A case of acute tubulointerstitial nephritis following administration of the Oxford-AstraZeneca COVID-19 vaccine: a case report.

BACKGROUND: More than 4 billion doses of the Coronavirus disease (COVID-19) vaccine have been administered worldwide but the relationship between the different vaccines and the development of renal disease is unknown. We present a case of tubulointerstitial nephritis following administration of the Oxford-AstraZeneca COVID-19 vaccine. CASE PRESENTATION: A previously fit and well 51-year-old female presented on 27th May 2021 with a one-month history of weight loss, fatigue, nausea, and a metallic taste. She had an acute kidney injury with a creatinine of 484 umol/L. She was on no regular medications and denied taking any over-the-counter or alternative medicines. She had received her first dose of the Oxford-AstraZeneca vaccine on 23rd March 2021 and her second dose on 20th May 2021. A renal biopsy was performed the following day. The 19 glomeruli appeared normal to light microscopy but the tubulointerstitial compartment contained a dense inflammatory infiltrate including many eosinophils. There was widespread acute tubular injury with tubulitis, but no established or longstanding atrophy. A diagnosis was made of an acute tubulointerstitial nephritis. She was commenced on oral prednisolone and her renal function improved. She did not require renal replacement therapy at any time. CONCLUSIONS: To our knowledge, this was the first described case of acute tubulointerstitial nephritis following administration of the Oxford-AstraZeneca COVID-19 vaccine, although a number of cases have emerged more recently. In our case the patient was very fit and well, had no previous past medical history and had not taken any recent prescribed, over-the-counter or alternative medications. The absence of these provoking factors in our case makes the vaccine the most likely explanation for the development of tubulointerstitial nephritis although the pathophysiology behind this remains unknown. Given the unprecedented number of vaccinations being delivered around the world, nephrologists should be aware of this possible link although more research into the topic is required.

Painless expanding facial swelling.

A previously healthy 11-year-old girl sustained a mosquito bite on her right cheek while on holiday in rural Bangladesh. A painless lump developed at the site, and over the ensuing 2 months gradually expanded. She was otherwise completely asymptomatic; there was no family history of note. On examination, there was obvious swelling affecting the right cheek and visible abnormality of the upper gum with displacement of the right upper central incisor (figure 1).

Mesangiocapillary glomerulonephritis complicating pulmonary tuberculosis.

Glomerulonephritis in tuberculosis may be a direct manifestation of renal infection or a result of immune-complex deposition complicating extra-renal infection, such as in pulmonary tuberculosis. A 17-year-old adolescent boy from Somalia was found to have pulmonary tuberculosis during routine health screening performed on entering Malta, with computed tomography of the chest showing scarring and calcification of the left upper lobe, left lower lobe consolidation, and a small left-sided pleural effusion. Five days after starting anti-tuberculous therapy, he developed lower limb and sacral oedema: urinary albumin: creatinine ratio was > 400 µg albumin/mg creatinine, and 24-h urinary protein showed nephrotic-range proteinuria of 4.963 g/day. In view of worsening lower limb, sacral and periorbital oedema and ascites, he was started on oral prednisolone, omeprazole and penicillin V prophylaxis. As heavy proteinuria persisted, a renal biopsy was performed after 8 days of prednisolone treatment, which confirmed the presence of mesangiocapillary glomerulonephritis (MCGN), with electron microscopy showing effacement of the podocytes, with hypercellularity and subendothelial immune deposits, confirming an immune-mediated pathophysiology. Ziehl-Neelsen staining did not reveal acid-fast organisms. The patient received a total of 3 weeks of oral prednisolone with subsequent tailing doses, 2 months of pyrazinamide and ethambutol and 6 months of rifampicin and isoniazid with complete resolution of his clinical and radiological signs, though heavy proteinuria persisted, so he was commenced on oral enalapril. This case highlights the potential association of MCGN with tuberculosis in adolescence. Timely recognition and treatment can prevent progression to chronic kidney disease.

Treatment of renal AA-Amyloidosis associated with human immunodeficiency virus infection: a case report.

We present a case of a young adult male who was treated successfully for renal AA-amyloidosis secondary to human immunodeficiency virus (HIV) infection using highly active anti-retroviral therapy (HAART). He presented with lobar pneumonia, acute kidney injury, nephrotic syndrome and newly diagnosed HIV infection and was initiated on HARRT and haemodialysis. Kidney biopsy was consistent with amyloid deposition of the AA-type. His clinical condition improved gradually and after 10 months of therapy, he regained sufficient excretory function to become dialysis independent. Two years later, he remained well, with a recovered CD4 count and a glomerular filtration rate of 63 mL/min/1.73 m2. Patients with renal AA-amyloidosis typically present with slowly progressive chronic kidney disease, often leading to end-stage kidney disease within months. To our knowledge, this is the first reported case of biopsy proven renal AA-amyloidosis in a newly diagnosed HIV positive patient to present with acute kidney injury leading to dialysis dependence over a period of 2 weeks, which was successfully treated using HAART.