A Nephrologist Perspective on Obesity: From Kidney Injury to Clinical Management

Abstract

Obesity is one of the epidemics of our era. Its prevalence is higher than 30% in the U.S. and it is estimated to increase by 50% in 2030. Obesity is associated with a higher risk of all-cause mortality and it is known to be a cause of chronic kidney disease (CKD). Typically, obesity-related glomerulopathy (ORG) is ascribed to renal hemodynamic changes that lead to hyperfiltration, albuminuria and, finally, impairment in glomerular filtration rate due to glomerulosclerosis. Though not only hemodynamics are responsible for ORG: adipokines could cause local effects on mesangial and tubular cells and podocytes promoting maladaptive responses to hyperfiltration. Furthermore, hypertension and type 2 diabetes mellitus, two conditions generally associated with obesity, are both amplifiers of obesity injury in the renal parenchyma, as well as complications of overweight. As in the native kidney, obesity is also related to worse outcomes in kidney transplantation. Despite its impact in CKD and cardiovascular morbility and mortality, therapeutic strategies to fight against obesity-related CKD were limited for decades to renin-angiotensin blockade and bariatric surgery for patients who accomplished very restrictive criteria. Last years, different drugs have been approved or are under study for the treatment of obesity. Glucagon-like peptide-1 receptor agonists are promising in obesity-related CKD since they have shown benefits in terms of losing weight in obese patients, as well as preventing the onset of macroalbuminuria and slowing the decline of eGFR in type 2 diabetes. These new families of glucose-lowering drugs are a new frontier to be crossed by nephrologists to stop obesity-related CKD progression.

Combined Donor-Recipient Obesity and the Risk of Graft Loss After Kidney Transplantation

“…Notably, risk of DCGL was more exaggerated than that of all-cause graft loss in both NOD-OR and OD-OR. This finding is in keeping with other studies which have shown a comparable mortality risk between obese recipients and those with a normal BMI ( 4 , 6 , 12 ). While this appears counter-intuitive given the greater burden of co-morbidities in obese individuals and the association of obesity with mortality in the general population ( 40 ), there are a number of possible explanations.…”

“…The global rise in obesity is reflected in the kidney transplant population, with the proportion of recipients with a body mass index (BMI) in excess of 30 kg/m 2 doubling every 15 years ( 3 ). As obesity rates increase in the general population, the number of obese transplant candidates and kidney donors, both living and deceased, is also expected to increase ( 4 ).…”

Obesity‐related glomerulopathy: Current approaches and future perspectives

“…8,22 Finally, it is also important to highlight the impact of hypertension or T2DM (both highly prevalent in obesity) on renal outcomes in ORG. 23 These two conditions contribute to hyperfiltration and glomerular hypertension due to increased renal plasma flow and impaired autoregulatory capacity and may amplify kidney damage in patients with ORG. 23…”

“… 23 These two conditions contribute to hyperfiltration and glomerular hypertension due to increased renal plasma flow and impaired autoregulatory capacity and may amplify kidney damage in patients with ORG. 23 …”

Serum creatinine versus corrected cockcroft-gault equation according to poggio reference values in patients with arterial hypertension

“…In the group of obese patients, the standard error was smaller if a correction for actual body weight was used, which was a very important factor for assessing creatinine clearance. [ 16 17 ] Luke et al . compared inulin clearance, creatinine clearance with five formulas for assessing creatinine clearance and glomerular filtration, which use gender, age, body height, body weight.…”