Academic journal article Public Health Reviews; Rennes

On the Rationale of Population Screening for Chronic Kidney Disease: A Public Health Perspective

Academic journal article Public Health Reviews; Rennes

On the Rationale of Population Screening for Chronic Kidney Disease: A Public Health Perspective

Article excerpt


Chronic kidney disease (CKD) and its complications represent an enormous and increasing public health burden worldwide [1]. More than one in ten adults suffers from CKD in the general population [2], with a majority of people being in its early stages (i.e. 1 to 3) [2]. In the general population, the prevalence of CKD sharply increases with age [3]. CKD can be considered as a condition associated with premature ageing with accelerated vascular disease [4]. The large number of people with CKD, or at high risk of CKD (i.e. patients with hypertension, diabetes and/or CVD), implies that primary care providers and specialists other than nephrologists frequently encounter patients with CKD [5], a situation in which most CKD cases are diagnosed via opportunistic kidney function screening or automated eGFR reporting.

The aim of this review is to discuss the rationale and currently available evidence for, or against, population-based screening for CKD. The focus will be on the situation of screening asymptomatic individuals at early stages of CKD regardless of the presence or absence of CKD risk factors.

Challenges in measuring renal function

Kidney function is usually measured by estimating glomerular filtration rate (GFR), which is currently considered to be the best index. A direct measurement of GFR is possible, such as by assessing urinary iothalamate or inulin clearance, but this is cumbersome and not suitable for route clinical or population screening. Several equations have been proposed to estimate GFR (eGFR) from serum creatinine and the currently recommended equation for adults is the Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI) equation [6]. The CKD-EPI equation also takes age, sex and race into account, because of their association with muscle mass, which influences the generation of creatinine. It is particularly challenging to accurately estimate eGFR in older adults, because the increase in serum creatinine reflecting reduced kidney function is paralleled by an age-related decrease in muscle mass [7]. Another issue is the need to calibrate serum creatinine assays across laboratories to use them to estimate GFR [8, 9]. Because creatinine depends on muscle mass and other factors, such as diet, that influence creatinine generation, there have been efforts to identify a marker of glomerular filtration that does not suffer from these limitations. Cystatin C, an endogenous protein produced by nearly all human cells that is freely filtered by the glomeruli, has recently been proposed as a new marker. Cystatin C-based equations to estimate GFR are now available [10-14]. Compared to creatinine, cystatin C-based equations better predicted all-cause mortality and cardiovascular events in people older than 65 years [15] as well as all-cause mortality and end-stage renal disease (ESRD) in general adult populations [11]. Cystatin C may be combined with creatinine to estimate GFR [11], as demonstrated by some recently published equations cited above [13, 14]. Markers of glomerular filtration (e.g. serum creatinine and cystatin C) and markers of kidney damage (e.g. albuminuria, renal biopsy findings) are also part of the tests used to define CKD-staging.

How to diagnose chronic kidney disease?

CKD is defined by the Kidney Disease: Improving Global Outcomes Initiative (KDOQI) as abnormalities of kidney structure or function, present for more than 3 months, with implications for health [16]. The following criteria are considered as markers of kidney damage: albuminuria (albumin excretion rate of 30 mg/24 h or higher or albumin-creatinine ratio???30 mg/g); abnormal urine sediment; abnormal histology; structural abnormalities detected at imaging; history of kidney transplantation or present of kidney damage; eGFR?

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