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Title: Microscopic haematuria in giant cell arteritis
Authors: Vanderschueren, Steven ×
Depoot, I
Knockaert, Daniel
Verbeken, Eric
Zaman, Zahur
Bobbaers, Herman #
Issue Date: Sep-2002
Series Title: Clinical rheumatology vol:21 issue:5 pages:373-7
Abstract: Giant cell arteritis (GCA) is traditionally considered to spare the kidney, although an uncontrolled study reported microscopic haematuria in 10 out of 30 patients with GCA. To study the frequency and the characteristics of microscopic haematuria in GCA, we retrospectively studied 42 patients with biopsy-proven GCA, 39 patients with polymyalgia rheumatica (PMR) and 62 control patients >or=60 years of age, admitted to the general internal medicine unit. Patients with pyuria, significant bacteriuria or a known haematuric disorder were excluded. Microscopic haematuria was defined as the presence of >5 red blood cells (RBC) per high-power field (sediment counts) or of >8 RBC/microl (direct counting). Microscopic haematuria was present at presentation in 47.6% of the GCA patients, versus 17.9% of the PMR patients (P = 0.005) and 21.0% of the control patients (P = 0.008). Urinary RBC were predominantly dysmorphic in all GCA patients in whom RBC morphology was assessed (n = 7). Presenting symptoms, renal function, arterial blood pressure and degree of leukocyturia did not differ significantly between GCA patients with or without haematuria. After the initiation of corticosteroid therapy, microscopic haematuria was no longer detectable in 25 of 35 GCA patients (71.4%). Microscopic haematuria of renal origin is frequent but generally benign in patients with GCA. Its presence, if unassociated with blood pressure elevation or renal function deterioration, helps to rule in rather than to rule out the diagnosis of GCA. In the typical setting invasive urologic and nephrologic work-up may not be warranted.
URI: 
ISSN: 0770-3198
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Translational Cell & Tissue Research
Laboratory for Clinical Infectious and Inflammatory Disorders
× corresponding author
# (joint) last author

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