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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 2, March/April 2020

AFRICA

93

proportions were compared by the large-sample

z

‑test and

the c

2

statistic, respectively. As HOMA-IR and circulating

concentrations of inflammatory markers were non-normally

distributed, they were transformed to improve on the

distribution (Table 1). Bivariate correlations were assessed from

Pearson’s correlation coefficients. Independent relations were

assessed from linear, logistic or stepwise regression analysis with

appropriate adjustors. Probability values were further adjusted

for non-independence of family members using the method of

maximum likelihood as implemented by the mixed procedure as

defined in the SAS package.

To determine the relative contribution of risk factors to

variations in eGFR, standardised

β

-coefficients were determined.

As DM is so strongly associated with renal dysfunction, in the

primary analysis we assessed relationships in the sample that

excluded those with DM. However, to compare the impact

of metabolic changes with that of DM on renal function at a

community level and to ensure that the exclusion of DM did not

result in a selection bias, we also performed the same analysis in

the whole sample, including those with DM.

Results

Table 2 shows the characteristics of the non-diabetic participants

in the study sample and Table 3 shows the characteristics

of all participants in the study sample. More women than

men participated and a high prevalence of hypertension and

obesity was noted, with many hypertensives being untreated or

uncontrolled; 33.9% of the non-diabetic sample had an eGFR

=

60–90 ml/min/1.73 m

2

and 4.4% an eGFR

=

20–60 ml/min/1.73

m

2

; 34.9% of the full study sample had an eGFR

=

60–90 ml/

min/1.73 m

2

and 6.4% an eGFR

=

20–60 ml/min/1.73 m

2

.

In the non-diabetic cohort, only blood glucose, low-density

lipoprotein (LDL) cholesterol concentrations and metabolic

syndrome features (MDRD eGFR only) showed weak

independent relationships with eGFR. No adiposity index or

other obesity-associated metabolic abnormality (lipids) was

independently associated with eGFRor creatinine concentrations

(Table 4).

However, in multivariate regression models, independent

of conventional risk factors, including metabolic syndrome

Table 1. Distribution of circulating inflammatory markers or the

homeostasis model of insulin resistance (HOMA-IR) before and after

transformation of data (

n

=

1 010)

Parameter

Skewness

Kurtosis

Shapiro

Wilk

Untransformed

C-reactive protein

4.22

31.2

0.64

Resistin

2.81

15.8

0.80

HOMA-IR

4.33

26.3

0.57

Logarithm of:

C-reactive protein

0.37

0.04

0.99

Resistin

0.12

0.52

1.00

HOMA-IR

0.36

0.24

0.98

Table 2. Participant characteristics without diabetes mellitus

Characteristics

All

With 24-hour BP

With PWV

Number (% female)

872 (63.1)

600 (63.0)

779 (61.4)

Age (years)

41.7

±

17.8

41.5

±

17.5

41.2

±

17.9

Body mass index (kg/m

2

)

28.6

±

7.7

28.1

±

7.4

28.0

±

7.2

% overweight/obese

23.4/38.2

24.8/35.2

23.9/35.6

Waist circumference (cm)

88.8

±

16.2 (

n

=

850)

87.9

±

15.8 (

n

=

584)

87.7

±

15.6 (

n

=

762)

% abdominal obesity

40.6

37.3

37.6

Waist:hip ratio

0.82

±

0.10 (

n

=

850)

0.82

±

0.10 (

n

=

584)

0.82

±

0.10 (

n

=

762)

Regular tobacco (% subjects)

15.6

15.5

16.9

Regular alcohol (% subjects)

21.3

21.8

22.1

% females postmenopausal

37.4

35.2

36.4

% hypertension

39.1

37.7

37.9

Current antihypertensive meds (%)

17.1

15.7

16.2

Glucose (mmol/l)

4.72

±

0.86

4.74

±

0.91

4.70

±

0.82

LDL-C (mmol/l)

2.58

±

0.93

2.58

±

0.96

2.57

±

0.94

HDL-C (mmol/l)

1.43

±

0.42

1.43

±

0.41

1.44

±

0.42

Triglycerides (mmol/l)

1.13

±

0.86

1.13

±

0.94

1.12

±

0.87

Metabolic syndrome (%)*

31.9/25.9/11.9/6.6

32.2/24.7/12.3/6.5

32.6/25.4/11.0/5.4

Insulin (

µ

U/ml)

8.05 (3.86 to 15.00)

8.46 (3.94–16.45)

7.87 (3.77–14.70)

HOMA-IR

1.60 (0.75–3.07)

1.74 (0.80–3.59)

1.58 (0.72–2.99)

Resistin (ng/ml)

10.6 (7.6–15.2)

10.5 (7.5–14.6)

10.6 (7.7–15.1)

C-reactive protein (ng/ml)

3.35 (1.27–7.72)

3.06 (1.17–7.55)

3.14 (1.22–7.44)

Office SBP/DBP (mm Hg)

127

±

22/83

±

13

126

±

22/83

±

12

126

±

22/83

±

12

24-hour SBP/DBP (mm Hg)

117

±

14/72

±

10 (

n

=

600)

117

±

14/72

±

10

117

±

14/72

±

10

Aortic PWV (m/s)

5.95

±

2.36 (

n

=

779)

6.06

±

2.36 (

n

=

529)

5.95

±

2.36

Aortic SBP (mm Hg)

119

±

22

118

±

22

118

±

22

Creatinine (

µ

mol/l)

74.0

±

16.8

74.4

±

16.4

73.9

±

16.7

eGFR (MDRD) (ml/min/1.73 m

2

)

96.1

±

25.8

95.6

±

25.4

97.0

±

25.6

eGFR (CKD-EPI) (ml/min/1.73 m

2

)

97.1

±

21.4

96.8

±

21.3

97.9

±

21.4

Data shown are mean

±

SD, median and interquartile range and proportions. PWV, pulse-wave velocity; LDL-C, low-density lipoprotein cholesterol; HDL-C, high-

density lipoprotein cholesterol; HOMA-IR, homeostasis model of insulin resistance; SBP, systolic blood pressure; DBP, diastolic BP; eGFR, estimated glomerular

filtration rate; MDRD, Modification of Diet in Renal Disease equation; CKD-EPI, Chronic Kidney Disease Epidemiology equation. *Metabolic syndrome (%) is

percentage of individuals with one/two/three/four components of the metabolic syndrome.