Health Disparities in Kidney Disease

Health Disparities in Kidney Disease

Despite advances in the management of hypertension and diabetes—the two risk factors accounting for over 70% of all cases of chronic kidney disease (CKD)—the prevalence of CKD in the general population has risen from about 10% two decades ago to 14.8% in 2017, surpassing that of diabetes (9.4%) (1) and making it a major public health problem in the United States.

Many patients with CKD invariably experience progression, slow or fast, to later CKD stages and require renal replacement therapy at some point. Controlling the primary risk factors for CKD has been shown to slow progression of CKD but does not prevent the development of ESRD. The mechanisms underlying slow or fast progression of CKD are complex but are generally attributable to nephron loss from the primary disease, which sets a vicious circle of further nephron loss, characterized by hypertrophy and hyperfiltration of the remaining nephrons, intraglomerular hypertension, proteinuria, and toxicity of filtered proteins on tubular epithelial cells (13). Although these forces have been attributed to pertain to many glomerular diseases, the processes are particularly described in diabetic nephropathy, in which podocyte loss may be a downstream effect (4).

The best chance to slow or reverse the progression of chronic kidney disease (CKD) is in CKD stage 1, when GFR is still preserved. The strategy in stage 1 CKD is to control comorbidities (treat to target) and to perform risk assessment and intervention for cardiovascular disease (1). Unfortunately, many patients, particularly those of minority extraction, do not get this early referral benefit, as noted in the previous section. Current evidence-based progression-specific treatment approaches in CKD include treating BP to acceptable goals, blockade of the renin-angiotensinogen aldosterone system (RAAS), and controlling metabolic acidosis. Trials of antioxidants by the use of bardoxolone, an inhibitor of oxidative stress that failed phase 3 clinical trials, was associated with worsened albuminuria and heart failure (2). Antagonists of inflammation, renal fibrosis, extracellular matrix deposition, and endothelin 1 have not yielded any meaningful clinical application. Interestingly, antagonists of the mineralocorticoid receptor have demonstrated reduced albuminuria but have been associated with high blood potassium levels, which may limit their use in patients with advanced CKD (3). Of the progression-specific treatment approaches, the RAAS system and BP control exhibit significant racial disparities, as detailed below.

Kidney transplantation is the renal replacement therapy (RRT) of choice for most patients with ESRD because it is associated with improved survival and improved quality of life, and it is less expensive than dialysis. The process leading to transplantation is complex, with multiple necessary steps that must be completed before transplantation. Despite improvement in outcomes, disparity across the board in the transplantation process continues to be a major problem.

Smooth transition from CKD stage 5 to renal replacement therapy (RRT) remains a challenge. This transition period bears a high risk for mortality (1); hence, it requires a multidisciplinary pre-ESRD team approach (2) to address all aspects of care aimed at improving survival and providing adequate patient education about transplantation, in-center hemodialysis (HD), and home-based therapies (3).

Population-based screening and identification strategies for patients with CKD remain a challenge. Data from the Behavioral Risk Factors Surveillance System suggest that most patients with CKD do not know they have the condition. Screening strategies such as albuminuria and serum creatinine determinations are not widely used in the general population and are performed only on indication; hence, most patients with CKD go undetected, for several reasons.