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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2018  |  Volume : 29  |  Issue : 4  |  Page : 971-975
Acute renal infarction induced by heavy marijuana smoking


Department of Nephrology, King Fahd University Hospital, Alkhobar, Saudi Arabia

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Date of Submission26-Jul-2017
Date of Acceptance03-Sep-2017
Date of Web Publication28-Aug-2018
 

   Abstract 

Acute renal infarction usually occurs in patients with severe atherosclerosis or valvular heart disease. We here report a 42-year Saudi male who presented with severe abdominal pain nausea and vomiting associated with hematuria, after heavy smoking of marijuana. Computed tomography abdomen revealed bilateral renal infarction. Serum anti phospholipids antibody and anti-cardio lipid antibody were positive. To the best of our knowledge, the association between marijuana and secondary lupus anticoagulant-induced renal infarction has not been reported previously.

How to cite this article:
Al-Hwiesh AK, Bahbhani H, Alhwiesh A, Saad I, AlMohama F. Acute renal infarction induced by heavy marijuana smoking. Saudi J Kidney Dis Transpl 2018;29:971-5

How to cite this URL:
Al-Hwiesh AK, Bahbhani H, Alhwiesh A, Saad I, AlMohama F. Acute renal infarction induced by heavy marijuana smoking. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2019 Dec 9];29:971-5. Available from: http://www.sjkdt.org/text.asp?2018/29/4/971/239652

   Introduction Top


The two major causes of renal embolic disease are thromboembolic (clot emboli) and athero-emboli (cholesterol emboli). The former usually originate from a thrombus in the heart or aorta, whereas the latter occurs in patients with the erosive atheromatous disease, most often after aortic manipulation.[1],[2] In situ thrombosis of a stenotic renal artery is a less common cause of renal infarction.[3] Clot emboli causes clinical renal infarction by completely occluding a renal artery or branch vessel. In comparison, atheroemboli are small, irregularly-shaped, and no distensible, leading to incomplete vascular occlusion or occlusion of very small vessels; thus, distal ischemia rather than infarction usually occurs. Most reports of renal infarction due to clot emboli are in patients with atrial fibrillation, although many patients also have diffuse atherosclerosis.[2],[4] The major sources of clot embolism include the left atrium or left atrial appendage in atrial fibrillation, a left ventricular thrombus in patients with myo-cardial infarction, and thrombo-emboli originating from complex plaque in the aorta.[2],[4] The reported incidence of renal thromboembolism in patients with atrial fibrillation was 2%.[5] Other potential embolic sources include valvular vegetations in infective endocarditis, and rare tumor and fat emboli and paradoxical embolism through a patent foramen ovale.[6]

Renal artery occlusion may also result from renal artery thrombosis (typically superimposed on the preexisting atherosclerotic renovascular disease or following a traumatic intimal tear), spontaneous or iatrogenic renal artery or aortic dissection, or as a complication following endovascular (aortic or renal) intervention.[3],[7],[8],[9],[10],[11] In addition, acute thrombosis has been described with cocaine, marijuana and the antiphospho-lipid syndrome. Our patient presented with severe abdominal pain, nausea, vomiting, and hematuria, discovered to have bilateral renal infarction and secondary antiphospholipid syndrome induced by heavy marijuana smoking.

To the best of our knowledge, this is the first case report of such association. Marijuana as a risk factor for secondary lupus anticoagulant needs to be considered.


   Case Report Top


A 34-year-old Saudi male reported to our hospital with a history of the left flank pain of two weeks duration. The pain was colicky in nature, radiating to groin on and off, with no specific aggravating or relieving factors and was associated with nausea, vomiting, dysuria, frequency, and hematuria. The pain was so severe to the limit he could not carry out his usual activities. There was no history of fever, chills, or rigors. He gave a history of anorexia and weight loss of about 5 kg during the preceding four weeks. No previous history of any similar episode or history of renal stone or gouty arthritis, but he gave a history of marijuana smoking on a daily basis for four weeks. There was no history of arthritis, skin rash, Reynaud phenomena or previous history of deep vein thrombosis. No history of chest pain, palpitation, orthopnea, or paroxysmal nocturnal dyspnea. He was seen at the emergency room where he was diagnosed with renal colic and was send home on supportive treatment. One week later, he reported with severe bilateral loin pain radiating to the groins associated with nausea and vomiting.

Clinical examination revealed a young male in distress with pain, conscious and oriented to time, place, and person. Vital signs showed that he was afebrile with blood pressure 190/90 mm Hg, pulse 90/min regular, respiratory rate 22/min. The chest was clear and cardiovascular system normal S1 and S2 no add sound or murmur.

Abdomen showed diffuse abdominal tenderness but no organomegaly. There was bilateral renal angle tenderness with bilateral renal bruit. Bowel sounds were normal, lower limbs showed no edema but had weak peripheral pulses bilaterally, fundoscopy showed grade two hypertensive retinopathy. He was admitted with the differential diagnosis of possible renal infarction possibly due to polyarteritis nodosa or Takayasu arteritis or acute mesenteric ischemia.

Investigations showed: White blood cells (WBC) 17.4, hemoglobin 13.5 g/dL, platelet 229, blood urea nitrogen 21, serum creatinine 2 mg/dL, serum sodium 140 mEq/L, potassium 4 mEq/L, CO3 22 mEq/L, anion gap 13, total protein 6 g/dL, albumin 2 g/dL, SGOT 56, SGPT 119, LDH 1338, creatinin phosphokinase 600, and GGTP 57.

The urine analysis revealed pH 6, protein 30 mg/dL, red blood cell 1–2 HPF, WBC 1–2, and under microscopy few granular casts. ECG and echcocardiogram was normal. Abdominal computed tomography (CT) scan [Figure 1] and [Figure 2] showed multiple wedge-shaped hypodensity area seen in both kidneys more in the left one, feature suggestive of renal infarction. Urine was positive for cannabis, antinuclear antibody (ANA) was positive 1:160, antidouble stranded DNA negative, lupus anticoagulant was positive, antiB2 glycoprotein IGM and IGg were positive, c3, c4, protein S, protein C, and antithrombin III were negative. Hepatitis C, B, HIV, and syphilis were all negative. The patient was started on amlor 10 mg, codiovan 95.5 mg, warfarin, and aspirin and hydroxychloroquine and we were discharged in a stable condition. Six months later after stopping marijuana, repeated tests for lupus anticoagulant, antiB2 glycoprotein, and ANA remained negative.
Figure 1: CT scan showing multiple wedge-shaped hypodensity area.

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Figure 2: CT scan showing bilateral wedge shape hypo density area seen in both kidney more in left one

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   Discussion Top


Patients with acute renal infarction usually present with persistent abdominal, flank, or low-back pain. Detection can be delayed or missed, because the condition is rather uncommon and its clinical presentations are nonspecific. Many patients have a history of conditions associated with a high risk of thromboembolism. Atrial fibrillation, previous embolism, and valvular or ischemic heart disease are the usually encountered major risk factors for acute renal infarction.[12],[13],[14] These risk factors generally are recognized early, at the time of history taking or during clinical examination. However, acute renal infarction also has been associated with rare conditions. These include trauma, hereditary and acquired clotting disorders, cocaine use, vessel anomalies such as fibromuscular dysplasia or hereditary diseases such as Marfan syndrome or Ehlers-Danlos syndrome. Other less recognized conditions are medical interventions such as surgery for valve replacement, kidney transplantation, endovascular catheterization, and application of intraluminal stents, and also, malignant disease.[15],[16]

The diagnosis of acute renal infarction is usually based on clinical findings that are rather nonspecific, but with reasons for increased risk for thromboembolism,[17],[18] a profile that was present in our patient. Even if at this point a physician did not consider acute renal infarction, additional laboratory results such as hematuria and elevated LDH should suggest the possible diagnosis of acute renal infarction.

Urinalysis by dipstick is a simple screening test for many renal diseases. The sensitivity of this test to detect hematuria is high in contrast to a low specificity because of cross-reaction in the presence of myoglobinuria.[18] Domanovits et al[1] reported that hematuria was present at admission in 74% of their patients, but in another 11% the test became positive within the next 24 h. Consequently, serial urinalysis within the first 24 h of pain onset should be performed to increase its diagnostic value.

Serum LDH as a characteristic marker for cell necrosis is known to be elevated in patients with acute renal infarction.[17],[18],[19],[20] As serum LDH is highly sensitive but not specific, other causes of LDH elevation, such as acute myocardial infarction, tumor, mesenteric embolism, and hemolysis, must be excluded as soon as possible. Spirsal (helical) CT without contrast is usually the preferred initial test for flank pain, being the gold standard for the diagnosis of kidney and ureteral stones which are much more common than renal infarction.[16] If there is no evidence of stone disease on unenhanced spiral CT, an enhanced CT scan should be performed to assess for renal infarction. The classic finding is a wedge-shaped perfusion defect. If CT is indeterminate, a radioisotope scan may show a segmental or generalized decrease in renal perfusion. Ultrasonography is much less sensitive. The sensitivity of these imaging procedures was addressed in a series of 44 patients with atrial fibrillation and a diagnosis of embolic renal infarction.[2] The sensitivity was 97% (36/37) with the renal radioisotope scan, 80% (12/15) with contrast-enhanced CT, and only 11% with renal ultrasound.[2]

The optimal treatment for renal infarction due to thromboembolic, in situ thrombosis, or renal artery dissection is uncertain, given the absence of comparative studies. Reported approaches include anticoagulation, endovascular therapy (thrombolysis/thrombectomy with or without angioplasty),[20],[21],[22],[23],[24],[25],[26] and open surgery. Reperfusion therapies should only be considered in patients who do not yet have atrophy of the affected kidney on imaging studies, and who do not have prolonged duration of occlusion. A small kidney on the affected side suggests that there has been prolonged ischemia and collateral circulation may have formed, thus decreasing the potential benefits of correcting the renal artery occlusion; prolonged acute ischemia reduces the likelihood that there will be viable tissue. Our patient was managed with anticoagulation and good blood pressure control one year later his blood serum creatinine was 1.7 mg/dL and repeated renal CT was normal. Repeated tests for lupus anticoagulant and B2 glycoprotein six months after marijuana was stopped came to be negative, so we concluded that marijuana as risk factors of secondary lupus anticoagulant induce renal infarction to need to be considered.


   Acknowledgment Top


The authors are pleased to express their great thanks and appreciation to the staff nurses the Intensive Care Unit and the male medical ward for their valuable support during the patient's hospitalization

Conflict of interest: None declared.

 
   References Top

1.
Domanovits H, Paulis M, Nikfardjam M, et al. Acute renal infarction. Clinical characteristics of 17 patients. Medicine (Baltimore) 1999;78: 386-94.  Back to cited text no. 1
    
2.
Hazanov N, Somin M, Attali M, et al. Acute renal embolism. Forty-four cases of renal infarction in patients with atrial fibrillation. Medicine (Baltimore) 2004;83:292-9.  Back to cited text no. 2
    
3.
Paris B, Bobrie G, Rossignol P, et al. Blood pressure and renal outcomes in patients with kidney infarction and hypertension. J Hypertens 2006;24:1649-54.  Back to cited text no. 3
    
4.
Tunick PA, Nayar AC, Goodkin GM, et al. Effect of treatment on the incidence of stroke and other emboli in 519 patients with severe thoracic aortic plaque. Am J Cardiol 2002;90: 1320-5.  Back to cited text no. 4
    
5.
Frost L, Engholm G, Johnsen S, et al. Incident thromboembolism in the aorta and the renal, mesenteric, pelvic, and extremity arteries after discharge from the hospital with a diagnosis of atrial fibrillation. Arch Intern Med 2001;161: 272-6.  Back to cited text no. 5
    
6.
Carey HB, Boltax R, Dickey KW, Finkelstein FO. Bilateral renal infarction secondary to paradoxical embolism. Am J Kidney Dis 1999; 34:752-5.  Back to cited text no. 6
    
7.
Cosby RL, Miller PD, Schrier RW. Traumatic renal artery thrombosis. Am J Med 1986;81: 890-4.  Back to cited text no. 7
    
8.
Krämer SC, Seifarth H, Pamler R, et al. Renal infarction following endovascular aortic aneurysm repair: Incidence and clinical consequences. J Endovasc Ther 2002;9:98-102.  Back to cited text no. 8
    
9.
Ivanovic V, McKusick MA, Johnson CM 3rd, et al. Renal artery stent placement: Complications at a single tertiary care center. J Vasc Interv Radiol 2003;14:217-25.  Back to cited text no. 9
    
10.
Böckler D, Krauss M, Mansmann U, et al. Incidence of renal infarctions after endo-vascular AAA repair: Relationship to infra-renal versus suprarenal fixation. J Endovasc Ther 2003;10:1054-60.  Back to cited text no. 10
    
11.
Stawicki SP, Rosenfeld JC, Weger N, Fields EL, Balshi JD. Spontaneous renal artery dissection: Three cases and clinical algorithms. J Hum Hypertens 2006;20:710-8.  Back to cited text no. 11
    
12.
Krishnan P, Anandh U, Fernandes DK, Somiah S, Vincent L. Renal failure in a patient with primary antiphospholipid syndrome. J Assoc Physicians India 2002;50:964-6.  Back to cited text no. 12
    
13.
Bolderman R, Oyen R, Verrijcken A, Knockaert D, Vanderschueren S. Idiopathic renal infarction. Am J Med 2006;119:356.e9-12.  Back to cited text no. 13
    
14.
Bemanian S, Motallebi M, Nosrati SM. Cocaine-induced renal infarction: Report of a case and review of the literature. BMC Nephrol 2005; 6:10.  Back to cited text no. 14
    
15.
Rosenberger C, Griethe W, Gruber G, et al. Cellular responses to hypoxia after renal segmental infarction. Kidney Int 2003;64:874-86.  Back to cited text no. 15
    
16.
Lumerman JH, Hom D, Eiley D, Smith AD. Heightened suspicion and rapid evaluation with CT for early diagnosis of partial renal infarction. J Endourol 1999;13:209-14.  Back to cited text no. 16
    
17.
Lessman RK, Johnson SF, Coburn JW, Kaufman JJ. Renal artery embolism: Clinical features and long-term follow-up of 17 cases. Ann Intern Med 1978;89:477-82.  Back to cited text no. 17
    
18.
Korzets Z, Plotkin E, Bernheim J, Zissin R. The clinical spectrum of acute renal infarction. Isr Med Assoc J 2002;4:781-4.  Back to cited text no. 18
    
19.
London IL, Hoffsten P, Perkoff GT, Pennington TG. Renal infarction. Elevation of serum and urinary lactic dehydrogenase (LDH). Arch Intern Med 1968;121:87-90.  Back to cited text no. 19
    
20.
Winzelberg GG, Hull JD, Agar JW, Rose BD, Pletka PG. Elevation of serum lactate dehydro-genase levels in renal infarction. JAMA 1979; 242:268-9.  Back to cited text no. 20
    
21.
Blum U, Billmann P, Krause T, et al. Effect of local low-dose thrombolysis on clinical outcome in acute embolic renal artery occlusion. Radiology 1993;189:549-54.  Back to cited text no. 21
    
22.
Moyer JD, Rao CN, Widrich WC, Olsson CA. Conservative management of renal artery embolus. J Urol 1973;109:138-43.  Back to cited text no. 22
    
23.
Steckel A, Johnston J, Fraley DS, et al. The use of streptokinase to treat renal artery throm-boembolism. Am J Kidney Dis 1984;4:166-70.  Back to cited text no. 23
    
24.
Salam TA, Lumsden AB, Martin LG. Local infusion of fibrinolytic agents for acute renal artery thromboembolism: Report of ten cases. Ann Vasc Surg 1993;7:21-6.  Back to cited text no. 24
    
25.
Rouvière O, Berger P, Béziat C, et al. Acute thrombosis of renal transplant artery: Graft salvage by means of intra-arterial fibrinolysis. Transplantation 2002;73:403-9.  Back to cited text no. 25
    
26.
Cheng BC, Ko SF, Chuang FR, et al. Successful management of acute renal artery thrombo-embolism by intra-arterial thrombolytic therapy with recombinant tissue plasminogen activator. Ren Fail 2003;25:665-70.  Back to cited text no. 26
    

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Correspondence Address:
Prof. Abdullah K Al-Hwiesh
Department of Nephrology, King Fahd University Hospital, Alkhobar
Saudi Arabia
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DOI: 10.4103/1319-2442.239652

PMID: 30152437

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    Abstract
   Introduction
   Case Report
   Discussion
   Acknowledgment
    References
    Article Figures
 

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