Case Report

Endocrinology Division

HYPOTHYROIDISM AND ACUTE

KIDNEY INJURY

Ati Salami
INTRODUCTION
 Hypothyroidism results from a lack of thyroid hormone
production, either due to a defect in the gland (primary
hypothyroidism), or due to a lack of stimulation from
Thyroid Stimulating Hormone, TSH.

 This disorder can manifest from birth (congenital) or

because of causal acquired.
INTRODUCTION
 Acute Kidney Injury  sudden decrease in renal function
with the loss of the kidney's ability to maintain body
homeostasis.
 Nowdays, the term used is Acute Kidney Injury (AKI) to
increase alertness to early-stage disorders of the kidneys.
 Classification in children  pRIFLE : risk, injury, failure,
end stage and loss.
 This disorder can be caused by Pre-renal, Renal, or
Post renal causes.
INTRODUCTION
 One Renal cause that is rarely found to cause acute renal
impairment is Hypothyroidism.

 The main mechanisms of hypothyroidism causing acute renal

impairment are not fully known, but the tendency for renal
impairment is due to reduced plasma flow of the kidneys and
glomerular filtration rate (GFR) resulting from hypodinamic
circulation.
CASE REPORT

We report a case of AKI as the complication of

Hypothyroidism
A.A.J, ♀,12 years 8 months, admitted to
pediatric department with a major febrile
complaint (Figure 1). Fever experienced
since about 4 days before entering hospital.
Another complaint in the form of a history of
blood-colored 2 days before entering the
hospital. History of irregular defecation.
Urination <<. Currently the child is able to
speak but seems slow. Children can walk at
the age of 5 years.
Image 1. Picture the patient on
the first day of treatment
 DATA
Weakness since born, she rarely
History taking : Fever  4 days cries. was not able to walk until the
before admitted, no convulsion. No age of 5 years. Starts talking at the
cough, no dyspnea, no vomiting. No age of 9 years, was only able to say
direct contact with DHF patient. one word at a time. Not able to talk
in full sentence.
CASE
General condition: moderately There was dismorphic face ,puffy
ill/well nourished/alert; T face, pale, hypertelorism, no low set
37,8 oC, other vital sign ears, macroglossi, nor simian line.
within normal limit; BW 23 Dry Skin .pubertal state A1M1P1.
kg; H 105 cm Ascites, shifting dullness
Image 2. Body Height < 3th
percentile (Short stature)
LAB. & RO ( RSWS, 15/04/2017)
GDS 101 mg/dl, Ureum 174
Hemoglobin 7,3 g/dl, MCV 85,2 fL,
mg/dl, kreatinin 8,69 mg/dl, (GFR
MCH 28,4 pg, hematokrit 21,9 %,
6,6 ),SGOT 59 U/l, SGPT 24 U/l,
lekosit 4.590/mm3, trombosit
albumin 3,0 g/dl, DHF IgG
40.000/mm3, eritrosit 2,57
Negatif, IgM DHF negatif, Natrium
juta/mm3. Hitung jenis: neutrofil
133 mmol/L, Kalium 4,7 mmol/L,
48,8%, limfosit 9,4%.
&Chlorida 100 mmol/L

Urinalysis :
Abdominal Ultrasound
Dark yellow, pH 6, protein, : Bilateral Mild
Leukosit +-/15, blood Hydronephrosis & minimal
+3/200, sed leu 3 lpb, sed ascites
eryt 40 lpb
Image 3. abdominal ultrasound : Bilateral Mild Hydronephrosis &
Minimal Ascites
WORKING DIAGNOSIS
 Chronic Kidney Disease stage V
 Bilateral Hydronephrosis
 Mild-Moderate acute diarrhea
 Hypothyroidism DD Down’s Syndrome
 Short Stature
 Anemia on chronic Disease
 Trombocitopenia
MANAGEMENT
- Rehydration with Ringer lactate
- Zinc 20 mg / 24 hours / oral
- Paracetamol 230 mg / 8 hours / intravenous
- Nephrology division cooperation, MSCT
urography plan (without contrast)
- Cooperation to the division of Hematology,
Tracking anemia
- Tracking Hypothyroidism
- Nutritional care
Day 2 Subjective /objectives Planning

watery stool 2x; urination 0,68 ml/BW Nepgrology :

Cefotaxime

Laboratory :
FT4 0,08 ng/dL ( Normal : 0,932-1,71
mg/dL) Endocrinology:
TSHs >60 mlU/ml (Normal: 0,270-4,20 L-thyroxine 50 mcg/24
mlU/ml) jam/oral

ureum 205 mg/dl, kreatinin 9,1 mg/dl,

PT/aPTT 9,8 detik/22,8 detik (INR 0,94), Hemathology :

ferritine >1200 ng/ml Epo 2000 iu/iv

Bone Age : 4 year

MSCT Urography : hepatomegaly,sistitis,
Hypothyroid
pneumovesika
 BONE AGE (according to Greulich and Pyle)
THIS PATIENT

4 years, 2 months old female Patient (12 years, 8 months) 12 years old female
Image 4. MSCT Scan
Urograpy : :
Hepatomegaly, cystitis
with pneumovesica,
bilateral pleural efusi
Day 3 Subjective /objectives Planning
tachypneu (+), RR 32 x/mt, Fever (-) Hematology :
urination 0,99 ml/BW Blood transfusion
lab :
HGB 6,6 gr/dl , WBC 9.730/mm3, PLT 109.000/mm3 L-Thyroxine continued

Day 6 Subjective /objectives Planning

coomunicative, bowel problem (-), urination 0,83
ml/BW L-Thyroxine continued
Lab :

Hb 8,1 gr/dl; WBC 6600/mm3; PLT 231.000/mm3

Ureum 194 mg/dl; Creatinine 4,50 mg/dl
total protein 5,2 gr/dl; Albumine 2,1 gr/dl;
total cholesterol 134 mg/dl. Calcium 7,7 mg/dl (N= 6,8-10,2)
urine culture (17-06-2016): no growth
Blood culture (17-06-2016): no growth
Image1. After 4 days of L-thyroxine
therapy
Day 9 Subjective /objectives Planning
urination 1,38 ml/BW
lab : Congenital Hypothyroidism
Hb 7,5 gr/dl; WBC 6900/mm3; PLT 390.000/mm3 Acute Kidney Injury
Ur 87 mg/dl; Cr 1,40 mg/dl; Total Cholesterol 205
mg/dl
Total protein 6,1 gr/dl; Albumin 2,9 gr/dl
thyroid ultrasound : Bilateral Thyroid Hypoplasia
with cystic nodule

Day 13 Subjective /objectives Planning

lab : OPD

Hb 10,1 gr/dl; WBC 6400/mm3; PLT 447.000/mm3

Ureum 34 mg/dl; Creatinine 0,30 mg/dl;
Calcium 10,2 mg/dl

FT4 1,39 ng/dl; TSHs 0,08 mlU/ml

 DEFINITIVE DIAGNOSIS

 Congenital Hypothyroidism
 Acute Kidney Injury
 Anemia on chronic disease
DISCUSSION
DISCUSSION
Role of thyroidhormon in Metabolism
 Renal Physiology
 affect protein synthesis and cell growth. Thyroid hormone
status affects renal mass function (renal mass to the
body), hypothyroidism reduces this ratio.
 However, severe hyperthyroidism leads to the breakdown
of protein and kidney atrophy in the end.
 In addition, children with congenital hypothyroidism have a
high incidence of congenital renal abnormalities.
 function of the neonate kidney. Thusthyroid hormones play
an important role in kidney development and early kidney
function.
 Renal Blood Flow (RBF) decreases with decreased cardiac
output (negative chronotropic and inotropic effects),
increases peripheral vascular resistance, intrarenal
vasoconstriction, reduces renal response to vasodilators, and
decreases renal vasodilator expression such as vascular
endothelial growth factor ( VEGF) and insulin like growth
factor-1 (IGF-1).
 Pathological changes in the glomerular structure of
hypothyroidism, such as thickening of the glomerular
basement membrane and mesangial matrix expansion, may
also lead to reduced RBF
These patient
Chronic Kidney Disease

Acute Kidney Injury

CKD
1. Kidney damage> 3 months à abnormality of a / f (x) kidney
with / without decrease (GFR) structure, which manifests as
one or more symptoms:
a. Abnormalities of urine composition
b. Imaging abnormality
c. Kidney biopsy abnormalities

2. GFR <60 mL / min / 1.73 m2 for> 3 months with /

without any other renal impairment mentioned.
These patients
 Fall in GFR of more than 90% and is
accompanied by anemia so that the patient is
diagnosed with CKD.
 Hormone therapy (Levothyroxine), a serum
creatinine decrease that shows kidney damage is
still reversible  Acute Kidney Injury.
 No Renal Congenital Abnormalities (Imaging)
Zhenhua et al. (Shanghai, 2015)

HYPOTHYROIDIS
Systemic M
• Mucopolysacchari
Metabolism de deposition
Interstitial mucin Myocardial • Glomerular
accumulation
Blood lipid
myxedema membrane
• Organ thickening
dysfunction • Endothelial cell
• Protein Heart Atherosclerotic proliferation
synthesis contractility blood vessels • Tubular epithelial
• Weakened cell cytoplasm
muscle Vascular content
contraction Bradicardia resistance
• Myxedema
• Water
trapping Cardiac output
Renal plasma
flow Restrict blood
flow

Plasma Atrial Natriuretic Renal

HYPOVOLEMIA GFR
Peptide release
vasoconstriction
Thyroid hormones in Erythropoiesis
Increased oxygen consumption in cells will increase the
production of erythropoietin in the erythropoesis system.
However, blood volume does not increase due to red cell
turnover process. Thyroid hormones increase 2,3-
diphospogliserat contained erythrocytes so that oxygen levels
in hemoglobin and tissue increase. Thus, in case of
hypothyroidism, this process will be disrupted.
Child Growth and Development

 The role of hormonal factors in growth depends on age and

developmental phase.
 The development of endocondral ossification and linear growth is
closely regulated by local feedback mechanisms involving :
- Indian hedgehog (IHH) and PTHrP,
- other factors including systemic hormones (thyroid hormone,
GH, IGF-1, glucocorticoids, sex steroids), various cytokines, and
growth factors (BMP, FGF, vascular endothelial growth factor) that
act in paracrine and autocrine ways.
 Linear growth continues until melting growth plate during
puberty (Figure 7).
Thyroid hormone is one element that is
involved in the process of bone lengthening,
then in children who have thyroid hormone
disorders can occur short stature.
Short Stature
Short stature is less height than the percentile-3 on the curve
that is appropriate for gender, age and race.

 Not a final diagnosis, but the first step is to determine

whether the SS is pathological or physiological (normal
variant).
 Height between -2SD and -3SD approximately 80% is a
normal variant. Whereas if height> -3SD then pathological
possibility is 80%.
These patient :
Height below the 3rd
percentile based on the
CDC curve
Caused By
Hypothyroidism
Neurodevelopment
Thyroid hormones are essential for brain development :
 Neurogenesis
 Neuron migration,
 Neuronal and glial cell differentiation,
 Myelination
 Synaptogenesis.
Congenital Hypothyroidsm
Hypothyroidism : primary and secondary, or congenital and
acquired, as well as persistent or transient.
Congenital hypothyroidism is the most common cause of
mental retardation, due to inadequate production of thyroid
hormones in newborns.
Congenital hypothyroidism may occur due to an anatomic
defect in the thyroid gland, inborn errors of thyroid
metabolism, or iodine deficiency.
Incidence rate women : men 2:1.
Cause of CH
Thyroid dysgenesis is the most common cause of nonendemic
congenital hypothyroidism, approximately 85-90% of cases
of congenital hyperthyroidsm.
Thyroid dysgenesis may be the absence of total thyroid tissue
(agenesis), or partial (hypoplasia) that can result from failure
of thyroid gland to neck (ectopic).
Genetic and environmental factors may play a role in the
etiology of thyroid dysgenesis, but most of the causes are
unknown.
These Patient
 Congenital hypothyroid because thyroid ultrasound results
show thyroid hypoplasia. This indicates the presence of
thyroid gland but because of its small size so that the ability
to produce hormones is also disrupted.
 The therapy given is giving Levothyroxine (Euthyrox) at a
dose of 50 mcg per day
 Age Levo thyroxine (μg /
KgBB / day

0 – 3 bulan 10-15
3 – 6 bulan 8-10
6 – 12 bulan 6-8
1 – 3 tahun 4-6
3 – 10 tahun 3-4
10 -15 tahun 2-4
> 15 tahun 2-3
Summary
Reported one case of Acute Kidney Injury in Congenital
Hypothyroidism in a girl, aged 12 years and 8 months. Diagnosis is
based on history taking that is short stature, defecation disorder
that the child defecate once every 3 days, delays in the
development which child can walk by the age of 5 years, the child
seemed very slow in every movement. Physical examination
showed a pale, dysmorphic face, hypertelorism, makroglossi, and
at the height lies far below percentile 3rd. Investigations showed
anemia, thrombocytopenia, azotemia, hypoalbuminemia,
increased levels of TSHs and decreased levels of FT4. Treatment
given is hormonal therapy and supportive. Prognosis of this case is
dubia.
Thank You
Stadium GFR Deskripsi

1 >90 GFR normal/meningkat

2 60-89 Penurunan GFR ringan

3 30-59 Penurunan GFR sedang

4 15-29 Gagal ginjal

5 <15 (dialisis)