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    "textoCompleto" => "<p class="elsevierStylePara">Dear Editor&#44;</p><p class="elsevierStylePara">Optic neuropathy is a syndrome and not a mere common injury of the optic nerve&#59; its aetiology is broad and greatly varies&#46; Ischaemic optic neuropathies influenced by local and systemic factors are particularly noteworthy&#44; many of which are difficult to understand&#46; These processes occur in the field of other specialisations with surgical manoeuvres and&#47;or aggressive diagnoses&#44; in which the patient is compromised&#44; as the initial diagnosis could be problematic&#46;<span class="elsevierStyleSup">1</span> Ophthalmologists are well aware of the process&#44; however&#44; doctors of other specialisations do not realise the possibility for this clinical condition&#44; being familiar with its existence only when it appears&#46; Various risk factors exist for ischaemic optic neuropathy &#40;ION&#41;&#44; however&#44; we must emphasise sudden hypotension&#44; which does not allow for the autoregulation mechanisms of the optic nerve to compensate&#44; particularly if the patient suffers from previous hypotension&#44; anaemia&#44; sudden and&#47;or recurrent haemorrhage&#44; serious facial oedema&#44; chronic kidney disease&#44; bleeding surgeries and&#44; generally&#44; all situations associated with arteriosclerosis&#46;</p><p class="elsevierStylePara">Based on the few reports in the literature of patients with chronic kidney disease &#40;CKD&#41;&#44; we report the cases of 2 patients in haemodialysis with a diagnosis of acute bilateral loss of vision due to a previous ischaemic optic neuropathy &#40;PION&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Case 1</span></p><p class="elsevierStylePara">A 29-year-old woman with a diagnosis of CKD owing to GEFS was hospitalised for haemodialysis at the age of 25&#46; Three years after the haemodialysis&#44; she showed signs of severe secondary hyperparathyroidism &#40;SHPT&#41; with PTH i &#62; 1&#44;000pg&#47;ml&#44; ostealgia&#44; asthenia&#44; pruritus and persistent symptomatic hypotension&#46; There were no arterial or cardiovascular calcifications&#46; A diagnostic ultrasound of the parathyroid glands was carried out with no visualisation with 99Tc and MIBI with diffuse increase in the fixation of the left and right inferior parathyroid lobes&#46; Treatment for the SHPT was carried out with calcium binders and intermittent calcitriol IV for hyperphosphatemia&#46; Subtotal parathyroidectomy was prescribed&#44; taking into consideration the patient&#191;s age and transplant suitability&#46; The previous laboratory results were as follows&#58; HCT 37&#37;&#44; Hb 12&#46;1&#44; Ca 9mg&#47;dl&#44; P 6mg&#47;dl&#44; K 5 meq&#47;l&#46; Normal coagulation test results&#46; Biopsy of the parathyroid glands&#58; bilateral hyperplasia&#46; During the surgery she developed hypotonia &#40;average BP of 90&#47;60&#41;&#46; Six days following surgery&#44; she experienced partial loss of vision in the RE and total in the LE&#44; mild hypocalcaemia and symptomatic hypotension&#46; Laboratory&#58; HCT 36&#37;&#44; Hb 12&#44; Ca 6&#46;3&#44; Ca i 0&#46;2l&#44; P 3&#46;5 and Mg 1&#46;9&#46; The hypocalcaemia values were corrected&#46;</p><p class="elsevierStylePara">Normal results of the collagen and coagulation tests&#46; Results of anticardiolipin antibodies&#44; lupus anticoagulant&#44; ANCAp and c and serology for toxoplasmosis and syphilis were negative&#46;</p><p class="elsevierStylePara">Neurological examination was carried out&#44; showing right nasal hemianopsia and vision restricted to profiles on the left eye&#46; Discus-shaped pupil in the RE and LE at<span class="elsevierStyleSup">3</span> and 4mm&#44; respectively&#46; Ophthalmological examination&#58; AV with vision&#44; counted fingers at 50cm in the LE and slight drop in vision in the RE&#46; A reactive mydriasis in the LE and reactive in the RE&#46; Inner eye&#58; attached retina&#44; normal macula and congestion of the papilla with degenerative oedema &#40;L and RE&#41; and PO 10&#47;10mmHg&#46; Normal MRI of the brain and bulb&#46; Evoked visual potential in the RE and LE of average range and prolonged central latency&#44; compatible with moderately affected areas of the optical route that is consistent with optic neuropathy&#46; Visual sharpness&#58; 0&#46;5 in the LE and 0&#46;8 in the RE&#46; Campimetry&#58; outwith the normal limits for the LE&#44; with an alteration in the relative feeling and a restriction of the blind spot &#40;increased&#41;&#46; There was a total decrease in feeling in the LE&#46;</p><p class="elsevierStylePara">Corticosteroids &#40;prednisone&#41; were prescribed as a treatment at a dose of 1mg&#47;kg&#47;day for 30 days&#46;</p><p class="elsevierStylePara">The papillary oedema increased in both eyes&#44; with a vision restricted to profiles in the RE and amaurosis in the LE&#46;</p><p class="elsevierStylePara">Within two months&#44; an almost total atrophy of the right optical nerve was detected in the inner eye&#44; with dilation and venous tortuosity&#44; while there was total atrophy of the left optical nerve&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Case 2</span></p><p class="elsevierStylePara">In 1993&#44; a 25-year-old man with CKD owing to obstructive nephropathy was hospitalised to receive haemodialysis&#46; In November 1995&#44; he was given a renal transplant from a compatible donor&#46; In December 1995&#44; he experienced FAV and received blood transfusions at various times&#46; In September 2003&#44; he was once again admitted to hospital for haemodialysis due to the transplant&#191;s chronic nephropathy&#46; In the period from 2004-2009 he suffered from multiple blockages of the vascular access&#46;</p><p class="elsevierStylePara">Anaemia with partial response to EPO&#46; Severe SHPT with persistent hyperparathyroidism&#46; Did not follow the diet and took in an excessive amount of fluids&#44; leading to a significant interdialytic excess weight and severe hypotension&#46; Deficient dialysis suitability with minor KTVsp at 1&#46;4&#46; Haematological tests were carried out for his medical history with thrombophilia&#44; consistent with the inhibitory lupus effect and a slightly increased plasma homocysteinemia&#46; Treatment with acetylsalicylic acid&#44; folic acid &#43; vitamin B complex and anticoagulation was administered&#46; A short anticoagulant treatment was administered for lack of performance&#46;</p><p class="elsevierStylePara">In March 2009&#44; the patient showed symptoms of loss of vision in the RE and partial loss of vision in the LE&#46; Inner eye&#58; with bilateral papillary oedema&#46; Normal ocular pressure&#46; There is no medical history of headaches&#46; Normal MRI of the brain&#46; Neurological examination&#58; negative AV light&#44; abolished reflexes &#40;areactive mydriasis&#41;&#46; Inner eye&#58; diffuse-edge papilla with papillary oedema &#43; &#40;no haemorrhage&#41; &#40;LE&#41;&#44; diffuse- edge papilla with papillary oedema&#43;&#43;&#43;&#46; Visual PE with severely affected areas of the optical route that is consistent with optic neuropathy&#46; Results of laboratory tests&#58; HCT 26&#44; Hb 8&#46;1&#44; Upre 129&#44;Upost 18&#44; P 6&#46;9&#44; Ca 8&#46;2 and PTH 2&#46;431&#46; Normal results for connective disease tests&#46; Normal values for anticardiolipin IgG and IgM&#46; Results of ANCAp and c and serology for HBs Ag&#44; HCVAc&#44; HIV&#44; toxoplasmosis and syphilis were negative&#46;</p><p class="elsevierStylePara">Beginning of treatment with&#58; corticosteroids &#40;prednisone&#41; at a dose of 1mg&#47;kg&#47;day&#44; with no response at 30 days&#46; Inner eye test &#40;2 months&#41;&#44; bilateral atrophy&#46; The patient is clinically damaged with bilateral amaurosis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Discussion</span></p><p class="elsevierStylePara">We have come across 16 cases of PION in patients with substitutive renal treatment&#44; 10 of which correspond to patients following a programme of periodic haemodialysis <span class="elsevierStyleSup">2-13</span> and the rest to DPCA&#46;<span class="elsevierStyleSup">11&#44;12</span> In general&#44; all cases shared a medical history of hypotension episodes in dialysis&#44;<span class="elsevierStyleSup">2&#44;8&#44;13</span> one of which showed no hypotension&#44;<span class="elsevierStyleSup">9</span> while another was associated to Sildenafil&#46;<span class="elsevierStyleSup">10</span> The visual deficit was bilateral&#44; and in 15 of the cases it manifested as anterior ischemic optic neuropathy&#44; with only one case showing it afterwards&#46; They showed a partial response to a corticosteroids dose&#46; In the cases presented&#44; we could not avoid thinking about the possible association of severe secondary hyperparathyroidism with calcific uremic arteriolopathy &#40;calciphylaxis&#41; in arterioles that moisten the optic nerve&#46; Korzets et al<span class="elsevierStyleSup">13</span> observed an acute loss of vision in 2 patients with a diagnosis of PION&#44; a biopsy of the choroid of the temporal artery of whom showed signs of hypotension and calcification&#44; taking into account that hypoperfusion could have occurred from calciphylaxis of the arterioles moistening the top of the optic nerve&#46; Furthermore&#44; the association of the ischaemic ocular pathology with the antiphospholipid syndrome is well known&#44;<span class="elsevierStyleSup">14&#44;15</span> as shown in the second case&#44; where the patient has clinical and laboratory symptoms of primary antiphospholipid syndrome &#40;PAPS&#41;&#44; and in which the ocular affectation associated with the presence of these symptoms includes vaso-occlusive retinopathy&#44; estimated to be present in 29&#37; of the patients with PAPS&#44; and optic neuropathy of a likely ischaemic nature&#46; </p>"
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Previous ischaemic optic neuropathy in haemodialysis
Neuropatía óptica isquémica anterior en hemodiálisis
Luis Roberto Leóna, C.. Marinaroa
a DIAVERUM, CERER, S.A., San Justo, Buenos Aires, Argentina,
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    "textoCompleto" => "<p class="elsevierStylePara">Dear Editor&#44;</p><p class="elsevierStylePara">Optic neuropathy is a syndrome and not a mere common injury of the optic nerve&#59; its aetiology is broad and greatly varies&#46; Ischaemic optic neuropathies influenced by local and systemic factors are particularly noteworthy&#44; many of which are difficult to understand&#46; These processes occur in the field of other specialisations with surgical manoeuvres and&#47;or aggressive diagnoses&#44; in which the patient is compromised&#44; as the initial diagnosis could be problematic&#46;<span class="elsevierStyleSup">1</span> Ophthalmologists are well aware of the process&#44; however&#44; doctors of other specialisations do not realise the possibility for this clinical condition&#44; being familiar with its existence only when it appears&#46; Various risk factors exist for ischaemic optic neuropathy &#40;ION&#41;&#44; however&#44; we must emphasise sudden hypotension&#44; which does not allow for the autoregulation mechanisms of the optic nerve to compensate&#44; particularly if the patient suffers from previous hypotension&#44; anaemia&#44; sudden and&#47;or recurrent haemorrhage&#44; serious facial oedema&#44; chronic kidney disease&#44; bleeding surgeries and&#44; generally&#44; all situations associated with arteriosclerosis&#46;</p><p class="elsevierStylePara">Based on the few reports in the literature of patients with chronic kidney disease &#40;CKD&#41;&#44; we report the cases of 2 patients in haemodialysis with a diagnosis of acute bilateral loss of vision due to a previous ischaemic optic neuropathy &#40;PION&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Case 1</span></p><p class="elsevierStylePara">A 29-year-old woman with a diagnosis of CKD owing to GEFS was hospitalised for haemodialysis at the age of 25&#46; Three years after the haemodialysis&#44; she showed signs of severe secondary hyperparathyroidism &#40;SHPT&#41; with PTH i &#62; 1&#44;000pg&#47;ml&#44; ostealgia&#44; asthenia&#44; pruritus and persistent symptomatic hypotension&#46; There were no arterial or cardiovascular calcifications&#46; A diagnostic ultrasound of the parathyroid glands was carried out with no visualisation with 99Tc and MIBI with diffuse increase in the fixation of the left and right inferior parathyroid lobes&#46; Treatment for the SHPT was carried out with calcium binders and intermittent calcitriol IV for hyperphosphatemia&#46; Subtotal parathyroidectomy was prescribed&#44; taking into consideration the patient&#191;s age and transplant suitability&#46; The previous laboratory results were as follows&#58; HCT 37&#37;&#44; Hb 12&#46;1&#44; Ca 9mg&#47;dl&#44; P 6mg&#47;dl&#44; K 5 meq&#47;l&#46; Normal coagulation test results&#46; Biopsy of the parathyroid glands&#58; bilateral hyperplasia&#46; During the surgery she developed hypotonia &#40;average BP of 90&#47;60&#41;&#46; Six days following surgery&#44; she experienced partial loss of vision in the RE and total in the LE&#44; mild hypocalcaemia and symptomatic hypotension&#46; Laboratory&#58; HCT 36&#37;&#44; Hb 12&#44; Ca 6&#46;3&#44; Ca i 0&#46;2l&#44; P 3&#46;5 and Mg 1&#46;9&#46; The hypocalcaemia values were corrected&#46;</p><p class="elsevierStylePara">Normal results of the collagen and coagulation tests&#46; Results of anticardiolipin antibodies&#44; lupus anticoagulant&#44; ANCAp and c and serology for toxoplasmosis and syphilis were negative&#46;</p><p class="elsevierStylePara">Neurological examination was carried out&#44; showing right nasal hemianopsia and vision restricted to profiles on the left eye&#46; Discus-shaped pupil in the RE and LE at<span class="elsevierStyleSup">3</span> and 4mm&#44; respectively&#46; Ophthalmological examination&#58; AV with vision&#44; counted fingers at 50cm in the LE and slight drop in vision in the RE&#46; A reactive mydriasis in the LE and reactive in the RE&#46; Inner eye&#58; attached retina&#44; normal macula and congestion of the papilla with degenerative oedema &#40;L and RE&#41; and PO 10&#47;10mmHg&#46; Normal MRI of the brain and bulb&#46; Evoked visual potential in the RE and LE of average range and prolonged central latency&#44; compatible with moderately affected areas of the optical route that is consistent with optic neuropathy&#46; Visual sharpness&#58; 0&#46;5 in the LE and 0&#46;8 in the RE&#46; Campimetry&#58; outwith the normal limits for the LE&#44; with an alteration in the relative feeling and a restriction of the blind spot &#40;increased&#41;&#46; There was a total decrease in feeling in the LE&#46;</p><p class="elsevierStylePara">Corticosteroids &#40;prednisone&#41; were prescribed as a treatment at a dose of 1mg&#47;kg&#47;day for 30 days&#46;</p><p class="elsevierStylePara">The papillary oedema increased in both eyes&#44; with a vision restricted to profiles in the RE and amaurosis in the LE&#46;</p><p class="elsevierStylePara">Within two months&#44; an almost total atrophy of the right optical nerve was detected in the inner eye&#44; with dilation and venous tortuosity&#44; while there was total atrophy of the left optical nerve&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Case 2</span></p><p class="elsevierStylePara">In 1993&#44; a 25-year-old man with CKD owing to obstructive nephropathy was hospitalised to receive haemodialysis&#46; In November 1995&#44; he was given a renal transplant from a compatible donor&#46; In December 1995&#44; he experienced FAV and received blood transfusions at various times&#46; In September 2003&#44; he was once again admitted to hospital for haemodialysis due to the transplant&#191;s chronic nephropathy&#46; In the period from 2004-2009 he suffered from multiple blockages of the vascular access&#46;</p><p class="elsevierStylePara">Anaemia with partial response to EPO&#46; Severe SHPT with persistent hyperparathyroidism&#46; Did not follow the diet and took in an excessive amount of fluids&#44; leading to a significant interdialytic excess weight and severe hypotension&#46; Deficient dialysis suitability with minor KTVsp at 1&#46;4&#46; Haematological tests were carried out for his medical history with thrombophilia&#44; consistent with the inhibitory lupus effect and a slightly increased plasma homocysteinemia&#46; Treatment with acetylsalicylic acid&#44; folic acid &#43; vitamin B complex and anticoagulation was administered&#46; A short anticoagulant treatment was administered for lack of performance&#46;</p><p class="elsevierStylePara">In March 2009&#44; the patient showed symptoms of loss of vision in the RE and partial loss of vision in the LE&#46; Inner eye&#58; with bilateral papillary oedema&#46; Normal ocular pressure&#46; There is no medical history of headaches&#46; Normal MRI of the brain&#46; Neurological examination&#58; negative AV light&#44; abolished reflexes &#40;areactive mydriasis&#41;&#46; Inner eye&#58; diffuse-edge papilla with papillary oedema &#43; &#40;no haemorrhage&#41; &#40;LE&#41;&#44; diffuse- edge papilla with papillary oedema&#43;&#43;&#43;&#46; Visual PE with severely affected areas of the optical route that is consistent with optic neuropathy&#46; Results of laboratory tests&#58; HCT 26&#44; Hb 8&#46;1&#44; Upre 129&#44;Upost 18&#44; P 6&#46;9&#44; Ca 8&#46;2 and PTH 2&#46;431&#46; Normal results for connective disease tests&#46; Normal values for anticardiolipin IgG and IgM&#46; Results of ANCAp and c and serology for HBs Ag&#44; HCVAc&#44; HIV&#44; toxoplasmosis and syphilis were negative&#46;</p><p class="elsevierStylePara">Beginning of treatment with&#58; corticosteroids &#40;prednisone&#41; at a dose of 1mg&#47;kg&#47;day&#44; with no response at 30 days&#46; Inner eye test &#40;2 months&#41;&#44; bilateral atrophy&#46; The patient is clinically damaged with bilateral amaurosis&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Discussion</span></p><p class="elsevierStylePara">We have come across 16 cases of PION in patients with substitutive renal treatment&#44; 10 of which correspond to patients following a programme of periodic haemodialysis <span class="elsevierStyleSup">2-13</span> and the rest to DPCA&#46;<span class="elsevierStyleSup">11&#44;12</span> In general&#44; all cases shared a medical history of hypotension episodes in dialysis&#44;<span class="elsevierStyleSup">2&#44;8&#44;13</span> one of which showed no hypotension&#44;<span class="elsevierStyleSup">9</span> while another was associated to Sildenafil&#46;<span class="elsevierStyleSup">10</span> The visual deficit was bilateral&#44; and in 15 of the cases it manifested as anterior ischemic optic neuropathy&#44; with only one case showing it afterwards&#46; They showed a partial response to a corticosteroids dose&#46; In the cases presented&#44; we could not avoid thinking about the possible association of severe secondary hyperparathyroidism with calcific uremic arteriolopathy &#40;calciphylaxis&#41; in arterioles that moisten the optic nerve&#46; Korzets et al<span class="elsevierStyleSup">13</span> observed an acute loss of vision in 2 patients with a diagnosis of PION&#44; a biopsy of the choroid of the temporal artery of whom showed signs of hypotension and calcification&#44; taking into account that hypoperfusion could have occurred from calciphylaxis of the arterioles moistening the top of the optic nerve&#46; Furthermore&#44; the association of the ischaemic ocular pathology with the antiphospholipid syndrome is well known&#44;<span class="elsevierStyleSup">14&#44;15</span> as shown in the second case&#44; where the patient has clinical and laboratory symptoms of primary antiphospholipid syndrome &#40;PAPS&#41;&#44; and in which the ocular affectation associated with the presence of these symptoms includes vaso-occlusive retinopathy&#44; estimated to be present in 29&#37; of the patients with PAPS&#44; and optic neuropathy of a likely ischaemic nature&#46; </p>"
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