Nefrología Vol. 38 Issue 1 Year 2018
Nefrologia (English Version) 2018;38:107-8 | doi: 10.1016/j.nefroe.2018.01.001

Obesity and kidney function; epidemiological study data: Prevalence of chronic kidney disease in Spain. EPIRCE study

Obesidad y funcion renal .datos del estudio epidemiologico: Prevalencia de la enfermedad renal cronica en España. Estudio EPIRCE


a Servicio de Nefrología, Complexo Hospitalario Universitario de Ourense, Ourense, Spain
b Servicio de Nefrología, Hospital Marqués de Valdecilla, Santander, Cantabria, Spain
c Centro de Salud Oroso-XXI de Santiago, Instituto de Investigación Sanitaria de Santiago de Compostela, Santiago de Compostela, La Coruña, Spain
d Instituto de Salud Carlos III, Centro Nacional de Epidemiología, Madrid, Spain

We would like to take advantage of World Kidney Day 2017 with the slogan “Obesity and Kidney Disease”, to share epidemiological data from the study into the epidemiology of chronic kidney disease in Spain (EPIRCE).1

It is well known that obesity is a public health problem, and for several years different epidemiological studies have shown a clear relationship between obesity and the risk of developing chronic kidney disease (CKD).2 The associated nephropathy is a result of hyperfiltration, glomerular hypertrophy and increased synthesis of vasoactive and fibrogenic substances and dyslipidaemia.3

The EPIRCE study is an observational study of a randomly-selected multistage sample in 42 sampling points (towns) stratified by habitat, age and gender, providing a representative cohort of the Spanish population (n: 2746). The prevalence of obesity (BMI >30kg/m2) was 26.1% and the odds ratio (OR) of CKD development was 3.5 (95% confidence interval [CI]: 2.0–6.0) while the prevalence of another cardiovascular risk factor, such as arterial hypertension (HTN), was 42% and the OR for CKD development was 6.2 (95% CI: 4.0–9.6).

Table 1 shows that the obese population is significantly more hypertensive and dyslipidaemic, with a higher rate of insulin resistance, and the higher BMI is associated with conventional risk factors (HTN, dyslipidaemia, HOMA) and with “worse” kidney function and higher proteinuria rate (Alb/creatinine). However, these changes are also seen in the “global” population, whether they are hypertensive or not.

Table 1.

BMI and cardiovascular risk factors.

  BMI <25 (kg/m2BMI 25–30 (kg/m2BMI >30 (kg/m2p value (BMI) 
Age
HTN  56.45  60.65  59.61  0.0016 
NHTN  39.01  44.39  46.19  0.0000 
Global  42.84  51.59  54.53  0.0000 
SBP; mmHg
HTN  149.63  151.3  150.25  0.4889 
NHTN  114.58  120.29  123.23  0.0000 
Global  122.27  133.97  140.01  0.0000 
DBP; mmHg
HTN  85.93  86.6  87.86  0.0606 
NHTN  71.24  74.08  76.83  0.0000 
Global  74.45  79.6  83.68  0.0000 
Ct; mg/dl
HTN  211.02  209.64  210.64  0.0000 
NHTN  192.16  205.64  205.91  0.0000 
Global  196.41  207.39  208.85  0.0000 
Tg; mg/dl
HTN  96.11  126.44  136.07  0.0000 
NHTN  79.41  102.45  124.57  0.0000 
Global  82.99  112.97  131.72  0.0000 
HDL-C; mg/dl
HTN  77.86  69.65  68.22  0.0000 
NHTN  78.69  70.64  66.52  0.0000 
Global  78.56  70.22  67.58  0.0000 
LDL-C; mg/dl
HTN  130.08  130.94  129.85  0.8895 
NHTN  114.42  129.01  128.91  0.0000 
Global  117.94  129.84  129.49  0.0000 
eGFR; ml/min
HTN  83.25  79.22  79.27  0.0203 
NHTN  88.88  87.11  85.24  0.0049 
Global  87.64  83.65  81.54  0.0000 
HOMA
HTN  1.52  2.04  2.52  0.0000 
NHTN  1.54  1.88  2.53  0.0000 
Global  1.54  1.95  2.52  0.0000 
Alb/Cr; mg/g
HTN  10.22  9.99  16.23  0.0007 
NHTN  7.29  6.69  10.16  0.0077 
Global  7.89  8.17  13.93  0.0000 

Alb/Cr: albumin/creatinine; Ct: total cholesterol; DBP: diastolic blood pressure; eGFR: estimated glomerular filtration rate; Global: general study population; HDL-C: HDL cholesterol; HOMA: homeostatic model assessment; HTN: hypertension; LDL-C: LDL cholesterol; NHTA: normotensive; SBP: systolic blood pressure; Tg: triglycerides.

ANOVA “t” test.

The pathogenic mechanisms of nephropathy seem to be linked to: glomerular hyperfiltration and haemodynamic changes, the dyslipidaemia itself and a greater activation of the renin-angiotensin system, hyperinsulinaemia and a greater synthesis of leptin, oestrogen and TGF-β1.4 Regarding the therapeutic approach it is essentially to lose weight, and the progression of nephropathy is reduced through blood pressure control, improvement of insulin resistance and lipid profile, as well as reduction of leptin and RAAS.4 It should be noted that this association of HTN, obesity, dyslipidaemia or proteinuria is not a metabolic syndrome, a syndrome questioned not only by Reaven5 himself but by the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD)6 because the presence of a unique pathogenic substrate has not been proven. Many authors agree that the usefulness of the concept of metabolic syndrome is to highlight the association of multiple CVRFs when making clinical decisions.5 We also consider that CKD is the principal CVRF7 and the existence of a common pathogenic substrate which might explain the coexistence of obesity and CKD.4

Bibliography
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A. Otero,A.L.M. de Francisco,P. Gayoso,F. Garcia,EPIRCE Study Group
Prevalence of chronic renal disease in Spain: results of the EPIRCE study
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Predictors of new-onset kidney disease in a community based population
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Obesity, proteinuria and progression of renal failure
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Relación entre obesidad y desarrollo de insuficiencia renal
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G.M. Reaven
The metabolic syndrome: is this diagnosis necessary?
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The metabolic syndrome: time for a critical appraisal Joint Statement from the American Diabetes Association and the European Association for the Study of Diabetes
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A.S. Go,G.M. Chertow,D. Fan,C.E. McCulloch,C.Y. Hsu
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