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Sir, The relationship of human parvovirus B 19 (HPB 19) with renal disease is rare, with only two studies describing glomerulonephritis in patients with erythema infectiosum and sickle cell disease (SCD) [1]. We describe a case of acute nephritis associated with HPB 19, which, to the best of our knowledge, is the first case reported without associated SCD. A 54-year-old Caucasian woman was admitted to a medical ward with a 3-week history of generalized malaise, arthralgia and a widespread macular rash. She was in frequent contact with her grandson, who had been recently diagnosed with erythema infectiosum (fifth disease). She had a past history of Raynaud’s disease, migraine, sinusitis and breast carcinoma, previously treated with surgery and radiotherapy. Her only long-term medication was tamoxifen. There was no family history of autoimmune or renal disease. Although she was discharged, the patient failed to improve, and was subsequently re-admitted to our renal unit with haematuria and proteinuria. On examination, she was apyrexial, tachycardic and hypertensive, with a blood pressure of 163/90mmHg. There was a widespread macular rash with a mottled appearance, consistent with erythema infectiosum. Although previously normal, the patient’s serum creatinine was elevated to 195mmol/l. There was a normochromic normocytic anaemia with haemoglobin of 9.5 g/dl. Serum ANCA, anti-GBM and ANA titres were negative, with a weakly positive dsDNA antibody. Complement C3 and C4 levels were reduced at 0.34 g/l (normal range: 0.70–1.70 g/l) and 0.10 g/l (normal range: 0.18–0.58 g/l) respectively. Other investigations showed rheumatoid factor increased at 43 IU/ml (normal range 20 IU/ml) and creatinine clearance reduced to 15 ml/min (normal range: 60–140ml/min) with a proteinuria of 0.97 g/24 h (normal range: 0.15 g/24 h). The C-reactive protein was elevated at 30mg/l (normal range: <5mg/l) with an ESR of 26mm/h (normal range: <20mm/h). Renal ultrasonography, immunoglobulins, paraproteinaemia and cryoglobulins were normal. Subsequently, polymerase chain reaction (PCR) for HPB 19 was positive, confirming current infection. Her condition improved with symptomatic treatment. The laboratory abnormalities, including urinary protein, microscopic haematuria and rash improved within a few days; renal functions and complement levels returned to the normal range and her dsDNA became negative. A link between renal disease and human parvovirus was first implied by Markenson et al. [2], who described two siblings with SCD and hypoplastic crises, who developed nephrotic syndrome. Similarly, Wierenga et al. [1] described seven patients with homozygous SCD who showed proliferative segmental glomerulonephritis with proteinuria and nephritic syndrome after aplastic crisis induced by HPB 19. There have recently been several reports indicating that HPB 19 infection may elicit symptoms and laboratory findings resembling those of systemic lupus erythematosus, such as polyarthritis, positive antinuclear antibodies and hypocomplementaemia [3]. However, these reports have not demonstrated renal abnormalities as a complication of the disease. Although HPB 19 infection has been reported to be associated with vasculitis including Henoch–Schlonlein purpura [4] and necrotizing vasculitis resembling polyarteritis nodosa [5], there has been no previous accounts of involvement of the renal vasculature. Our patient with confirmed erythema infectiosum suffered an acute nephritis manifesting as acute renal failure with an active urinary sediment. The temporal relationship between the two conditions strongly suggests causality. Nephritis with HPB 19 infection has not been previously reported in patients without SCD. As the patient’s condition improved spontaneously, renal biopsy to confirm a glomerulonephritis was not justified. In conclusion, infection with HPB 19 should be considered as a possible cause of acute nephritis in adults. This usually occurs in patients with SCD but can also occur in its absence.

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