A 67-year-old woman came to the emergency department of our centre referred by her primary care physician with a one-week history of dyspnoea, orthopnoea and oedema in the lower limbs. Her personal history included arterial hypertension, diabetes mellitus treated with oral antidiabetics, dyslipidaemia, permanent atrial fibrillation anticoagulated with acenocoumarol and prosthetic mitral valve replacement 6 years ago due to rheumatic stenosis with severe pulmonary hypertension. It should be mentioned that the patient had no history of known nephrourological pathology, with analytical studies prior to admission showing normal renal function, without proteinuria or sediment alterations. He was admitted to Cardiology with the diagnosis of a first episode of decompensation of heart failure, with no clear trigger.  A transthoracic echocardiogram was performed showing a normal functioning mitral prosthesis, aortic valve calcification and severe right ventricular dysfunction, with no other significant findings. On the third day of admission he presented with a fever peak related to peripheral phlebitis, so blood cultures were taken, the IV was changed and empirical antibiotic therapy with Ceftriaxone was started. In the following 24 hours, the growth of SAMS was confirmed in the blood cultures, and Ceftriaxone was replaced by intravenous Cloxacillin. A transesophageal echocardiogram was performed to rule out infective endocarditis, revealing an anchored vegetative image at the level of the posterolateral mitral annulus and another, smaller, anterolateral filiform image. In view of these findings, a diagnosis of infective endocarditis due to methicillin-sensitive S. aureus (SAMS) on the prosthetic valve was made, and Rifampicin was added to the aforementioned treatment. The patient was assessed by the Cardiac Surgery Department and it was decided to surgically replace the prosthesis. Since then, she has had a long and complicated postoperative period, with initial multi-organ dysfunction in the context of cardiac tamponade that required urgent reintervention. In a situation of severe haemodynamic failure, with no evidence of sepsis and maintaining antibiotic coverage, he developed acute oligoanuric renal function deterioration attributed to hypoperfusion with the need for extra-renal depuration by continuous venovenous haemofiltration for a week.  Urine studies performed at this time showed decreased sodium excretion (FENa < 1%) without proteinuria or sediment alterations. In the following days, haemodynamic recovery is accompanied by a progressive increase in diuresis and improvement in renal function parameters (Crp 0.8 mg/dL), and haemofiltration can be withdrawn. He developed multiple complications during the following months, of which the most relevant are highlighted below. Eight weeks after the operation, he suffered an episode of upper gastrointestinal bleeding, for which an endoscopic study was carried out, revealing millimetric gastric erosions of uncertain origin. Two weeks later, non-pruritic raised petechiae were found on the trunk, extremities, folds and slopes. Coinciding with the above, the urinary sediment showed proteinuria of less than 1 gram per day, with normal renal function (Crp 0.84 mg/dl). Urgent determination of anti-neutrophil cytoplasmic antibodies (ANCAs) and anti-glomerular basement membrane antibodies (anti-GBM) was requested, which were negative. The dermatology department was consulted and a skin biopsy was taken, which was compatible with leukocytoclastic vasculitis, and treatment with Prednisone at a dose of 0.5 mg/kg/day was indicated.  One week later he presented with anaemia without externalisation of bleeding and a chest X-ray showed bilateral de novo interstitial infiltrates.  All this coincided with a new deterioration of renal function (Crp 1.78 mg/dL), oliguria, proteinuria of 850 mg/day, macroscopic haematuria and the presence of dysmorphic red blood cells and haematic and leukocyte casts in the urinary sediment.  Given the suspicion of pulmonary haemorrhage in an anticoagulated patient, fibrobronchoscopy was performed, confirming the presence of fresh haematic debris in both bronchial trees, suggestive of alveolar haemorrhage. Renal function progressively deteriorated, and the patient remained in a situation of oligoanuria and secondary hydrosaline overload, with persistent haematuria and proteinuria. Given the clinical diagnosis of nephritic syndrome with pulmonary haemorrhage, an immunological study was completed, highlighting a decrease in C3 (78.8 mg/dL) and C4 (14.4 mg/dL) levels, the presence of circulating immunocomplexes and positive rheumatoid factor (190 mg/dL), with negative ANAs, antiDNA, ANCAs and antiMBG, as well as negative cryoglobulins. The patient's respiratory condition progressively deteriorated, anticoagulation was discontinued, and it was decided to start treatment with plasmapheresis, oral cyclophosphamide (100 mg/day) and increasing the dose of prednisone (1 mg/kg/day) in view of the renopulmonary syndrome. Prior to the start of the immunosuppressive regimen, blood cultures were taken on several occasions and were persistently negative, although all of them were removed and the patient continued with antibiotherapy. With these measures, there was a slight improvement from the respiratory point of view, both clinically and radiologically, but the progressive deterioration of renal function persisted, again requiring extra-renal depuration by means of continuous venovenous haemofiltration. Finally, as there was no improvement in the following days, a renal biopsy was performed with the suspicion of acute glomerulonephritis related to the infection. The renal biopsy showed areas of increased mesangial matrix and presence of thickening in the membranes of the glomerular capillaries. Direct immunofluorescence techniques showed granular mesangial IgA and C3 fixation, with a predominance of IgA deposits, and therefore compatible with infection-related IgA-dominant glomerulonephritis.  In view of these findings and the extrarenal manifestations characteristic of Henoch-Schönlein purpura, we requested an extension of the immunofluorescence of the skin biopsy, which also showed IgA deposits. All these findings were therefore compatible with IgA-dominant glomerulonephritis related to infective endocarditis due to SAMS with manifestations of Schönlein-Henoch purpura ("Schönlein-Henoch like"). Despite therapeutic measures, the patient had a torpid evolution with massive alveolar haemorrhage and no recovery of renal function, finally leading to exitus.
