Procalcitonin and minimal-change nephropathy: a pilot study.

INTRODUCTION Minimal-change nephropathy (MCN) is the most common cause of nephrotic syndrome in childhood. It is generally accepted that MCN emerges by way of cytokine derangement since neither cellular nor immune complex deposits are detected.(1) T-cells and podocytes share a regulatory mechanism that illustrates one possible indirect link between immune responses and podocytes.(2) Despite managing with low-dose steroids given daily or on alternate days, approximately 60% of patients experience five or more relapses, especially if they have intercurrent infections with MCN.(3) Procalcitonin (PCT), a 13-kDa protein, is a precursor of calcitonin that is physiologically synthesised by the C-cells of the thyroid gland, pulmonary neuroendocrine cells (in minute quantities) and especially, peripheral blood mononuclear cells during inflammation and sepsis. Serum PCT has been established as a very accurate and specific marker of severe systemic infection in patients with normal renal function. Current findings suggest that PCT may not only be a valid marker for infection and inflammation but also a pro-inflammatory cytokine-like mediator.(4) This study aimed to assess the levels of PCT in patients with MCN and the role of PCT in the differentiation of MCN relapses due to proteinuria flares co-existent with intercurrent infection. METHODS The records of 34 patients with histopathologically confirmed MCN were retrospectively evaluated. The patients were constituted as three groups: patients with relapse (Group I; n = 26); patients with proteinuria attacks co-existent with intercurrent infection (Group II; n = 28); and patients in remission (Group III; n = 25). For comparison purposes, patients who had infections similar to those in Group II but were nephrologically healthy (Group IV; n = 25) and controls (Group V; n = 25) were prospectively enrolled. Relapse (Group I) was def ined as albuminuria > 300 mg/day, hypoalbuminaemia, hyperlipidaemia and oedema. Proteinuria attacks co-existent with intercurrent infection (Group II) was defined as the co-existence of findings of infection (clinical: fever, cough, sore throat, otitis media, tonsillitis; and laboratory: acute elevations of erythrocyte sedimentation rate [ESR], PCT, C-reactive protein [CRP]) with proteinuria > 300 mg/day and a reduction of proteinuria following antibiotic treatment). Patients in remission (Group III) were recruited from among Group I and II patients during their remission period. Group IV patients or the infection group had coexistent clinical and laboratory findings of infection without any kidney involvement. Patients in Groups IV and V were matched for age and infection site to the other three patient groups. Procalcitonin and minimal-change nephropathy: a pilot study