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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44; </span></p><p class="elsevierStylePara">Parkinson&#8217;s disease &#40;PD&#41; is a common neurodegenerative disease that can be caused by mitochondrial dysfunction&#44; oxidative stress&#44; apoptosis or inflammation&#46;<span class="elsevierStyleSup">1 </span>Between 50&#37; and 80&#37; of PD patients show intolerance to glucose&#44; which can be exacerbated by levodopa treatment&#46;<span class="elsevierStyleSup">2</span> We describe the case of a patient with PD and poorly controlled diabetes mellitus&#44; who was initially treated with anti-diabetic drugs and later required insulin therapy and who came for consultation with a nephrotic syndrome &#40;NS&#41;&#46;</p><p class="elsevierStylePara">The patient was a 74-year-old man with a 9-year history of diabetes mellitus &#40;initially treated with anti-diabetic drugs and for the last 3 years with insulin&#41;&#59; diagnosed with infarctional ischaemic heart disease and post-infarction angina&#44; he had undergone double coronary bypass surgery&#46; Previous episodes of deep vein thrombosis and pulmonary thromboembolism&#44; and hypercoagulability had been confirmed &#40;heterozygotic mutation of homocysteine gene&#41;&#46; For 10 years he had had PD&#44; which was being treated with carbidopa&#47;entacapone&#47;levodopa&#44; ropinirole and rasagiline&#46; Other medical conditions included prostate adenoma&#44; hiatus hernia and chronic renal failure with previous plasma creatinine levels of 1&#46;4-1&#46;5mg&#47;dl&#46;</p><p class="elsevierStylePara">The patient was referred to the emergency department by his GP&#44; owing to symptoms of anasarca&#46; In the days prior to his visit to the emergency department he had noticed a decrease in the frequency of diuresis accompanied by weight gain&#46; He did no report blood-stained or dark-coloured urine&#46; A week before he had developed very itchy petechiae on his arm and the back of his hands&#46;</p><p class="elsevierStylePara">The physical examination revealed that the patient&#8217;s general condition was good&#44; and he was conscious and orientated&#46; There was slight jugular vein ingurgitation and his blood pressure was 150&#47;78mm Hg&#46; Body temperature was normal&#46; As far as the rest of the examination is concerned&#44; notable symptoms included pitting oedema of the lower limbs and signs of venous insufficiency&#46;</p><p class="elsevierStylePara">In the complementary tests&#44; the blood analysis showed&#58; haematocrit&#58; 44&#37;&#44; leukocyte&#58; 7060&#44; platelets&#58; 152 000&#59; pH&#58; 7&#46;32&#44; bicarbonate&#58; 28mEq&#47;l&#44; glucose&#58; 241mg&#47;dl&#44; creatinine 2&#46;2mg&#47;dl and calcium 7&#46;7mg&#47;dl&#46; The rest of the on-the-spot analysis was normal&#46;</p><p class="elsevierStylePara">In the routine blood analysis the findings were as follows&#58; uric acid&#58; 11&#46;8mg&#47;dl&#44; cholesterol&#58; 297mg&#47;dl&#44; triglycerides&#58; 141mg&#47;dl&#44; albumin&#58; 1&#46;9g&#47;dl&#44; total protein&#58; 5&#46;2g&#47;dl&#44; LDH&#58; 629U&#47;l&#44; glycosylated haemoglobin&#58; 8&#46;5&#37;&#46; Immunological analysis&#58; C-reactive protein 1&#46;9mg&#47;dl&#59; rheumatoid factor&#44; ASLO&#44; ANCA&#44; antinuclear antibodies&#44; anti-Ro&#44; anti-La&#44; anti-Sm and anti-RNP antibodies were within normal limits&#46; Tumour markers&#44; including ACE&#44; CA19-9&#44; AFP and PSA were acceptable&#46; Blood electrophoresis&#58; hypoproteinaemia&#44; reduced albumin levels&#44; raised alpha-2 and beta globulins with a polyclonal increase in gammaglobulins&#46; Thyroid hormones were normal&#46; Serological tests for the hepatitis C and HIV virus were negative&#46; HBsAg positive&#44; anti-HBc and anti-HBs negative&#59; hepatitis B virus DNA less than 2000 copies&#47;ml&#46; Herpes virus 1-2 IgG positive&#46;</p><p class="elsevierStylePara">The urine analysis on admission showed proteins &#43;&#43;&#43;&#44; blood &#43;&#43; and the presence of casts &#40;cylindruria&#41;&#46; Protein quantification in 24-hour urine was 13g&#47;24 h&#46;</p><p class="elsevierStylePara">Chest X-ray&#58; enlarged heart with no signs of acute heart failure&#46; Electrocardiogram&#58; sinus bradyarrhythmia at 50bpm&#46; A Doppler ultrasound scan showed no pathological findings&#46;</p><p class="elsevierStylePara">Given the patient&#8217;s history of poorly controlled diabetes mellitus and his admission owing to recent fluid retention&#44; it was decided that a renal biopsy should be performed&#46; Our findings were as follows&#58; six glomeruli&#44; two of which were completely sclerotic&#46; In two of the other four glomeruli&#44; focal&#44; nodular lesions of the glomerular tuft &#40;Kimmelstiel-Wilson nodules&#41; were identified&#46; The result of the immunofluorescence assay was negative&#46; Moderate interstitial fibrosis associated with tubular atrophy and chronic inflammatory infiltrate was observed&#46; The vascular component presented no lesions&#46; The definitive diagnosis was nodular glomerulosclerosis with a morphological substrate of diabetic nephropathy &#40;DN&#41;&#46;</p><p class="elsevierStylePara">With this diagnosis&#44; the initially established treatment&#44; which consisted of diuretics&#44; irbesartan&#44; atenolol&#44; statins and oral anticoagulants&#44; was maintained and the patient was discharged&#46;</p><p class="elsevierStylePara">Twelve days later the patient was re-admitted for fluid retention&#44; and he responded favourably to diuretic treatment&#46; Subsequent outpatient follow-up showed the analytical changes depicted in Table 1 and the patient has not presented new episodes of fluid retention&#46;</p><p class="elsevierStylePara">DN is a common complication of diabetes and is currently an important public health problem&#44; as diabetic renal disease is the main cause of terminal chronic kidney disease in Western countries&#46;<span class="elsevierStyleSup">3</span> Diabetic patients with a history of DN who develop slow-onset proteinuria&#44; are not usually subjected to a biopsy&#44; on the assumption of the presence of DN&#46; However&#44; non-diabetic glomerular disease may also develop in diabetic patients&#44; which is why a renal biopsy may be indicated&#46;<span class="elsevierStyleSup">4</span> In our case&#44; the patient had longstanding diabetes mellitus&#44; which was poorly controlled metabolically&#46; We are unaware whether he had proteinuria prior to his first admission&#44; although the onset of anasarca and fluid retention was sudden&#44; so we decided to perform a renal biopsy and the diagnosis was DN&#46;</p><p class="elsevierStylePara">In the medical literature cases of NS due to minimal change disease have been reported in diabetic patients&#46;<span class="elsevierStyleSup">5&#44;6</span> In the case described by Donaire et al&#44; the suspicion of a cause other than diabetes was founded on the short history of diabetes&#44; the absence of retinopathy and the fact that a previous check-up proved negative for proteinuria&#46;<span class="elsevierStyleSup">5</span> Although in our case the established diagnosis was DN&#44; the sudden onset of symptoms with severe proteinuria which led to fluid retention on more than one occasion and subsequently spontaneous remission&#44; and then a proteinuria of less than 0&#46;5g&#47;24 h during follow-up&#44; suggested the possibility that the patient might have a comorbid minimal change nephropathy&#46; This might have gone unnoticed during the histological analysis when an underlying DN substrate was found and electron microscopy test was not performed&#46; The patient might have had an unrelated infectious process prior to his first admission&#46; In fact&#44; he had developed cutaneous lesions on his upper limbs&#46; This process could have been triggered by an immune mechanism&#44; leading to an increase in glomerular permeability and&#44; subsequently&#44; severe NS with spontaneous remission some months later&#46;</p><p class="elsevierStylePara">To conclude&#44; we described a case of NS with clinical symptoms indicating a minimal change aetiology&#44; which could have gone unnoticed in the renal biopsy because we found a DN histological substrate associated to the base pathology &#40;long-term diabetes mellitus&#41;&#46;</p><p class="elsevierStylePara"><a href="grande&#47;10784&#95;108&#95;17673&#95;en&#95;t1&#46;10784&#46;jpg" class="elsevierStyleCrossRefs"><img src="10784_108_17673_en_t1.10784.jpg" alt="Follow-up of laboratory results"></img></a></p><p class="elsevierStylePara">Table 1&#46; Follow-up of laboratory results</p>"
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