- Clinical Findings & Diagnostic Criteria
- Risk Factors
- Etiology
- Pathology
- Epidemiology
- Management & Treatment
- Prevention
- Complications
- Prognosis
- Research Frontier
- Clinical Case Studies
- Study Questions
Symptoms
acute kidney injury and severe metabolic alkalosis
. These crystals are also identified in light and electron microscopy. We hypothesize that heroin crystalizes in an alkaline pH, resulting in tubular obstruction and acute kidney injury. Management is mainly supportive as there is no known specific therapy for this condition. This paper highlights the utility of urine microscopy in diagnosing the etiology of acute kidney injury and proposes a novel disease called heroin crystal nephropathy.
Signs
Urinalysis
Urine microscopy showed numerous broomstick-like crystals
Typically, patients present with azotemia, hematuria and nephrotic-range proteinuria [3].
Reference: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4440465/
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Alcohol
Alcohol can interfere with the function of each of these components, thereby causing impotence, infertility, and reduced male secondary sexual characteristics.1 In the testes, alcohol can adversely affect the Leydig cells, which produce and secrete the hormone testosterone. Studies found that heavy alcohol consumption results in reduced testosterone levels in the blood. Alcohol also impairs the function of the testicular Sertoli cells that play an important role in sperm maturation. In the pituitary gland, alcohol can decrease the production, release, and/or activity of two hormones with critical reproductive functions, luteinizing hormone and follicle-stimulating hormone. Finally, alcohol can interfere with hormone production in the hypothalamus.
In 1970, an association between nephrotic syndrome and chronic heroin and cocaine use was reported [2].
Kidney biopsies of African Americans who abuse heroin showed focal segmental glomerulosclerosis as the predominant finding while membranoproliferative glomerulonephritis was the common pathologic description in affected Caucasians [4, 5]. Of note, these studies included patients concomitantly infected with either hepatitis C or human immunodeficiency virus; thus, this led some authors to postulate that the biopsy findings are the result of the viral infection rather than heroin's effect on the glomeruli. Importantly, morphine, the active metabolite of heroin, is known to have a direct cytotoxic effect on the renal parenchyma including mesangial cell and glomerular epithelial cell hyperplasia. This is thought to be mediated by activated macrophages that ultimately cause mesangial matrix synthesis and injury from oxidative stress [6–9]. Both an increased incidence of amyloidosis and rhabdomyolysis-induced acute tubular necrosis have also been described in heroin abuse [10].
Heroin production is a four-step process, which begins with extraction of raw opium from Papaver somniferum [11], followed by synthesis of morphine and then its acetylation into heroin. Alkalinization of heroin into its base form is achieved by the addition of bicarbonate or ammonia. The final step is the transformation of the heroin base into the salt form with the addition of hydrochloride acid and ether. This final step is critical in making heroin water-soluble for injection [12, 13]. More than twenty substances have been used as adulterants or diluents for heroin including procaine, caffeine, paracetamol, mannitol, acetic acid, quinine, dextrose, paracetamol, phenobarbital, methanol, and acetone [14, 15].
Taken intravenously, heroin bypasses first-pass metabolism in the liver where heroin is metabolized into its active form morphine glucoronides [16]. Only 20–40% of heroin is bound to albumin or erythrocytes. It has a volume of distribution of 60–100 L and a half-life of 1.3–7.8 min [17]. Micropuncture studies have shown that heroin is freely filtered, actively secreted in the proximal convoluted tubule and partly reabsorbed in the distal segments, resulting in net tubular excretion [18, 19]. This concept is important in establishing the possible causal relationships between tubular injury and heroin use. The presence of acute kidney injury also potentiates heroin toxicity.
Mainly a disease of concentration, crystal nephropathy is dependent on both the renal tubular fluid composition and substrate concentration. In addition, the deposition of crystals into the renal epithelium depends upon the integrity of the renal tubular epithelial cells [20]. Crystal deposition is more likely to occur in the presence of tubular epithelial injury. In rats, crystals do not adhere to normal epithelial cells but more easily deposit in damaged ones [21]. Acute kidney injury (AKI) results from either obstruction of the tubular lumen or direct cytotoxicity of the crystals on the renal epithelium. The former is mainly influenced by the solubility of certain substances in the normally acidic urine [22]. Certain substances are known to crystalize in acidic urine (e.g. calcium, calcium oxalate) while others in alkaline urine (e.g. calcium phosphate, struvite, protease inhibitors and quinolones) [23–27]. Direct cytotoxicity to the renal epithelium can result from the production of inflammatory substances such as IL-1β that stimulate cytokine release and neutrophil recruitment, ultimately resulting in tissue remodeling and renal failure [28].
Existing literature on heroin crystals is exclusive to experimental microcrystalline studies used in forensic drug analysis. There is no published report of heroin crystal causing direct nephropathy. In this paper we present a possible case of acute kidney injury as a result of heroin crystal deposition in the renal tubules.
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Complications of Injecting Drug Use
- Local problems—Abscess (Figures 240-2
and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of Richard P. Usatine, MD.)
- IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
- Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
- IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
- Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.
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A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?
The correct answer is A. You answered A.
Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.
Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?
The correct answer is A. You answered A.
The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.