THESIS PROTOCOL

DEPARTMENT OF NEPHROLOGY
DHAKA MEDICAL COLLEGE, DHAKA, BANGLADESH
PART-A

Title: Association of Left ventricular Hypertrophy with Hypertension

and Hyperparathyroidism in ESRD Patients

1. Principal Investigator: Dr. Shanjida Sultana Juthy

MD Resident (Phase B)
Department of Nephrology,
Dhaka Medical College, Dhaka
2. Guide: Dr. Md. Nazrul Islam
Professor & Head
Department of Nephrology
Dhaka Medical College & Hospital,
Dhaka
3. Co-guide: NA
4. Place of the study: Dhaka Medical College & Hospital, Dhaka

5. Duration of the study: 18 months

6. Study period: February 2021 to August 2022

7. Type of study: Hospital based prospective observational

study
8. Total cost: 3,70,000 Taka

9. Signature of the Principal

Investigator:

Dr. Shanjida Sultana Juthy

MD Resident (Phase B)
Department of Nephrology, Signature
Dhaka Medical College, Dhaka
10. Signature of Guide:
Dr. Md. Nazrul Islam
Professor & Head
Department of Nephrology
Dhaka Medical College & Hospital, Signature
Dhaka
Title: Association of Left ventricular Hypertrophy with Hypertension
and Hyperparathyroidism in ESRD Patients

Summary
Cardiovascular dieases are major causes of mortality among patients with end-stage

renal disease( ESRD) (Sliva LS et al, 2012), who are highly at risk of developing left

ventricular hypertrophy (LVH) (Charytan D, 2014). LVH is a powerful predictor of

mortality and several independent factors contribute to the development of LVH in

dialysis patients including fluid overload, anemia, hypertension, hyperparathyroidism

and arteriovenous fistula. HTN is a crucial factor for LVH development in ESRD

patients. However , recently parathormone has been identified as a important cardio-

toxin which causes deleterious effects on myocardial metabolism and function by

intracellular influx of calcium and activates cardiac fibroblasts which in turn causes

cardiac fibrosis (N.Al-Hilali,2009). So early detection of hyperparathyroidism and

proper management of both HTN and hyperparathyroidism may reduce the

cardiovascular burden in ESRD patients. As there are very few studies regarding the

association between HTN and hyperparathyroidism with LVH in ESRD patients ,the

present study is designed to examine the close relation of HTN and elevated intact

parathyroid hormone in LVH and to evaluate their synergistic effect as risk factor for

LVH as well as LV ejection fraction in hemodialysis patients without other major risk

factors . This hospital based prospective observational study will be conducted at the

department of Nephrology in Dhaka Medical College and Hospital. Total 96 CKD

patients, fulfilling the criteria will be included in the study .Patients will be

subdivided into three groups on the basis of mean arterial pressure and level of

parathyroid hormone and a comparative study will be done among three groups .A

pre-tested questionnaire will be used for interview. The study duration will be for 18
months after approval of the protocol. Informed written consent will be obtained in all

cases. Following completion of the data collection, data analysis will be done SPSS

version 23.

Introduction

Cardiovascular risk factors are a significant burden in end-stage renal disease patients

under hemodialysis and cardiovascular-related diseases are the leading cause of death

among these patients and are responsible for almost half of all deaths in dialysis

patients (Nasri H, Baradaran A, 2004). Dialysis patients are subject to atherosclerosis

and consequent ischemic heart disease, but myocardial dysfunction and overt heart

failure are also highly prevalent. Eighty-four percent of patients have left ventricular

hypertrophy (LVH), left ventricular (LV) dilatation, low fractional shortening at the

initiation of ESRD therapy, and LVH has been found in 38% of patients with chronic

renal failure (CRF) prior to the requirement for dialysis (Rahn KH et al ,2000).

Left ventricular hypertrophy (LVH) is frequent in maintenance dialysis patients(Nasri

H, Baradaran,2004). LVH is a condition in which exhibit myocyte hypertrophy, loss

of myocardial capillaries, increased interstitial fibrosis, and reduced capillary-to-

myocyte ratio (Vida Nesarhosseini et al, 2019) .The pathogenesis of LVH in ESRD is

multifactorial including fluid overload, anemia, hypertension, hyperparathyroidism,

disturbed elasticity of central arteries, arterio-venous fistula, hypoalbuminemia,

sympathetic over activity and hormonal factors such as endothelin ,renin etc (Randon

RB etal,2005). LVH causes difficulty of the heart’s left ventricle in pumping blood
and consecutively causes systolic and diastolic dysfunction, reduces blood supply in

coronary arteries, and eventually gives rise to side effects such as ischemia,

myocardial infarction, heart failure, and sudden death. The physiological factors

responsible for LVH are isometric exercise, pregnancy, old age, obesity, and salt

intake; the pathological factors implicated in the disease are relevant to hypertension

(HTN), aortic stenosis (AS), aortic insufficiency, hypertrophic cardiomyopathy, and

other cardiomyopathies (Cerasola G et al,2011). The specific incidence rate of LVH

among patients with ESRD is 68% to 89%, and the disease often occurs in

progressive form (London GM et al, 2001). The prevention of LVH can improve the

survival of ESRD patients. For example, a 10% reduction in LVH results in a 28%

decrease in the risk of cardiac mortality among patients on dialysis (Ferrario CM ,

2006).

Recently, parathyroid hormone (PTH) has been identified as an important cardio-

toxin in end stage renal disease. Parathyroid hormone (parathormone) is a main

regulator of calcium and is a principal regulator of bone and mineral homeostasis

(Bacchetta J et al, 2007). Heart and vessel disease starts early during the progression

of chronic renal failure and is the mainly common cause of death in these individuals

(Bacchetta J et al,2007). Parathyroid hormone is a polypeptide containing 84 amino

acids secreted by parathyroid glands (Palmer SC et al, 2015). Mechanisms of

extension of heart and vessel disease are ill-understood. However, dysregulated

homeostasis of parathyroid hormone, vitamin D, calcium and phosphorus are

responsible partly in cardiac dysfunction in chronic renal failure patients (Evenepoel

P,2014). Secretion of parathormone is moderated by alterations in concentration of

calcium in the blood. In fact, reduced calcium concentration stimulate PTH secretion
by the calcium-sensing receptors located in the parathyroid gland. Parathormone

forms a tightly controlled feedback cycle and to response to hypocalcemia, this

hormone has various targets to increase serum calcium concentration (Ketteler M

etal,2017). Parathormone is also a key stimulator of vitamin D production in renal

tissue and its major physiologic regulator is circulating ionized calcium. The impact

of parathormone on intestinal cells, renal tissue, and also bone leads to maintain

serum calcium levels within a narrow range. However, elevated levels of parathyroid

hormone have been correlated with increased risks of congestive heart failure,

cardiovascular mortality hypertension and hypertrophy of left ventricle (Dusso A et

al, 2011). Indeed, disturbed arterial function due to endothelia cell dysfunction is

responsible for the above mentioned organ dysfunctions. Thus, cardiac tissue is one of

the target organs of parathyroid hormone. Parathormone has a direct hypertrophic

property on heart myocytes by activating protein kinase C that further stimulates

hypertrophic growth and re-expression of fetal type proteins in heart tissue. PTH

increases calcium influx into cardiomyocytes (Van Ballegooijien et al,2016) and

activates fibroblasts (Nasri H, 2006). Calcium overload and interstitial fibrosis may

lead to impairment of left ventricular diastolic function.

The hypertrophic effect of parathyroid hormone on cardiac cells also is detected by a

close association between parathormone levels and proportion of left ventricular mass

in end stage renal disease (ESRD)(Gruson D etal ,2016). Previous studies have

supported the view that high serum PTH serum levels in uremic patients may cause

deleterious effects in myocardial metabolism and function (Massry SG,

Smogorzeweski M ,1996). Another study, Block et al. found that hyperphosphatemia

was an independent risk factor of cardiovascular mortality in dialysis patients (Block

G.A. et al, 1998). Also, high calcium × phosphorus (Ca × P) product is the marker of

elevated cardiac mortality risk.

Secondary Hyperparathyroidism (SHPT) is a major complication of CKD, resulting

from disturbances in the regulation of PTH, calcium, phosphorus, and vitamin D.

Although hyperphosphatemia appears to be particularly important in the development

of SHPT, the complication often occurs early in stage 3 of kidney failure, before the

development of hyperphosphatemia (Sela-Brown A et al,1999 and Slatopolsky E et al,

1994) A majority, if not all, of untreated CKD patients will develop SHPT as a result

of the kidney’s inability to maintain mineral homeostasis.

Several investigators have found that myocyte hypertrophy and increased interstitial

collagen matrix in renal failure are related to PTH concentrations and LVH has been

noted in uremic patients with high PTH levels. In some clinical studies, LV

dysfunction was observed with uremia and an improvement of cardiac function, BP

reduction, and LVH regression were observed after proper treatment of

hyperparathyroidism (Parfrey PS et al,1987 and Drueke T et al,1980). Treatment of

the contributing factors may result in regression of LVH with the subsequent

improvement in patient outcome. The relationship between elevated PTH and LVH

was further explored in a retrospective study by Goto et al., who determined that

parathyroidectomy in CKD patients with advanced SHPT led to a significant

improvement of left ventricular ejection fraction and function.67 A prospective study

of 15 patients by Park et al. confirmed the association with SHPT, finding that PTH-

suppressive calcitriol therapy led to a regression in myocardial hypertrophy in dialysis

patients(Cheol Whee Park et al,1998).

Hypertension is frequently (80-90%) seen in patients with end stage renal disease ( N.

Al-Hilali et al,2009). LVH as a consequence of HTN usually presents with an

increase in wall thickness with or without an increase in cavity size. Hypertensive

patients in hemodialysis have higher left ventricular mass indices than normotensive

patients, but similar to those of no uremic hypertensive patients signifying that

hypertension is a crucial factor for LVH development.

The present study will be conducted to examine the role of excess PTH and HTN in

the development of LVH as well as LV ejection fraction and to evaluate their

synergetic effect as risk factors for LVH in hemodialysis patients without other major

risk factors.
Rationale of the study

It is well known that half of the patients on chronic hemodialysis (HD) die of

cardiovascular disease, predominantly congestive heart failure, ischemic heart disease

resulting from left ventricular hypertrophy (LVH), considered as the major single

reason for such high mortality. Among the multiple factors involved in the origin of

LVH, the association of uremia, high blood pressure, anemia and elevated parathyroid

hormone are specific to ESRD. Association of LVH with secondary

hyperparathyroidism and hypertension is commonly observed in hemodialysis

patients. Therefore, this association might contribute in escalating LVH. By early

assessment and management of secondary hyperparathyroidism and HTN, may

address cardiovascular complications and thus reduce morbidity and mortality

burden of end stage renal disease (ESRD) patients .As there is no such study in

Bangladesh and it becomes a burning issue so this study aims to determine the

association of LVH with HTN and hyperparathyroidism on hemodialysis patients .

Research question:

What is the association of Left ventricular Hypertrophy with Hypertension and

Hyperparathyroidism in ESRD Patients
Objectives:

General objective:

Association of Left ventricular Hypertrophy with Hypertension and

Hyperparathyroidism in ESRD Patients

Specific objectives:

1. To determine the association between left ventricular hypertrophy and

HTN in ESRD Patients.
2. To evaluate the association between left ventricular hypertrophy and
secondary hyperparathyroidism in ESRD patients.
3. To assess the relation between left ventricular dysfunction and
hyperparathyroidism along with HTN in ESRD patients.

RESEARCH METHODOLOGY
Study Design: Prospective observational study

Place of Study: Dhaka Medical College and Hospital

Period of study: February 2021 – August 2022

Study population: End stage renal disease (ESRD) patients on

hemodialysisHD)

Sample size:

The sample size of this study will be determined by following equation:

Here, 
zα= Z value (two tail) of standard normal distribution at 95%

confidence level or 5% level of significance = 1.96 (when α = 0.05

at 5% level of significance)

zβ= Z value (one tail) at 90% power = 1.28 (when β = 0.1 and

Power = (1-β)

σ1= 13 (Standard deviation of eGFR in CKD patients before fasting in

Ramadan) (NasrAllah MM et al, 2014)

σ2= 15 (Standard deviation of eGFR in CKD patients after fasting in

Ramadan) (NasrAllah MM et al, 2014)

µ1- µ2= 8.5 (mean change in eGFR in patients) (NasrAllah MM et al, 2014)

Therefore,

n=
=57.2
 

Total 57 patients will be included in this study.

Sampling technique: Purposive sampling

 Selection criteria:

Inclusion criteria:

 Age: >18 years of both sex

 All patients received their dialysis treatment 2 times per

week, 4 h per session (12 h ???weekly) for atleast 6
months

Exclusion criteria:

• Patients with severe anemia

• Coronary artery disease

• Cardiomyopathies

• Valvular heart disease

• Previous parathyroidectomy, and

• connective tissue diseases

Variables:

Demographic variable:
 Age
  Sex

Clinical variable:
 Body mass index(BMI)-??
 Anemia
 Blood pressure
 Duration of dialysis
 Underlying cause of CKD
 Medications-vit D3

Laboratory variable:
 Hemoglobin
 Serum Calcium
 Serum phosphorus(p)
 Ca x p products
 Fasting lipid profile
 iPTH
 Serum Albumin

Outcome variables:

 Serum Creatinine/ Estimated glomerular filtration rate

(eGFR)

Investigations:

 Complete blood count (CBC)

  Serum Calcium

 Serum phosphorus

 Fasting lipid profile

 Serum Albumin

 iPTH

 ECG

 Echo cardiogram

 USG of Whole Abdomen

Operational definitions:

CKD: CKD will be defined as kidney damage or estimated glomerular filtration

rate (eGFR) of < 60 ml/min/1.73 m2 for > 3 months as per NKF-K/DOQI
guidelines. To determine the evidence of kidney damage abdominal ultrasonography
will be done. (Levey, A.S et al, 2002)
Stages of CKD: (Levey, et al, 2002)
CKD stages will be defined as per NKF-KDOQI guidelines-
•Stage 1: Patients with > 90 eGFR (ml/min/1.73 m2) and evidence of kidney
damage,
•Stage 2: Patients with 60-89 eGFR (ml/min/1.73 m2) and evidence of kidney
damage,
•Stage 3: Patients with 30-59 eGFR (ml/min/1.73 m2),
•Stage 4: Patients with 15-29 eGFR (ml/min/1.73 m2) and
•Stage 5: Patients who will have <15 eGFR (ml/min/1.73 m2) or on dialysis.
Modification of Diet in the Renal Disease (MDRD) equation will be used to
estimate eGFR [eGFR = 186 x (creatinine in umol/L/88.4)-1.154 x (age in yrs)-0.203
x (0.742 if female) x (1.21 if black)].

Stable Serum Creatinine:

It is defined as fluctuations of <10% in at least three readings during the 3 months
prior to the month of Ramadan. (Kara E, Sahin OZ et al ; 2017)

Pre-existing cardiovascular disease:

Defined as stable heart failure, coronary heart disease, stroke or peripheral vascular

disease documented at least 3 months before onset of the study. (M. NasrAllah, N

Osman et al; 2014)

Deterioration of renal functions: It is defined as ≥30% rise in serum creatinine and/

or ≥25% drop in eGFR levels from baseline after at least 7 days of fasting or after 3

months of Ramadan. (Kara E, Sahin OZ et al ; 2017)

Study procedure:

Before starting the study, formal ethical approval will be taken from the Ethical
review committee (ERC) of DMC. Selection of the patients will start according to
inclusion and exclusion criteria from beginning of the 2021 and end of 2022
respectively. Patients who will choose have to receive their dialysis 2 times per week
4 h per session for at least 6 months. After selection of participants in according to
the inclusion and exclusion criteria, patients will be approached for inclusion of study.
Following informed about the study aim, objectives and procedure, informed written
consent will be taken from each participant. History taking focusing clinical features,
disease duration along with physical examination will be done as per standard
protocol. Polysulfone dialyzers and a bicarbonate bath with a dialysate Ca
concentration of 1.25 mmol/L and Na concentration of 136 mmol/L will be used for
dialysis. The blood flow rate will be ≥300 mL/min and the dialysate flow rate will be
800 mL/min. All patients will be receiving recombinant erythropoietin intravenously
2-3 times postdialysis. No dialyzers will be reused in our unit. The dialysis dose as
Kt/V will be calculated according to DOQI guidelines. All patients will be subjected
to M-mode echocardiography. Echocardiograms will be performed when the patient
reached their estimated ideal weight. Left ventricular diameters and wall thicknesses
will be measured from 2-dimensional targeted M-mode echocardiography. Left
ventricular mass (LVM) will be calculated by using Devereux's formula, and will be
indexed (LVM index) for body surface area,[17,18] considering the diastolic
measurements of left ventricular internal diameter (LVID), interventricular septal
thickness (IVST) and posterior wall thickness (PWT): LVMI (g/m ) 5 (1.04 [(IVST 1
LVID 1 PWT) 3-LVID3]-14 g)/Body surface area. Body surface area (BSA) will be
calculated using the Du Bois formula: BSA (m 2 ) =0.007184 X weight (kg)0.425 X
height(cm)0.725.[19] LVH will be defined as LV mass index (g/m ) greater than 131
g/m in men and greater than 100 g/m in women.[20] Blood pressure will be measured
by using a standard automatic blood pressure machine of the same for all patients. An
average of three measures will be taken to calculate the mean arterial blood pressure.
The mean arterial blood pressure (MAP) will calculated by the following equation:
MAP= DBP+1/3(SBP-DBP) .Mean arterial blood pressure (MAP) of 107 mmHg
will be considered to be high. Blood samples will be drawn from the arterial side of
the vascular access before starting dialysis and prior to heparin administration, in the
midweek session after a 48-h dialysis free interval. Serum levels of intact parathyroid
hormone, cholesterol, triglycerides, high density lipoprotein (HDL) and hemoglobin
will be measured. Sera of the patients will be analyzed for intact parathyroid hormone
(iPTH). Intact PTH will be measured with immune radiometric assay (IRMA) method
in the same laboratory. Other biochemical parameters will be carried out by
standardized clinical laboratory methods. Patients will be stratified into 3 groups
according to MAP and iPTH. Group 1 where BP will be less than 107 mm hg with
iPTH less than 300 ng/l ,group 2 where BP less than 107 mm hg with iPTH more
than 300 ng/l and group 3 where BP more than 107 mm hg and iPTH more than 300
ng/l. iPTH more than 300 ng/l and mean blood pressure (MAP) will be considered to
be high for the study. All collected information will be stored in separate data record
form. After checking all the data will be analysed by SPSS 23.

Data collection:

Data will be collected in a pre-tested questionnaire by taking history, examining the

patients clinically, laboratory finding and patient outcomes. The data will be collected

by researcher himself.

Analysis of the study:

Following data collection, the collected data will be assessed for completeness,

accuracy and consistency before analysis was commenced. Data analysis will be

carried out by using SPSS version 23 (IBM Corp., Armonk, NY). Exploratory data

analysis will be carried out to describe the study population where categorical

variables will be summarized using frequency tables while continuous variables will

be summarized using measures of central tendency and dispersion such as mean,

median, percentiles and standard deviation. Qualitative or categorical variables will be

described as frequencies and proportions. Repeated measure ANOVA will used to

compare the outcome in between three groups. Moreover, Kaplan-Meier life table

analysis will be used to document and test for any differences in the time to the

catheter removal event. A level of P< 0.05 will be considered statistically significant.

Time schedule for activities (18 months)

Sl.no Name of milestones Time

1. Topic selection 1 month

2. Literature search and review 1 month

3. Data collection 13 months

4. Data entry and Data analysis 3 months

Ethical consideration:

The researcher is duly concern about the ethical issues relate to the study. In this study

the following criteria will be followed to ensure maintaining the ethical values.

A. Formal ethical clearance will be taken from the ethical review committee of

the Dhaka Medical College for conducting the study.

B. Confidentiality of the person and the information was maintained, observed

and unauthorized persons didn’t have any access to the data.

C. Informed written consent will be taken from the subject.

D. The content of the consent requirements will be as such:

i. Explanation of the nature & purpose of the study.

ii. Explanation of the procedure of study.

iii. Explanation that they have the right to refuse, accept &

withdraw to participate in the study.

E. The participants don’t gain financial benefit from this study.

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BUDGET:

a). Total 2,70,000 Tk

b). Details:

1. Person cost 1,000 Tk

2. Supplies and materials 2,000 Tk

3. Internet 4,000 Tk

4. Office stationary 2,000 Tk

5. Data processing 10,000 Tk

6. Printing and reproduction 5,000 Tk

7. Dissemination of Results 10,000 Tk

8. Publication 15,000 Tk

9 Investigation cost 2,20,000 Tk

10. Others 1,000 Tk

Total (Two lac & seventy thousands taka only) 2,70,000 Tk