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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2016  |  Volume : 27  |  Issue : 1  |  Page : 153-156
Malignant hypertension-associated thrombotic microangiopathy following cocaine use


1 Nephrology Department, La Rabta Hospital, Tunis, Tunisia
2 Laboratory of Renal Pathology (LR00SP01), Charles Nicolle Hospital, Tunis, Tunisia

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Date of Web Publication15-Jan-2016
 

   Abstract 

Cocaine is one of the most commonly used illicit drugs with distribution and consumption throughout the world. Acute renal failure associated with rhabdomyolysis, direct vasoconstriction and hemodynamic alteration is well described in patients with cocaine intoxication. Cocaine use is associated with high blood pressure and may rarely induce malignant hypertension associated with thrombotic microangiopathy. We report the case of a patient who developed malignant hypertension associated with thrombotic microangiopathy after chronic consumption of cocaine. A kidney biopsy revealed thrombotic microangiopathy with fibrinoid necrosis of arterioles and glomerular tufts. He required dialysis sessions. Cocaine-mediated endothelial injury and platelet activation may play important pathogenetic roles in cocaine abusers who develop malignant hypertension associated with thrombotic microangiopathy. Clinicians need to be aware of this rare feature of cocaine intoxication.

How to cite this article:
Lamia R, El Ati Z, Fatma LB, Zouaghi K, Smaoui W, Rania K, Krid M, Hmida FB, Béji S, Moussa FB. Malignant hypertension-associated thrombotic microangiopathy following cocaine use. Saudi J Kidney Dis Transpl 2016;27:153-6

How to cite this URL:
Lamia R, El Ati Z, Fatma LB, Zouaghi K, Smaoui W, Rania K, Krid M, Hmida FB, Béji S, Moussa FB. Malignant hypertension-associated thrombotic microangiopathy following cocaine use. Saudi J Kidney Dis Transpl [serial online] 2016 [cited 2020 Jul 13];27:153-6. Available from: http://www.sjkdt.org/text.asp?2016/27/1/153/174195

   Introduction Top


Cocaine, a natural alkaloid derived from the coca plant, is one of the most commonly used illicit drugs. [1] Cardiovascular dysfunction and renal failure due to rhabdomyolysis are well described following cocaine use. [2],[3] Although hypertension is a well-known manifestation of cocaine use, [4] cocaine-induced malignant hypertension associated with thrombotic microangio pathy has been rarely reported.

We report the case of a patient who developed malignant hypertension associated with thrombotic microangiopathy after chronic consumption of cocaine.


   Case Report Top


A 26-year-old man was admitted to our unit because of intermittent fever, dyspnea and oliguria. The patient had a medical history of chronic otitis and septic arthritis treated three years ago. He complained of headaches with blurred vision for a few days. He was alcoholic with a habitual use of inhaled cocaine for several years.

Physical examination revealed 38°C fever, 190/110 mm Hg blood pressure, 17/min respiratory rate, 80 beats/min heart rate and proteinuria and hematuria in urinalysis. Cardiac, pulmonary, abdominal, neurologic, musculoskeletal and lymph node exams were normal. The ophtalmological exam revealed papillary edema. Laboratory investigations revealed 1.8 g/day proteinuria, 220 mg/dL blood urea nitrogen, 9.8 mg/dL serum creatinine, 3.8 mEq/L serum potassium, 522 U/L serum lactate dehydrogenase and 72 U/L serum creatinine kinase. Blood count also revealed 6.9 g/dL hemoglobin, 5700/mm 3 white blood cell count, 183,000/mm 3 platelet count and <1% schistocytes in the peripheral blood smear. Measurement of arterial blood gas showed pH 7.32, partial pressure of carbon dioxide (pCO 2) 20.3 mm Hg, partial pressure of oxygen (pO 2 ) 69 mm Hg and bicarbonate11 mEq/L.

Serological tests for C hepatitis were positive. Serological assays for human immunodeficiency virus, cytomegalovirus, Hepatitis B, cryoglobulin, antineutrophil cytoplasmic antibodies, antinuclear antibodies and rheumatoid factor were all negative.

Doppler echocardiography showed concentric hypertrophy of the left ventricle with normal systolic function. The renal ultrasound was normal and kidney biopsy was performed. The renal histological exam demonstrated that most of the glomeruli had global sclerosis. The rest showed hyperplasic and myxoid intimal change affecting interlobular arteries [Figure 1] with thrombotic microangiopathy lesions in the small arteries [Figure 2]. Severe interstitial fibrosis with tubular atrophy and multiple hyaline casts were also present [Figure 3]. The diagnosis of thrombotic microangiopathy caused by cocaine-induced malignant hypertension was therefore confirmed. Although hypertension was controlled using multiple antihypertensive medications, renal function did not improve and the patient required chronic hemodialysis.
Figure 1: Renal histology showing hyperplasic and myxoid intimal change affecting interlobular arteries (Masson trichrome staining ×200).

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Figure 2: Renal histology showing thrombotic microangiopathy lesions in small arteries (Masson trichrome staining ×200).

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Figure 3: Renal histology showing severe interstitial fibrosis with tubular atrophy and multiple hyaline casts (Masson trichrome staining ×200).

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   Discussion Top


The major pharmacologic effects of cocaine consist of blockage of norepinephrine reuptake and release of catecholamines from adrenal glands. [5] Cocaine use is associated with multiple complications; the most common are cardiovascular and neurological disorders. [6] Regular and continual use can result in severe arterial hypertension causing, sometimes, terminal chronic renal failure. [7],[8]

Acute renal failure can also happen to patients with acute cocaine intoxication and it is well known that the most common kidney complication is rhabdomyolysis. [7] The mechanism linking cocaine with rhabdomyolysis is unclear, but it could involve ischemia due to vasoconstriction and vasospasm caused by cocaine's sympathomimetic action. This triggers tissue hypoxia with myocytic necrosis, direct muscle toxicity, hyperpyrexia and an increase in muscle activity with repeated trauma due to the agitation after consumption. [7],[9],[10]

Otherwise, cocaine abuse is usually associated with high blood pressure, but accelerated hypertension reaching levels of malignant hypertension is uncommon. Indeed, cocaine-induced malignant hypertension associated with morphologic features of thrombotic microangiopathy has been rarely cited in the literature. [2]

Thakur and colleagues reported two chronic hypertensive patients who developed accelerated hypertension with renal failure after consuming cocaine. Histologic examination of kidney biopsies revealed typical hyperplastic vasculopathy with onion-skinning of the interlobular arteries and ischemic changes of the glomeruli. Segmental fibrinoid necrosis of an interlobular artery was also noted. [11] Reported cocaine-associated thrombotic microangiopathy is rare, with only four previously reported cases in the literature. [2],[12],[13] In those reported cases, the patients had hemolysis, thrombocytopenia, renal failure and other systemic manifestations mimicking thrombotic thrombocytopenic purpura. In our case, there was cocaine use associated with malignant hypertension and renal failure without any sign of cardiac or cerebral ischemia. Laboratory tests ruled out rhabdomyolysis. The kidney biopsies revealed typical features of thrombotic microangiopathy with fibrinoid necrosis of arterioles and glomeruli, vascular sclerosis and glomerulosclerosis. It is likely in our case that cocaine-induced toxicity and the hypertensive effect resulted in injury of endothelial cells. Damage to the endothelium and activation of platelets further triggered thrombosis and fibrinoid necrosis in small vessels and capillaries and resulted in the morphologic changes characteristic of thrombotic microangiopathy. [14],[15] Other factors such as chronic hypertension, arteriolosclerosis and low cholinesterase activity may also be involved in some cases.

In most cases, a history of cocaine abuse is not available. A high index of clinical suspicion is necessary when patients have renal failure associated with significantly high blood pressure and poor response to conventional treatment. Serum and urine testing for cocaine and cocaine metabolites are indicated in this clinical situation. Otherwise, the main renal lesion associated with cocaine use can be infarct, necrosis or myoglobinuria-related injury. The renal lesion can also be an acute tubular necrosis as a result of vaso-constriction or possibly as a direct toxic effect on the proximal tubular cells by cocaine metabolites. [16],[17],[18]

We conclude that cocaine-mediated endothelial injury and platelet activation may play important pathogenetic roles in cocaine users who develop malignant hypertension associated with thrombotic microangiopathy. Clinicians need to be aware of this rare feature of cocaine intoxication.

 
   References Top

1.
Zimmerman JL. Cocaine intoxication. Crit Care Clin 2012;28:517-26.  Back to cited text no. 1
    
2.
Gu X, Herrera GA. Thrombotic microangiopathy in cocaine abuse-associated malignant hypertension: Report of 2 cases with review of the literature. Arch Pathol Lab Med 2007;131: 1817-20.  Back to cited text no. 2
    
3.
Solano Remírez M, Velilla Alcubilla JP, Alvarez Frías MT. Acute intoxication due to cocaine. Review of one case. An Med Interna 2006;23:31-3.  Back to cited text no. 3
    
4.
Zafar H, Vaz A, Carlson RW. Acute complications of cocaine intoxication. Hosp Pract 1997;32:167-70, 175-7, 181.  Back to cited text no. 4
    
5.
Kuhn FE, Johnson MN, Gillis RA, Visner MS, Schaer GL. Effect of cocaine on the coronary circulation and systemic hemodynamics in dogs. J Am Coll Cardiol 1990;16:1481-91.  Back to cited text no. 5
    
6.
Furaz K, Bernis Carro C, Cirugeda García A, Pérez de José A, Sánchez Tomero JA. Renal infarction and acute renal failure induced by cocaine. Nefrologia 2008;28:347-9.  Back to cited text no. 6
    
7.
Van der Woude FJ. Cocaine use and kidney damage. Nephrol Dial Transplant 2000;15: 299-301.  Back to cited text no. 7
    
8.
Jaffe JA, Kimmel PL. Chronic nephropathies of cocaine and heroin abuse: A critical review. Clin J Am Soc Nephrol 2006;1:655-67.  Back to cited text no. 8
    
9.
el-Hayek BM, Nogué S, Alonso D, Poch E. Rhabdomyolysis, compartment syndrome and acute kidney failure related to cocaine consume. Nefrologia 2003;23:469-70.  Back to cited text no. 9
    
10.
Picazo Sánchez M, Cuxart Pérez M, Martín Romero F, Sans Lorman R. Cocaine use, high blood pressure and chronic kidney disease. Nefrologia 2010;30:706-7.  Back to cited text no. 10
    
11.
Thakur V, Godley C, Weed S, Cook ME, Hoffman E. Case reports: Cocaine-associated accelerated hypertension and renal failure. Am J Med Sci 1996;312:295-8.  Back to cited text no. 11
    
12.
Volcy J, Nzerue CM, Oderinde A, HewanIowe K. Cocaine-induced acute renal failure, hemolysis, and thrombocytopenia mimicking thrombotic thrombocytopenic purpura. Am J Kidney Dis 2000;35:E3.  Back to cited text no. 12
    
13.
Abd El-Rahman AM, Ammar H. Cocaineinduced acute hepatitis and thrombotic microangiopathy. JAMA 2005;293:2715-6.  Back to cited text no. 13
[PUBMED]    
14.
Jeffcoat AR, Perez-Reyes M, Hill JM, Sadler BM, Cook CE. Cocaine disposition in humans after intravenous injection, nasal insufflation (snorting), or smoking. Drug Metab Dispos 1989;17:153-9.  Back to cited text no. 14
    
15.
Lange RA, Hillis LD. Cardiovascular complications of cocaine use. N Engl J Med 2001; 345:351-8.  Back to cited text no. 15
    
16.
Togna G, Tempesta E, Togna AR, Dolci N, Cebo B, Caprino L. Platelet responsiveness and biosynthesis of thromboxane and prostacyclin in response to in vitro cocaine treatment. Haemostasis 1985;15:100-7.  Back to cited text no. 16
[PUBMED]    
17.
Schnetzer GW 3rd. Platelets and thrombogenesis - Current concepts. Am Heart J 1972;83:552-64.  Back to cited text no. 17
    
18.
Debien B, Clapson P, Lambert E, Lenoir B, Perez JP, Pats B. Acute cardiovascular complications of cocaine. About two case reports. Ann Fr Anesth Reanim 2006;25:397-400.  Back to cited text no. 18
    

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Correspondence Address:
Rais Lamia
Nephrology Department, La Rabta Hospital, Jabbari, 1007, Tunis
Tunisia
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DOI: 10.4103/1319-2442.174195

PMID: 26787585

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    Abstract
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