3 to 5 minutes.
2. 24-hour urine protein quantification
24-hour urine protein quantification (normal value ≤ 0.4 g / 24 hours) is significantly higher, there can be a large amount of protein in the urine, and in some cases, even up to dozens of grams per day; urine sediment erythrocyte count is increased, polymorphic leukocyturia can be seen, urinary complement C3 is increased (normal value of ≤ 2.76 mg / liter), urinary α2 macroglobulin is increased. Urine N-acetyl-β-aminotransferase increased (normal value ≤16.5U/g creatinine), 13 hours of water fasting urine osmolality decreased, urine sugar negative.
3. Blood tests
Leukocytes, hemoglobin, platelets, peripheral blood lymphocytes are basically normal or elevated. Blood albumin is decreased, blood lipids are increased, and blood creatinine and urea nitrogen are progressively increased.
4. IgG, IgA, IgM, C3, C4, C-reactive protein (CRP)
There may be abnormal changes, anti-streptococcal hemolysin is increased, anti-nuclear antibody, anti-double-stranded DNA antibody, anti-extractable nuclear antigen polypeptide antibody is negative. Hepatitis B 5 tests show that some patients are positive for HBsAg.
5. Kidney tissue biopsy
(1) light microscopy light microscopy can be seen in the glomeruli appear spherical abandonment, abandoned balloon still see fibrinous exudate individual glomeruli can be seen on the top of the lesion, the lesion at the segmental loop twisted and crumpled, the neighboring loops endothelial cells in pairs and foam cells single nucleated cells, the surrounding visceral epithelial cells swollen and proliferating cytoplasm see large vacuole formation, the other balloon visceral layer of the epithelial cells are also swollen, segmental tethered zone broadening tethered cells and stroma slightly proliferated. Segmental thickening of the wall of the Baumann’s capsule; PASM-Masson staining was negative. Acute tubular-interstitial lesions, mild tubular epithelial edema and degeneration, more fine vacuoles, focal tubular epithelial cells with brush border detachment, protein tubular pattern is seen in the lumen, no tubular cystic dilatation is seen, reduced number of tubules in medullary area, small focal tubular atrophy, basement membrane thickening medullary interstitial area slightly widened fibrosis, small focal cells infiltrating small arterial infiltrates; crescentic body formation is also seen. It is not easy to distinguish from other types of post-infectious glomerulonephritis.
(2) Electron microscopy Electron microscopy reveals subepithelial and basement membrane deposits usually with granular deposits of immunoglobulin and complement. In addition, electron microscopy also shows glomerulosclerosis, extensive podocyte lesions, obvious cytoplasmic microvilliosis, more vacuoles in the cytoplasm, part of the cytoplasm is pale, and there is a decrease in the number of organelles. Podocytes are extensively fused and flattened, and the gap of the non-fused podocytes narrows, and podocytes are occasionally peeled off from the basement membrane of the glomerulus.
(3) Immunofluorescence: IgG (+), IgA (+), IgM (++), diffusely distributed, granular deposits in the peritubular area and vascular loops; C3, C4, C1q are negative.
6. Ultrasound examination
In advanced stage, ultrasound shows bilateral renal shrinkage.
Diagnosis
The disease can be diagnosed with a history of heroin drug dependence, clinical presentation of massive microalbuminuria, hypoalbuminemia, hyperlipidemia, edema, progressive impairment of renal function and exclusion of hepatitis B viral glomerulonephritis, HIV-AN, renal amyloidosis, sepsis caused by bacteria or renal damage caused by infective endocarditis, and other renal diseases related to heroin drug dependence. Renal tissue biopsy, immunopathology and electron microscopy are helpful in the diagnosis.
Differential diagnosis
1. Differentiate from hepatitis B nephritis, AIDS, nephropathy, renal amyloidosis, infective endocarditis and septic kidney damage.
2. In HIV-positive patients, there is some difficulty in differentiating HIV-AN from HAN. Approximately 50% of patients with AIDS in New York are not infected with HIV through the intravenous drug dependence route, but rather through heterosexual, homosexual, or bisexual infections. This subset of patients can be identified on the basis of medical history. Pathologically HIV-AN renal tissue biopsies often show collapsing global sclerosis of the glomerular capillary plexus, with more severe proliferative microcystic formation of the renal tubules and tubular degeneration. Electron microscopy shows a large number of tubular meshwork structures in the glomerular endothelial cells. clinically, HIV-AN develops more rapidly than HAN, and patients often do not have hypertension, and there is no reduction in the size of the kidneys or even an increase in the size of the kidneys. hiv-an often occurs in patients with aids in the final weeks or months of the course of the disease.
3. The main points of differentiation from hepatitis viral glomerulonephritis include the presence of markers of hepatitis viral infection in the patient’s blood, and markers of hepatitis viral antigens in renal biopsy tissue. Patients with renal amyloidosis often have a history of long-term skin infections, ulcers, and positive staining with specific stains such as Congo red and thioredoxin T. Renal damage due to infective endocarditis and sepsis is often differentiated by clinical manifestations of the primary disease.
Treatment
For heroin nephropathy, the primary treatment is discontinuation of the drug, and there is no specific treatment, mostly symptomatic treatment. The prognosis of patients with glomerular damage is poor, and patients with end-stage renal failure need long-term replacement dialysis. For early cases such as timely withdrawal, active correction of acid-base imbalance, electrolyte disorders, etc., the prognosis may still be good.