Obesity, including morbid obesity, is a growing worldwide problem. The adverse effect of obesity on the kidneys is associated with the development of comorbid conditions, such as insulin resistance (IR), metabolic syndrome (MS), diabetes mellitus (DM), arterial hypertension (AH), which are the recognized risk factors of chronic kidney disease (СKD). Obesity also causes direct kidney damage with the development of non-immune focal segmental glomerulosclerosis. The leading pathophysiological mechanisms of kidney damage in obesity are intrarenal hemodynamic disorders with the formation of hyperfiltration and damaging effects of adipokines produced by adipose tissue. Bariatric surgery (BS) has taken a leading position in the treatment of morbid obesity, demonstrating its effectiveness not only in long-term weight loss, but also in the correction of IR, MS, DM, AH. Nephroprotective effect of significant and persistent weight loss is caused by the elimination of hyperfiltration and damaging effect of adipokines. Results of the observational studies of the immediate and long-term effects of BS have demonstrated positive renal outcomes, in particular, the decrease in albuminuria/proteinuria, the improvement or stabilization of glomerular filtration rate, the delay of end-stage renal failure development; surgical correction of body weight in dialysis patients with morbid obesity lets them realize subsequent kidney transplantation. Large, randomized prospective studies with a longer follow-up are needed; analysis of the long-term renal consequences of BS in obesity patients with pre-existing renal impairment, including dialysis patients, is required; stratification of the BS risk of renal complications (acute kidney damage, nephrolithiasis, nephrocalcinosis) and effective strategy for managing these risks need to be developed.
Long-term effects of the iron-based phosphate binder, sucroferric oxyhydroxide, in dialysis patients
