To  the editor:

Venography  is a procedure  intended  to  ascertain  the  location of veins in the arm in order to select  the most adequate  for performing the  arteriovenous fistula  required  for haemodialysis. The  case  of  a  73-year old  female  patient  with  a  history  of diabetes mellitus and high blood pressure,  both  starting  20 years  before, atrial fibrillation, mitral and aortic stenosis,  chronic  anaemia,  and  chronic kidney  disease  diagnosed  five  years before  and  monitored  at  our department of nephrology, with creatinine levels of 3 mg/dL and a creatinine clearance of 15 mL/min,  is  reported here. She  was  being  treated  with  insulin, acenocoumarol,  furosemide, oral  iron, doxazosin,  atenolol,  isosorbide  dinitrate  patches,  folic  acid,  and  omeprazole. The patient attended the hospital reporting  oligoanuria  (150  mL/24  h) for  the  past  24  hours  after  a  venography.  There  was  no  other  potential triggering factor of oligoanuria. Physical examination  found  no  fever  and blood  pressure  values  of  130/60 mmHg.  CA:  Rhythmic  heart  sounds. PA:  Preserved  vesicular  murmur. Lower  limbs: No  oedema  or  signs  of DVT. Laboratory  tests  showed  a  normal  WBC  differential,  haemoglobin 8.9, platelet count 159,000. Urea 104, creatinine 7.2, sodium 128, potassium 4.6, LDH 564,  elemental urine  analysis: pH 5, specific gravity 1005, positive  protein  (+++),  sodium  13  mEq/L, and  potassium  53 mEq/L.  The  ECG showed  atrial  fibrillation with  controlled  ventricular  response  at  approximately  80  bpm. Chest  and  abdominal X-rays revealed no radiographic changes.  During  admission,  patient  received  intravenous  fluid  therapy,  diuretics,  and  N-acetyl  cysteine,  showing basal  creatinine  levels  of 4 mg/dL at three days of admission.

Renal  failure  triggered  by  intravenous contrast after a venography is very uncommon,  but  has  been  reported  as one of  its  complications.1,2 Acute  renal failure caused by a contrast agent is defined  in  absolute  form  as  a 0.5 mg/dL increase and  in relative form as a 25% increase  in  creatinine  levels  48-72  h after administration.3

Contrast-induced  renal  failure  is more  common  in  patients  who  previously  have  some  grade  of  renal  insufficiency,  those  with  a  prediabetic state, those with diabetes mellitus starting  some  years  before,4-6 or  patients with  hyperuricemia7 (values  higher than 7 mg/dL in males and 5.9 mg/dL in  females). The most  common  clinical sign is oligoanuria from renal function impairment, occurring as a consequence  of  renal  vasoconstriction  and medullary hypoperfusion.8 There is no defined treatment for contrast toxicity, and  there  are  different  theories  about the most adequate treatment. Effective treatment  with  fluid  therapy and  Nacetyl  cysteine  has  been  reported  in the  literature,9 but  there  are  also  articles  reporting no benefits  from use of these treatments.10