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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#44; </span>&#160;</p><p class="elsevierStylePara">&#160;The functional relationship between thyroid and kidneys has been described since the mid-twentieth century<span class="elsevierStyleSup">1 </span>and has been the subject of many publications with differing pathophysiologic approaches&#46;<span class="elsevierStyleSup">2-5 </span>&#160;</p><p class="elsevierStylePara">&#160;Here we present the case of a patient with a striking recovery of glomerular filtration rate &#40;GFR&#41; after correction of a diagnosed hypothyroidism&#46; This was an 89-year-old woman with hypertension&#44; hypertensive cardiomyopathy&#44; atrial fibrillation &#40;AF&#41;&#44; mitral insufficiency&#44; and moderate aortic insufficiency&#44; cerebral small vessel disease&#44; and obesity-hypoventilation syndrome&#46; She had undergone a cholecystectomy in April 2008&#44; with plasma creatinine in the normal range at that time&#46;&#160;</p><p class="elsevierStylePara">&#160;From April 2008 and March 2009&#44; she required several hospitalisations for episodes of rapid AF&#44; lacunar infarct&#44; heart failure&#44; and digoxin toxicity&#46; Progressive deterioration of renal function &#40;RF&#41; was seen until May 2009&#44; at which point evaluation by the nephrology service was requested &#40;Table 1&#41;&#46; Ultrasound showed left renal atrophy &#40;76mm diameter with corticomedullary disruption&#41; and 118mm right kidney with moderate cortical atrophy&#46; At that time&#44; the patient was diagnosed with stage 4 chronic kidney disease &#40;CKD&#41; secondary to reduction of functional renal mass and severe cardiovascular comorbidity&#44; with therapeutic changes consistent with the degree of CKD&#46;&#160;</p><p class="elsevierStylePara">&#160;After laboratory detection of primary hypothyroidism and the subsequent diagnosis of multinodular goitre due to autoimmune thyroiditis&#44; hormonal treatment was started with levothyroxine&#46; In the subsequent 6 months&#44; adequate control of hypothyroidism was seen with progressive recovery of GFR and increased haemoglobin levels&#44; exceeding expectations of reversibility of renal impairment &#40;Table 1 and Figure 1&#41;&#46;&#160;</p><p class="elsevierStylePara">&#160;Thyroid disorders cause abnormalities in many locations with the heart and kidneys being the main targets of action of thyroid hormones&#46;<span class="elsevierStyleSup">2-5 </span>Primary hypothyroidism&#44; which develops after intrauterine growth&#44; is associated with impaired glomerular filtration which is reversible with hormonal treatment in approximately 55&#37; of cases&#46;<span class="elsevierStyleSup">2 </span>Hyponatraemia is common &#40;45&#37; of cases with coexisting CKD versus 21&#37; with previously normal renal function&#41;&#44; as is fluid overload&#46;<span class="elsevierStyleSup">2 </span>Renal function deterioration secondary to hypothyroidism involves heterogenous mechanisms dominated by haemodynamic abnormalities&#58; a negative inotropic effect on the heart&#44; reduced circulating intravascular volume&#44; and increased peripheral resistance with renal vasoconstriction&#46;<span class="elsevierStyleSup">2-4 </span>&#160;</p><p class="elsevierStylePara">&#160;Among the effects of thyroid hormones are the following&#58;&#160;</p><p class="elsevierStylePara">&#160;1&#46; Gene regulation of structural and regulatory proteins such as Na&#43;&#47;K&#43; ATPase&#44; Ca<span class="elsevierStyleSup">2</span>&#43; ATPase&#44; Na&#43;&#47;Ca<span class="elsevierStyleSup">2</span>&#43; exchanger&#44; betaadrenergic receptors&#44; adenylate cyclase&#44; phospholamban&#44; myosin&#44; voltage-gated potassium channels and G proteins&#44; among others<span class="elsevierStyleSup">3-7 </span>&#160;</p><p class="elsevierStylePara">&#160;2&#46; Extragenic regulation of Na&#43;&#44; K&#43;&#44; and Ca2&#43; channels in the cell membrane&#46;<span class="elsevierStyleSup">3&#44;7 </span>&#160;</p><p class="elsevierStylePara">&#160;3&#46; Correlation with the reninangiotensinaldosterone system&#46;<span class="elsevierStyleSup">4&#44;6</span>&#160;</p><p class="elsevierStylePara">&#160;4&#46; Correlation with levels of argininevasopressin &#40;ADH&#41;&#44;<span class="elsevierStyleSup">4&#44;5 </span>brain natriuretic peptide &#40;BNP&#41;&#44;<span class="elsevierStyleSup">4&#44;6 </span>and plasma creatinine not dependent on renal function<span class="elsevierStyleSup">8 </span>and erythropoietin&#46;<span class="elsevierStyleSup">4 </span>&#160;</p><p class="elsevierStylePara">&#160;5&#46; Activity on alpha-adrenergic receptor mediated vascular smooth muscle tone&#44; activity of nitric oxide synthase &#40;NOS&#41;&#44; and endothelial hyperpolarising factor &#40;EDHF&#41;&#46;<span class="elsevierStyleSup">3&#44;7 </span>&#160;</p><p class="elsevierStylePara">&#160;6&#46; Thyroid hormone deficits&#44; after foetal renal development&#44; may manifest both as functional abnormalities and anatomic abnormalities related to the presence of immune complexes in autoimmune thyroiditis&#46;<span class="elsevierStyleSup">9 </span>&#160;</p><p class="elsevierStylePara">&#160;7&#46; Functional abnormalities&#58; increased plasma creatinine&#44; hyponatraemia&#44; fluid retention&#44; loss of ability to concentrate urine&#44; and hyporegenerative anaemia&#46;&#160;</p><p class="elsevierStylePara">&#160;8&#46; Anatomic abnormalities<span class="elsevierStyleSup">10</span>&#58;&#160;</p><p class="elsevierStylePara">&#160;a&#41; Glomerular&#58; thickening of the glomerular basement membrane &#40;GBM&#41;&#44; amorphous mucopolysaccharide deposition in the mesangial matrix&#44; and mesangial cell vacuolisation&#46;&#160;</p><p class="elsevierStylePara">&#160;b&#41; Tubular&#58; thickening of the GBM&#44; cytoplasmic inclusions in the tubular epithelium&#44; and tubular necrosis in cases of rhabdomyolisis&#46;&#160;</p><p class="elsevierStylePara">&#160;The deterioration of renal function in hypothyroidism may present with hyponatraemia&#44; volume overload&#44; metabolic acidosis&#44; hypoaldosteronism relative low renin levels&#44; rhabdomyolysis with variable proteinuria&#44; and&#47;or anaemia&#44; but there is no common pattern of laboratory abnormalities&#46; Meanwhile&#44; CKD may cause abnormalities in the TSH circadian cycle&#44; reduce peripheral conversion of T4 and decrease renal secretion of iodine&#44; with prolongation of the Wolf- Chaikoff effect&#46;<span class="elsevierStyleSup">2 </span>The presence of subclinical hypothyroidism in patients with GFR less than 60ml&#47;min is 17&#46;9&#37; versus 7&#37; in patients with GFR greater than 90ml&#47;min&#46;<span class="elsevierStyleSup">2 </span>&#160;</p><p class="elsevierStylePara">&#160;There are numerous clinical case reports confirming the frequent association between hypothyroidism and decreased GFR&#44; both with advanced CKD<span class="elsevierStyleSup">8 </span>and in patients with preserved renal function&#46;<span class="elsevierStyleSup">11 </span>In published series of adult patients with primary hypothyroidism &#40;Montenegro&#44; with 41 patients<span class="elsevierStyleSup">12</span>&#41; or post-thyroidectomy &#40;Karanikas&#44; with 27 patients&#44;<span class="elsevierStyleSup">5 </span>Den Hollander&#44; with 37 patients&#44;<span class="elsevierStyleSup">13 </span>Baajafer&#44; with 124 patients&#44;<span class="elsevierStyleSup">14 </span>Kreisman&#44; with 24 patients<span class="elsevierStyleSup">15</span>&#41; there is a reversible decline in GFR that tends to recover 6-24 weeks after correction of thyroid function&#46; Muscular symptoms with CPK elevations were found in more than 90&#37; of cases&#46;<span class="elsevierStyleSup">8 </span>&#160;</p><p class="elsevierStylePara">&#160;In the case presented&#44; the spectacular recovery of the RF after correction of hypothyroidism forced us to review our initial diagnostic impression&#46; The advanced age of the patient with many cardiovascular risk factors&#44; respiratory disease&#44; and probable loss of function of the left kidney&#44; in addition to frequent hospital admissions&#44; made a diagnosis of multifactorial CKD very likely&#44; with little hope of improvement&#46; During follow-up&#44; there were no significant ionic changes in blood or urine&#46; No proteinuria&#44; metabolic acidosis&#44; or increased muscle enzymes were found&#46; There had been no changes to the standard treatment or other causes of renal failure to which we could attribute the progression&#44; nor was specific treatment implemented for the anaemia&#46; Both the improvement in GFR&#44; with the corresponding decline in serum creatinine&#44; as well as the spontaneous increase of haemoglobin levels are primarily attributable to the hormonal correction of hypothyroidism&#46; In our opinion&#44; thyroid function testing is recommended as part of the diagnostic process for renal failure of undetermined cause&#44; considering subclinical or manifest hypothyroidism among the possible causes of impaired renal function&#46;&#160;</p><p class="elsevierStylePara"><a href="grande&#47;10350&#95;18030&#95;5959&#95;en&#95;table1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10350_18030_5959_en_table1.gif" alt="Laboratory progression of plasma creatinine&#44; TSH&#44; T4&#44; sodium&#44; pH&#44; and haemoglobin"></img></a></p><p class="elsevierStylePara">Table 1&#46; Laboratory progression of plasma creatinine&#44; TSH&#44; T4&#44; sodium&#44; pH&#44; and haemoglobin</p><p class="elsevierStylePara"><a href="grande&#47;10350&#95;18030&#95;5960&#95;en&#95;figure1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10350_18030_5960_en_figure1.jpg" alt="Progression after stant of levothyroxine treatment&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Progression after stant of levothyroxine treatment&#46;</p>"
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Decrease in renal function associated with hypothyroidism
Deterioro de Función Renal Asociado a Hipotiroidismo
Vladimir Petkov Stoyanova, Juan A. Martín Navarroa, Evangelina Mérida Herreroa, Mª José Gutiérrez Sáncheza
a SECCIÓN DE NEFROLOGÍA, Hospital del Tajo, Aranjuez, Madrid, España,
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">Dear Editor&#44; </span>&#160;</p><p class="elsevierStylePara">&#160;The functional relationship between thyroid and kidneys has been described since the mid-twentieth century<span class="elsevierStyleSup">1 </span>and has been the subject of many publications with differing pathophysiologic approaches&#46;<span class="elsevierStyleSup">2-5 </span>&#160;</p><p class="elsevierStylePara">&#160;Here we present the case of a patient with a striking recovery of glomerular filtration rate &#40;GFR&#41; after correction of a diagnosed hypothyroidism&#46; This was an 89-year-old woman with hypertension&#44; hypertensive cardiomyopathy&#44; atrial fibrillation &#40;AF&#41;&#44; mitral insufficiency&#44; and moderate aortic insufficiency&#44; cerebral small vessel disease&#44; and obesity-hypoventilation syndrome&#46; She had undergone a cholecystectomy in April 2008&#44; with plasma creatinine in the normal range at that time&#46;&#160;</p><p class="elsevierStylePara">&#160;From April 2008 and March 2009&#44; she required several hospitalisations for episodes of rapid AF&#44; lacunar infarct&#44; heart failure&#44; and digoxin toxicity&#46; Progressive deterioration of renal function &#40;RF&#41; was seen until May 2009&#44; at which point evaluation by the nephrology service was requested &#40;Table 1&#41;&#46; Ultrasound showed left renal atrophy &#40;76mm diameter with corticomedullary disruption&#41; and 118mm right kidney with moderate cortical atrophy&#46; At that time&#44; the patient was diagnosed with stage 4 chronic kidney disease &#40;CKD&#41; secondary to reduction of functional renal mass and severe cardiovascular comorbidity&#44; with therapeutic changes consistent with the degree of CKD&#46;&#160;</p><p class="elsevierStylePara">&#160;After laboratory detection of primary hypothyroidism and the subsequent diagnosis of multinodular goitre due to autoimmune thyroiditis&#44; hormonal treatment was started with levothyroxine&#46; In the subsequent 6 months&#44; adequate control of hypothyroidism was seen with progressive recovery of GFR and increased haemoglobin levels&#44; exceeding expectations of reversibility of renal impairment &#40;Table 1 and Figure 1&#41;&#46;&#160;</p><p class="elsevierStylePara">&#160;Thyroid disorders cause abnormalities in many locations with the heart and kidneys being the main targets of action of thyroid hormones&#46;<span class="elsevierStyleSup">2-5 </span>Primary hypothyroidism&#44; which develops after intrauterine growth&#44; is associated with impaired glomerular filtration which is reversible with hormonal treatment in approximately 55&#37; of cases&#46;<span class="elsevierStyleSup">2 </span>Hyponatraemia is common &#40;45&#37; of cases with coexisting CKD versus 21&#37; with previously normal renal function&#41;&#44; as is fluid overload&#46;<span class="elsevierStyleSup">2 </span>Renal function deterioration secondary to hypothyroidism involves heterogenous mechanisms dominated by haemodynamic abnormalities&#58; a negative inotropic effect on the heart&#44; reduced circulating intravascular volume&#44; and increased peripheral resistance with renal vasoconstriction&#46;<span class="elsevierStyleSup">2-4 </span>&#160;</p><p class="elsevierStylePara">&#160;Among the effects of thyroid hormones are the following&#58;&#160;</p><p class="elsevierStylePara">&#160;1&#46; Gene regulation of structural and regulatory proteins such as Na&#43;&#47;K&#43; ATPase&#44; Ca<span class="elsevierStyleSup">2</span>&#43; ATPase&#44; Na&#43;&#47;Ca<span class="elsevierStyleSup">2</span>&#43; exchanger&#44; betaadrenergic receptors&#44; adenylate cyclase&#44; phospholamban&#44; myosin&#44; voltage-gated potassium channels and G proteins&#44; among others<span class="elsevierStyleSup">3-7 </span>&#160;</p><p class="elsevierStylePara">&#160;2&#46; Extragenic regulation of Na&#43;&#44; K&#43;&#44; and Ca2&#43; channels in the cell membrane&#46;<span class="elsevierStyleSup">3&#44;7 </span>&#160;</p><p class="elsevierStylePara">&#160;3&#46; Correlation with the reninangiotensinaldosterone system&#46;<span class="elsevierStyleSup">4&#44;6</span>&#160;</p><p class="elsevierStylePara">&#160;4&#46; Correlation with levels of argininevasopressin &#40;ADH&#41;&#44;<span class="elsevierStyleSup">4&#44;5 </span>brain natriuretic peptide &#40;BNP&#41;&#44;<span class="elsevierStyleSup">4&#44;6 </span>and plasma creatinine not dependent on renal function<span class="elsevierStyleSup">8 </span>and erythropoietin&#46;<span class="elsevierStyleSup">4 </span>&#160;</p><p class="elsevierStylePara">&#160;5&#46; Activity on alpha-adrenergic receptor mediated vascular smooth muscle tone&#44; activity of nitric oxide synthase &#40;NOS&#41;&#44; and endothelial hyperpolarising factor &#40;EDHF&#41;&#46;<span class="elsevierStyleSup">3&#44;7 </span>&#160;</p><p class="elsevierStylePara">&#160;6&#46; Thyroid hormone deficits&#44; after foetal renal development&#44; may manifest both as functional abnormalities and anatomic abnormalities related to the presence of immune complexes in autoimmune thyroiditis&#46;<span class="elsevierStyleSup">9 </span>&#160;</p><p class="elsevierStylePara">&#160;7&#46; Functional abnormalities&#58; increased plasma creatinine&#44; hyponatraemia&#44; fluid retention&#44; loss of ability to concentrate urine&#44; and hyporegenerative anaemia&#46;&#160;</p><p class="elsevierStylePara">&#160;8&#46; Anatomic abnormalities<span class="elsevierStyleSup">10</span>&#58;&#160;</p><p class="elsevierStylePara">&#160;a&#41; Glomerular&#58; thickening of the glomerular basement membrane &#40;GBM&#41;&#44; amorphous mucopolysaccharide deposition in the mesangial matrix&#44; and mesangial cell vacuolisation&#46;&#160;</p><p class="elsevierStylePara">&#160;b&#41; Tubular&#58; thickening of the GBM&#44; cytoplasmic inclusions in the tubular epithelium&#44; and tubular necrosis in cases of rhabdomyolisis&#46;&#160;</p><p class="elsevierStylePara">&#160;The deterioration of renal function in hypothyroidism may present with hyponatraemia&#44; volume overload&#44; metabolic acidosis&#44; hypoaldosteronism relative low renin levels&#44; rhabdomyolysis with variable proteinuria&#44; and&#47;or anaemia&#44; but there is no common pattern of laboratory abnormalities&#46; Meanwhile&#44; CKD may cause abnormalities in the TSH circadian cycle&#44; reduce peripheral conversion of T4 and decrease renal secretion of iodine&#44; with prolongation of the Wolf- Chaikoff effect&#46;<span class="elsevierStyleSup">2 </span>The presence of subclinical hypothyroidism in patients with GFR less than 60ml&#47;min is 17&#46;9&#37; versus 7&#37; in patients with GFR greater than 90ml&#47;min&#46;<span class="elsevierStyleSup">2 </span>&#160;</p><p class="elsevierStylePara">&#160;There are numerous clinical case reports confirming the frequent association between hypothyroidism and decreased GFR&#44; both with advanced CKD<span class="elsevierStyleSup">8 </span>and in patients with preserved renal function&#46;<span class="elsevierStyleSup">11 </span>In published series of adult patients with primary hypothyroidism &#40;Montenegro&#44; with 41 patients<span class="elsevierStyleSup">12</span>&#41; or post-thyroidectomy &#40;Karanikas&#44; with 27 patients&#44;<span class="elsevierStyleSup">5 </span>Den Hollander&#44; with 37 patients&#44;<span class="elsevierStyleSup">13 </span>Baajafer&#44; with 124 patients&#44;<span class="elsevierStyleSup">14 </span>Kreisman&#44; with 24 patients<span class="elsevierStyleSup">15</span>&#41; there is a reversible decline in GFR that tends to recover 6-24 weeks after correction of thyroid function&#46; Muscular symptoms with CPK elevations were found in more than 90&#37; of cases&#46;<span class="elsevierStyleSup">8 </span>&#160;</p><p class="elsevierStylePara">&#160;In the case presented&#44; the spectacular recovery of the RF after correction of hypothyroidism forced us to review our initial diagnostic impression&#46; The advanced age of the patient with many cardiovascular risk factors&#44; respiratory disease&#44; and probable loss of function of the left kidney&#44; in addition to frequent hospital admissions&#44; made a diagnosis of multifactorial CKD very likely&#44; with little hope of improvement&#46; During follow-up&#44; there were no significant ionic changes in blood or urine&#46; No proteinuria&#44; metabolic acidosis&#44; or increased muscle enzymes were found&#46; There had been no changes to the standard treatment or other causes of renal failure to which we could attribute the progression&#44; nor was specific treatment implemented for the anaemia&#46; Both the improvement in GFR&#44; with the corresponding decline in serum creatinine&#44; as well as the spontaneous increase of haemoglobin levels are primarily attributable to the hormonal correction of hypothyroidism&#46; In our opinion&#44; thyroid function testing is recommended as part of the diagnostic process for renal failure of undetermined cause&#44; considering subclinical or manifest hypothyroidism among the possible causes of impaired renal function&#46;&#160;</p><p class="elsevierStylePara"><a href="grande&#47;10350&#95;18030&#95;5959&#95;en&#95;table1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10350_18030_5959_en_table1.gif" alt="Laboratory progression of plasma creatinine&#44; TSH&#44; T4&#44; sodium&#44; pH&#44; and haemoglobin"></img></a></p><p class="elsevierStylePara">Table 1&#46; Laboratory progression of plasma creatinine&#44; TSH&#44; T4&#44; sodium&#44; pH&#44; and haemoglobin</p><p class="elsevierStylePara"><a href="grande&#47;10350&#95;18030&#95;5960&#95;en&#95;figure1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10350_18030_5960_en_figure1.jpg" alt="Progression after stant of levothyroxine treatment&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Progression after stant of levothyroxine treatment&#46;</p>"
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