Abstract

Introduction: Renal disease due to infective endocarditis (IE) is well established, with the earliest reports of glomerular lesions published over 100 years ago. Although initially believed to be primarily embolic it later became clear that over 80% of cases represented focal, segmental, or diffuse proliferative glomerulonephritis (GN) with prominent endo-capillary proliferation and occasional infiltrating leukocytes. However, the literature describing nephritis associated with IE still relies heavily on autopsy studies conducted in the pre- and early post-antibiotic era or small renal biopsy studies from the 1970s. Over the past decades, IE outcomes have not improved, and infection rates are steadily increasing.

Case Report: This thirty seven year old female patient came to OPD with chief complaints of facial puffiness, abdominal distension, swelling of feet, numbness of head since one month duration. She also complained of shortness of breath (SOB) which was insidious onset and gradually progressive NYHA Class 2. She was non-diabetic and non-hypertensive. She was anemic with bilateral pitting edema. She also had significant thyromegaly. Her cardiovascular examination revealed a regular, normo-volemic pulse at a rate of 120 bpm, blood pressure of 170/100 mm of Hg. On auscultation, both heart sounds were normally audible with early diastolic high pitched murmur heard best in left 2ndintercostal space during expiration. 2-dimensional echocardiography showed mild Aortic regurgitation with vegetation on the aortic valve. Her routines showed she was anemic, proteinuric (2400mg in 24 hr urine) with hypo-albuminemia (albumin:1.4g/l), hypothyroid, and hyperlipidemic (total cholesterol:408mg/dl). Her renal parameters were suggestive of pre-renal azotemia with serum urea of 40mg/dl. These findings led to a diagnosis of nephrotic syndrome. Her blood and urine culture showed negative findings. She underwent renal biopsy. Electron microscopic study of a renal biopsy specimen was suggestive of Focal Segmental Glomerulosclerosis. Her collagen profile was not suggestive of any collagen vascular disease.

She was started on immunosuppressive therapy for recurrent relapses. She had an episode of short duration weakness of left upper limb from which she recovered spontaneously within 10 minutes. Two-dimensional echocardiography and Transesophageal echocardiography showed healed vegetation over non-coronary cusp of aortic valve. Nephrologist opinion was taken regarding the nephrotic syndrome and healed vegetation over non-coronary cusp.

Conclusion: Nephrotic syndrome being immunodeficient state may lead to infective endocarditis in underlying valvular predisposing condition. Complementary to this subacute endocarditis may lead to nephrotic range proteinuria due to deposition of complements in glomeruli leading to massive proteinuria in some patients.

In this case, the patient presented with nephrotic syndrome with recurrent remissions and relapses which are quite a rare entity and further cases have to be studied regarding the implications of this complication in the management of nephrotic syndrome and infective endocarditis.