Journal Information
Vol. 28. Issue. 5.October 2008
Pages 475-573
Vol. 28. Issue. 5.October 2008
Pages 475-573
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Cryptococcosis in a patient with IgA nephropathy treated with corticosteroids
Criptococosis en paciente con GMN IgA tratado con esteroides
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Alejandra Rodriguez Garciaa, Rita Guerra Rodriguezb
a Hospital General de Fuerteventura, Fuerteventura, Islas Canarias, España,
b Hospital Universitario Insular de Gran Canaria, Gran Canaria, Islas Canarias, España,
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Sr. Director, la glomerulonefritis IgA (GMN IgA) es la primera causa de GMN primaria en el mundo1. Su evolución natural sin tratamiento es hacia una lenta progresión a la insuficiencia renal crónica en aproximadamente un 50 % de los pacientes2.
To the editor: IgA glomerulonephritis (IgA GMN) is the leading cause of primary GMN in the world.1 Its natural course without treatment is a slow pro- gression to chronic renal failure in approximately 50% of patients.
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To the editor: IgA glomerulonephritis (IgA GMN) is the leading cause of primary GMN in the world.1 Its natural course without treatment is a slow pro- gression to chronic renal failure in approximately 50% of patients.2 Because of  this  course,  use  of  corticosteroids has been postulated  in  recent years  in patients with  risk  factors  for  progression to chronic renal failure such as increased serum creatinine  levels  (SCr), proteinuria of approximately 500-1000 mg/day,  and  hypertension.1,3-5 We  report the case of a 60-year-old male patient  with  a  history  of  atrial  fibrillation,  type  2  diabetes  mellitus,  and dyslipidemia who was  referred  to our clinic  for  progressive  renal  function impairment from SCr 1.1 mg/dL to 2.7 mg/dL in three months with a creatinine clearance (ClCr) of 40mL/min, microhematuria, and proteinuria. A renal biopsy  allowed  for  diagnosing  IgA GMN  with  significant  tubulointerstitial  involvement. Treatment was  started with ACEIs (enalapril 10 mg/24 h) and  a  tapering  corticosteroid  regimen (80 mg/24 h). After two months of treatment,  the  patient  reported  fatigue, headache,  and  tinnitus,  and  showed renal  function  impairment  (SCr  4 mg/dL and ClCr  16 mL/min). A lumbar  puncture  was  performed,  and  the subsequent culture showed the presence of Cryptococcus neoformans. Imaging  tests  revealed  lesions  consistent with cryptococcoma  in  basal  ganglia and  the  left parasagittal  region. Corticosteroids were discontinued, and  treatment was  started with  amphotericin B and flucytosine for two weeks, plus oral  fluconazole  for  one  additional month.  Lesions  disappeared,  and  the patient  is  currently  asymptomatic, with  SCr  of  3.3 mL/min,  ClCr  of  31 mg/mL, and proteinuria of 1.0 g/24 h, and under  treatment with enalapril 10 mg/24 h.



In  summary,  corticosteroids  are  potent  immunosuppressants  of  both  humoral  and  cell-mediated  immunity,7

which causes patients treated with them to have a 40-fold greater predisposition than  untreated  patients  to  suffer  infection by opportunistic or atypical microorganisms.8 Thus, since use of immunosuppressants  is  a  standard  therapeutic weapon in our routine clinical practice, we should not forget its potential harmful  effects  and  should watch  patients who receive them for the occurrence of symptoms  and  signs,  however  trivial they may appear, in order to be able to take any adequate diagnostic and therapeutic actions. 
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