Hydralazine, a vasodilator, is commonly used as an adjunctive treatment for moderate to severe hypertension, heart failure and hypertensive emergencies in pregnancy. Hydralazine-induced lupus was first described in 1953. Clinical presentation ranges from arthralgia, myalgia, petechiae, or rash to single or multiorgan involvement. An occurrence of systemic vasculitis is a rare complication. When presented as the pulmonary–renal syndrome, it could have a rapidly progressive course which can be fatal. Here, we describe a case of hydralazine-associated rapidly progressive glomerulonephritis and pulmonary haemorrhage. We use this case to review the current literature and discuss and highlight the importance of a high degree of clinical acumen, early diagnosis and prompt treatment for better clinical outcomes.

A 58-year-old man with a prior history of coronary artery disease, hypertension, and radical prostatectomy for adenocarcinoma 6 years earlier presented with a 1-week history of headache and nausea, followed by a witnessed generalized tonic-clonic seizure. The history was positive for a 100 pack-year smoking history and an absence of intravenous drug use or sexual promiscuity. The physical examination, after resolution of the postictal state, was remarkable only for a tongue bite. Routine laboratory studies and toxicology screening were normal. An initial noncontrast computed tomography (CT) scan of the brain showed a questionable tiny arachnoid cyst adjacent to the right tentorium and ethmoid sinusitis (Fig 1). A magnetic resonance imaging (MRI) scan with contrast revealed a hypodense area with loss of gray-white differentiation on T1 imaging. Postgadolinium scan showed an enhanced 1.6 ϫ 1.3 cm mass in the left anteromedial temporal lobe (Figs 2A to 2C, arrows). There was also increased signal on T2 and flair images in the surrounding white matter suggestive of edema/mass effect (Figs 2D and 2E, arrows). There was a 0.65-cm area of increased signal on T2 and hypointense flair without enhancement on the postgadolinium measures in the right temporal region, likely representing a subarachnoid cyst. The differential included metastases, primary lymphoma, meningioma, and toxoplasmosis. A CSF

A 30-year-old Caucasian woman with no prior medical history presented with pedal oedema, arthralgias and abdominal pain with diarrhoea, following a respiratory infection. She had mild abdominal tenderness along with a purpuric rash on the extremities and was anaemic. Following initial workup for anaemia and rash, her condition deteriorated with renal impairment, respiratory failure and seizures necessitating ventilatory support, dialysis and steroids. Serologies were negative, and skin biopsy showed leucocytoclastic vasculitis without vascular IgA deposition, and renal biopsy showed subendothelial, mesangial deposits of IgA with C3 indicative of Henoch-Schonlein purpura (HSP). She was treated with steroids, haemodialysis and on 6-month follow-up recovered renal function. We present the case to illustrate that HSP, though rare in adults, can present with multiorgan failure, with renal, pulmonary and central nervous system involvement, and the need for early diagnosis and prompt treatment for rapid clinical recovery.

A 26-year-old Caucasian man with no medical history, except years of oral and intravenous drug abuse, presented with fatigue, shortness of breath, epistaxis and uncontrolled hypertension. He was pale with skin ecchymosis over his thighs and was anaemic, with severe renal failure and metabolic acidosis. Following initial clinical stabilisation of the patient, a renal biopsy was obtained, which showed vascular and glomerular changes consistent with thrombotic microangiopathic injury and advanced glomerulosclerosis. He was treated with antihypertensives and required haemodialysis. He admitted using ‘crystal meth’ regularly for many years, which is likely responsible for his renal failure. We present the case to illustrate methamphetamine-induced renal disease leading to end-stage renal disease and to bring awareness among practising clinicians, ancillary healthcare workers and public health professionals of this often undervalued cause of renal failure, which can be prevented.

Epicardial adipose tissue (EAT) is derived from splanchnic mesoderm, localized anatomically between the myocardium and pericardial visceral layer, and surrounds the coronary arteries. Being a metabolically active organ, EAT secretes numerous cytokines, which moderate cardiovascular morphology and function. Through its paracrine and vasocrine secretions, EAT may play a prominent role in modulating cardiac function. EAT protects the heart in normal physiological conditions by secreting a variety of adipokines with anti-atherosclerotic properties, and in contrast, secretes inflammatory molecules in pathologic conditions that may play a dynamic role in the pathogenesis of cardiovascular diseases by promoting atherosclerosis. Considerable research has been focused on comparing the anatomical and biochemical features of EAT in healthy people, and a variety of disease conditions such as cardiovascular diseases and renal diseases. The global cardiovascular morbidity and mortality in renal disease are high, and there is a paucity of concrete evidence and societal guidelines to detect early cardiovascular disease (CVD) in this group of patients. Here we performed a clinical review on the existing evidence and knowledge on EAT in patients with renal disease, to evaluate its application as a reliable, early, noninvasive biomarker and indicator for CVD, and to assess its significance in cardiovascular risk stratification.