Neuroblastoma Presenting with Acute Kidney Injury, Hyponatremic-Hypertensive-Like Syndrome and Nephrotic Proteinuria in a 10-Month-Old Child

• Main Authors: Giovanni Maria Poggi, Giuliana Fognani, Daniela Cuzzubbo, Antonio Liguori, Massimo Resti, Ivana Pela
• Format: Article
• Language: English
• Published: Karger Publishers 2011-08-01
• Series: Case Reports in Oncology
• Subjects: Neuroblastoma; Proteinuria; Acute kidney injury; Hyponatremic-hypertensive syndrome
• Online Access: http://www.karger.com/Article/FullText/331211

Neuroblastoma is the most common extracranial solid tumor in childhood. Its presenting signs and symptoms may be highly variable, depending on the location of the primary tumor and its local or metastatic diffusion and, rarely, with paraneoplastic syndrome such as opsoclonus-myoclonus-ataxia syndrome and gastrointestinal disturbances, due to autoantibodies or to aberrant secretion of vasoactive intestinal peptide. Herein we describe a 10-month-old child with neuroblastoma presenting with a complex clinical picture characterized by acute kidney injury manifested by renal insufficiency and signs and symptoms of tubulointerstitial damage, with polyuria, polydipsia, glucosuria, aminoaciduria and hypochloremic metabolic alkalosis, and of glomerular damage with heavy proteinuria. Imaging study documented a suprarenal mass enveloping the aorta and its abdominal and renal ramifications and bilaterally renal veins. This clinical picture shows some analogies with the hyponatremic-hypertensive syndrome concerning the renovascular disease; however, in absence of systemic arterial hypertension, the heavy proteinuria and the polyuria could be explained by sectional increased intraglomerular pressure, due to local renal blood vessels constriction. Hypochloremic metabolic alkalosis probably developed because of local production of renin, responsible of renin-angiotensin-aldosterone system activation, but above all because of chloride loss through sweating. The long lasting dehydration, due to vomiting, sweating and polyuria, caused prolonged prerenal failure evolving in proximal tubular damage manifestations.