A 25-year-old male with CRF secondary to obstructive nephropathy.
She was admitted for hemodialysis in 1993.
He underwent kidney transplantation with a compatible donor in November 1995.
Atrial fibrillation was diagnosed in December 1995.
She receives transfusions on several occasions.
She was readmitted for hemodialysis in September 2003 for chronic transplant nephropathy.
In 2004-2009, multiple etiologies of vascular access were identified.
Anemia with partial response to EPO.
Severe secondary HPT with persistent hyper-P.
It does not comply with the diet and provides excessive fluid intake, leading to significant interdialytic overweight and severe hypotension.
Poor dialysis adequacy with KTVsp < 1.4.
Pathological studies are performed due to its antecedents compatible in the thrombophilia service with a lopic-type inhibitory effect and slightly increased plasma homocysteinemia.
Treatment with ASA and folic acid + B complex and anticoagulation are indicated.
He underwent a short time of anticoagulant treatment due to lack of compliance.
In March 2009 the patient presented with loss of vision of the RE and partial of the LE.
Eye fundus: bilateral papilledema.
Normal eye pressure
She had no history of headache.
Normal brain MRI
Consultation with VA neurology negative light, abolished reflexes (reactive starch).
Eye fundus: diffuse edge papilla with papilla edema + (non-bleeding) (OI), papilla with diffuse edges and papilla edema +++.
Visual PE with severe optic pathway involvement, compatible with optic neuropathy.
Laboratory test results: Hto 26, Hb 8,1, Upre 129, Upost 18, P 6,9, Ca 8,2, PTH 2,431.
Normal collagenogram, anticardiolipin IgG and IgM with normal values, ANCAp and c and serology for HBs Ag, HCVAc, HIV, toxoplasmosis and syphilis were negative.
Treatment was initiated with corticosteroids (prednisone) at a dose of 1 mg/kg/day, with no response at 30 days.
Control eye fund (2 months), bilateral
The patient clinically remains with bilateral amaurosis.
