A 78 year old man presented with acute renal failure following a prolonged respiratory illness. A renal biopsy demonstrated severe suppurative interstitial nephritis with normal glomeruli. After nine weeks of antibiotics he remained anuric and a second biopsy demonstrated pauci-immune, necrotising glomerulonephritis. His subsequent clinical course was consistent with a diagnosis of Wegener's granulomatosis and antineutrophil cytoplasmic antibodies (ANCA) were detected. This is the first reported case of Wegener's granulomatosis presenting with an isolated tubulointerstitial lesion. (J Clin Pathol 2001;54:787-789)

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A 33-year-old non-diabetic, non-hypertensive man presented with fever followed by respiratory distress for the last 3 days prior to admission. There wasn't any history of chest pain, palpitation, paroxysmal nocturnal dyspnoea. Fever was associated with chills and rigor. On further enquiry the patient revealed that he had been diagnosed with some heart disease in the past and he had similar episodes of fever and respiratory distress.On examination he had tachycardia (120/min), tachypnoea (28/ min), fever (102.8 degree F), central cyanosis [Table/ Fig-1], clubbing [Table/ Fig-2] and coarse crepitations with increased bronchial breath sounds in the right lower zone of the lung suggestive of pneumonic consolidation. Cardiovascular system examination revealed a down and out apex beat (5 th intercostal space, 1.25 cm right of the midclavicular line) with a narrow and fixed split second heart sound. there was no murmur. ABG (arterial blood gas) revealed acidosis with hypoxia and hypercarbia. ECG revealed mild left axis deviation and there was neutrophilic leucocytosis in his peripheral blood (total count-13,400/cu.mm N82L16E2). Chest X ray showed right lower zone consolidation. Other investigations in his blood were within normal limits. Considering the history of some heart disease in childhood and central cyanosis, we performed a transthoracic echocardiography in which there was a septum secundum atrial septal defect (ASD) without any evidence of right to left shunt, pulmonary arterial hypertension or eisenmenger's physiology.Pulmonary artery pressure was 27/12 mmHg; mean 17 mmHg, right atrial pressure 9 mmHg, and left atrial pressure 10 mmHg as evidenced by a right heart catheterisation. Oxygen saturation was 75% in inferior vena cava, 70% in the right atrium, 96% in the pulmonary veins and 86% in the aorta. As we could not account for the central cyanosis in this patient from these reports, we did a bubble contrast echocardiography with agitated saline injection. It revealed that the patient had an ASD but interestingly in this case the Eustachian valve (valve of the inferior vena cava) was over-developed & located so close to the ASD that the jet of deoxygenated blood from the inferior vena cava (IVC) was practically draining into the left atrium [video-1]. The oxygenated blood of the left atrium was thus contaminated by the deoxygenated blood from the IVC thus giving rise to the central cyanosis. The blood from the superior vena cava was draining normally into the right atrium and was going to the right ventricle, as expected. As the flow through the right atrium and ventricle was reduced, there had been no right atrial or ventricular hypertrophy.Therefore, in this patient we made a diagnosis of right lower zone consolidation along with an IVC which is practically draining into the left atrium through a septum secundum ASD. As a result the major portion of the venous inflow to the heart was going to the left atrium directly without being oxygenated, thus giving rise to a functional right-to-left shunt. Cyanosis i...

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