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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#58;</span></p><p class="elsevierStylePara">Sodium retention is an expected situation in patients with proteinuria and hypoalbuminaemia&#46; Though the conventionally proposed mechanism is based on the low plasma oncotic pressure produced by hypoalbuminaemia&#44; a pathophysiological explanation that proposes a primary renal retention of sodium has recently been accepted&#46;<span class="elsevierStyleSup">1&#44;2</span> This mechanism is independent of aldosterone&#46; We present a case of membranous nephropathy with hyporeninaemic hypoaldosteronism&#46;</p><p class="elsevierStylePara">A 43-year-old male was referred to our clinic with three grams of proteinuria a day&#46; His history included common variable immunodeficiency that had required immunoglobulin infusion years before and idiopathic thrombocytopenic purpura untreated at present&#46; The physical examination at the time of the consultation revealed blood pressure of 125&#47;78mmHg&#44; with a heart rate of 70 beats per minute and minimal oedema&#46; The blood test showed the following parameters&#58; haemoglobin 14&#46;2g&#47;dl&#44; platelets 182&#44;000 per &#181;l&#44; sodium 143mEq&#47;l&#44; potassium 4&#46;2mEq&#47;l&#44; bicarbonate 25&#46;2mEq&#47;L&#44; creatinine 0&#46;73 mg&#47;dl&#44; urea 27mg&#47;dl&#44; albumin 3&#46;4g&#47;dl&#44; total protein 6&#46;0g&#47;dl&#44; cholesterol 247mg&#47;dl&#44; glycosylated haemoglobin 4&#46;4&#37;&#46; The following values were found in urine&#58; albuminuria 2868mg&#47;day &#40;albumin&#47;creatinine 1017mg&#47;g&#41; sodium 228mmol&#47;day and potassium 48 mmol&#47;l&#46; In the immunological study&#44; anti-neutrophil cytoplasmic&#44; anti-glomerular basement membrane&#44; anti-double-stranded DNA and anti-nuclear antibodies were negative&#46; Immunoglobulin and complement levels were also in the normal range&#46; At that time it was decided to perform a renal biopsy&#44; which revealed membranous nephropathy &#40;Figure 1&#41;&#46;</p><p class="elsevierStylePara">The patient was initially treated with renin-angiotensin-aldosterone system inhibitors&#44; with proteinuria decreasing to 500mg per day&#46; However&#44; this treatment had to be discontinued due to hyperkalaemia&#46; The transtubular potassium gradient was 4&#46;71 and the suprarenal study confirmed hyporeninaemic hypoaldosteronism &#40;aldosterone &#60;1&#46;6ng&#47;l&#44; plasma renin activity 0&#46;1ng&#47;ml&#47;h&#41;&#44; with a Synacthen test that stimulated cortisol and normal sex hormones&#46;</p><p class="elsevierStylePara">We consider that this case offers new pathways for understanding the role of aldosterone in patients with proteinuria&#46; There are currently two hypotheses that try to explain sodium and water retention in nephrotic syndrome&#58; <span class="elsevierStyleItalic">underfill and</span><span class="elsevierStyleItalic"> </span><span class="elsevierStyleItalic">overfill</span><span class="elsevierStyleItalic">&#46; </span>In the first of these&#44; the mechanism is based on low oncotic pressure produced by hypoalbuminaemia accompanying the nephrotic syndrome&#46;<span class="elsevierStyleSup">1</span> As a result&#44; there is renin and aldosterone stimulation&#44; generating water and sodium retention&#46; However&#44; there is some controversy over this theory as the only cause of volume overload&#59; as such&#44; it has been proven that albumin administration in these patients does not produce an increase in natriuresis and that proteinuria <span class="elsevierStyleItalic">per se</span> does increase urine sodium excretion independently of plasma albumin&#46;<span class="elsevierStyleSup">3&#44;4</span> Recently&#44; a new hypothesis regarding primary sodium retention by the kidney has been developed and&#44; as such&#44; Svenningsen et al&#46; have suggested that proteinuria includes the filtration of proteolytic enzymes capable of directly activating the collecting duct of the epithelial sodium channel&#44; allowing sodium retention and thus inhibiting aldosterone&#46;<span class="elsevierStyleSup">2&#44;5</span> Furthermore&#44; in the nephrotic syndrome there is increased activity of phosphodiesterase in the collecting duct&#44; allowing atrial natriuretic peptide and urodilatin degradation&#46; The experimental administration of phosphodiesterase inhibitors reversed this positive sodium balance situation&#46; This situation has also been demonstrated in patients with renal failure and cirrhosis&#46;<span class="elsevierStyleSup">6&#44;7</span> Filtered proteolytic enzymes in patients with proteinuria include plasmin&#44; which in normal conditions is not found in the urine&#46; However&#44; the conversion of plasminogen to plasmin by urokinase in these patients produces a direct action on the sodium channel gamma subunit in the collecting duct&#44; whose mission is to inhibit said channel &#40;and therefore mass sodium reabsorption&#41;&#46; This causes primary sodium retention independent of aldosterone &#40;which in these cases would be inhibited&#41;&#46;<span class="elsevierStyleSup">8</span></p><p class="elsevierStylePara">Very few cases have been published on this situation&#46;<span class="elsevierStyleSup">9&#44;10</span> The longest series includes 23 non-diabetic patients with nephrotic syndrome&#46; Five of them had low levels of renin and aldosterone&#46; Moreover&#44; as in our case&#44; these five patients had membranous nephropathy&#46;<span class="elsevierStyleSup">4</span> In the latest case published&#44; Hommos et al&#46; warn about the importance of the neurohumoral system for producing sodium retention in nephrotic states&#46; According to the authors&#44; it is necessary that the sympathetic nervous system is intact in order to permit intratubular reabsorption of sodium&#46;</p><p class="elsevierStylePara">Although in our case the renin-angiotensin-aldosterone system is inhibited&#44; starting blockers of this system reduced proteinuria to less than half a gram per day&#46;</p><p class="elsevierStylePara">We did not find any relationship in literature between variable common immunodeficiency and idiopathic thrombocytopenic purpura&#46;</p><p class="elsevierStylePara">Therefore&#44; patients with proteinuria could alternate between states of hypo and hyperaldosteronism as mechanisms responsible for sodium retention by the kidney&#46; Nevertheless&#44; longer series are necessary as well as a more extensive follow-up period and serial measurements of aldosterone&#44; natriuresis and proteinuria to explain what factors determine a patient being at one extreme or the other of the same clinical profile with different and alternative pathogenic pathways&#46;</p><p class="elsevierStylePara">In conclusion&#44; we can say that in the differential diagnosis of hyperkalaemia in the nephrotic syndrome we must exclude the uncommon presence of hyporeninaemic hypoaldosteronism&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><a href="grande&#47;11841&#95;16025&#95;46828&#95;en&#95;11841&#95;f1&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11841_16025_46828_en_11841_f1_copy1.jpg" alt="Renal biopsy"></img></a></p><p class="elsevierStylePara">Figure 1&#46; 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