Journal of The Association of Physicians of India ■ Vol. 66 ■ October 201880

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Bilateral Calcified Renal Artery Aneurysms: Not every Calcification is a Calculus!Nirmal Thampi John

Professor, Department of Urology, Christian Medical College, Vellore, Tamil NaduReceived: 20.03.2017; Accepted: 18.09.2017

Fig. 1: Plain radiograph of the abdomen showing “ring-like” calcification in both renal regions

Fig. 2: CT angiography showing bilateral calcified saccular renal artery aneurysms

Case Report

A 59 year old postmenopausal lady presented with back pain. She

had hypertension, well controlled on a single antihypertensive and a normal renal function. Plain radiograph (Figure 1) showed “ring-like” calcification in the

region of her kidneys. CT angiography revealed bilateral calcified saccular renal artery aneurysms (RAA) <2cms in size, arising from the segmental vessels at the hilum (Figure 2). Colour Doppler did not show any evidence of renal artery stenosis and renogram showed bilateral normal perfusion and function. Considering the low risk of complications in this patient, she was managed conservatively and was advised regular blood pressure monitoring and yearly follow up with imaging.

The incidence of RAA is estimated to be around 0.09-0.3% with only a fourth of these being bilateral. Poutasse1 had described 4 types of RAA: saccular, fusiform, dissecting and intrarenal; with the saccular type accounting for >75%.

Imaging is crucial for the diagnosis of RAA and presence of “ring-like” calcification on a plain abdominal radiograph should alert the physician.

As calcification in RAA is seen in >50% of the cases, further imaging is essential to dist inguish i t from renal calculi2 prior to embarking on therapy like extracorporeal shockwave lithotripsy. Angiography being the gold standard, affords a 100% diagnostic rate.3 However, non-invasive imaging like CT and MR angiography (MRA) are ideal with sensitivity and specificity of MRA being 78% and 100% respectively.

Majority of the RAA are small and asymptomatic but assume cl inical significance when associated with hypertension or impending rupture.4 Factors which may predispose to rupture include size > 2cms, absent or incomplete calcification, uncontrolled h y p e r t e n s i o n a n d p r e g n a n c y . Endovascular treatment with stenting is the treatment of choice in most cases, with high rates of technical success and negligible complication and recurrence rates.5

References1. Poutasse EF. Renal artery aneurysms.  J Urol  1975; 113:443-9.

2. Rha SE, Byun JY, Jung SE, Oh SN, Choi YJ, Lee A, Lee JM. The renal sinus: pathologic spectrum and multimodality imaging approach. Radiographics 2004; 24 suppl 1:S117–131.

3. Wason SE, Schwaab T. Spontaneous rupture of a renal artery aneurysm presenting as gross hematuria. Rev Urol 2010; 12:e193–6.

4. Novick AC. Renal arterial aneurysms and arteriovenousfistulas. In: Novick AC, Straffon RA, ed. Vascular Problems in Urologic Surgery. Philadelphia; WB Saunders: 1982:189-204.

5. Sédat J, Chau Y, Baque J. Endovascular treatment of renal aneurysms: a series of 18 cases. Eur J Radiol 2012; 81:3973–8.

Journal of The Association of Physicians of India ■ Vol. 66 ■ October 2018 81

“Amyloid Spells” - An Unusual TIA MimicAradhana Chauhan1, Pradeep G Divate2

1Neurology Resident, 2Senior Neurologist, Sahyadri Speciality Hospital, Pune, MaharashtraReceived: 10.08.2016; Accepted: 13.06.2017

Fig. 1 : (a) SWI shows blooming in right fronto-parietal & left anterior frontal region suggestive of SAH; (b) FLAIR sequences show hyperintensity in the same areas; (c) Non enhanced CT brain shows high attenuation acute subarachnoid blood within right frontal region.

An eighty-eight years old gentleman p r e s e n t e d t o t h e e m e r g e n c y

department with two episodes of left sided paresthesias , grip weakness and slurred speech which resolved completely in two hours. His past history was notable for IHD for which he was on dual antiplatelets. There was no h/o injury to head. The examination was unremarkable save for mild left hemi-hypoesthesia. His MRI showed right fronto-parietal and left anterior frontal Subarachnoid Hemorrhage (SAH) which was blooming on SWI (Susceptibil i ty weighted imaging) images (Figure 1a). FLAIR sequences (Figure 1b) showed hyperintensity in the same areas. Non-enhanced CT brain (Figure 1c) showed high attenuation acute SAH within right frontal region. His coagulat ion profi le , EEG and MRA were normal. The antiplatelets were withheld and he was initiated on Topiramate. There were no such further episodes on follow up after one month.

Cerebra l Amylo id Angiopathy (CAA) occurs due to deposition of beta amyloid in small and medium sized superficial cortical and leptomeningeal

vessels;1 vascular disruption leads to micro bleeds, Lobar Hemorrhages (LH) and Cortical Superficial Siderosis (CSS); less commonly the amyloid may cause inflammation of the vessels leading to amyloid angiitis.

In pat ients present ing with an acute convexity SAH or CSS, recent or prior head trauma needs be excluded. Reversible cerebral vasoconstriction syndrome occurs most commonly in younger patients and is associated with thunder clap headache. Other d i f ferent ia l s for acute convex i ty SAH are- bleeding diathesis due to thrombocytopenia or coagulopathy, infect ious aneurysms, transmural arterial dissection, cerebral venous s inus thrombosis , in fec t ious and noninfectious vasculitis , Posterior Reversible Encephalopathy Syndrome, cavernous angioma and dural arterio- venous fistula.

C A A r e l a t e d T r a n s i e n t F o c a l Neurological Episodes (TFNE) can resemble transient ischemic attacks, migraine auras or seizures.2,3 These CAA related TFNE are associated with an early risk of symptomatic LH,

hence requiring aggressive treatment of hypertension and avoidance of antithrombotic exposure.3

S o m e r e p o r t s s u g g e s t t h a t antiepileptics and migraine preventives may s top amyloid spe l l s . In one small study four out of six patients with amyloid spells responded to antiepileptic therapy alone.4

References1. Yamada M. Cerebral amyloid angiopathy: emerging

concepts. J Stroke 2015; 17:17–30.

2. Greenberg SM, Vonsattel JP, Stakes JW, Gruber M, Finklestein SP. The clinical spectrum of cerebral amyloid angiopathy : presentations without lobar hemorrhage. Neurology 1993; 43:2073-9.

3. Charidimou A, Peeters A, Fox Z, Gregoire SM, Vendermeeren Y, Laloux P, et al. Spectrum of transient focal neurological episodes in cerebral amyloid angiopathy: multicentre magnetic resonance imaging cohor t study and metaanalysis. Stroke 2012c; 43:2324-30.

4. Roch JA, Nighoghossian N, Hermier M, et al. Transient neurologic symptoms related to cerebral amyloid angiopathy: usefulness of T2*-weighted imaging. Cerebrovasc Dis 2005; 20:412-14.