Response to erythropoietin in pediatric patients with chronic kidney disease: insights from an in vitro bioassay

Gavish, Rachel; Watad, Salmas; Ben‐Califa, Nathalie; Goldberg, Ori; Haskin, Orly; Davidovits, Miriam; Koren, Gili; Falush, Yafa; Neumann, Drorit; Krause, Irit

doi:10.1007/s00467-018-4016-1

Cited by 1 publication

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“…The decreased serum level of EPO is a main cause of CKD-associated anemia. In addition to the reduced EPO production by the diseased kidney, the presence of erythropoiesis inhibitory substances in uremic sera is supported by the observation that sera from dialysis patients are able to inhibit the growth of the human leukemic cell line UT-7, whereas sera from healthy controls showed no effect [113].…”

Section: Erythropoietin and Ironmentioning

confidence: 94%

Immune Dysfunction in Uremia 2020

Cohen

2020

Toxins

106

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Cardiovascular disease and infections are major causes for the high incidence of morbidity and mortality of patients with chronic kidney disease. Both complications are directly or indirectly associated with disturbed functions or altered apoptotic rates of polymorphonuclear leukocytes, monocytes, lymphocytes, and dendritic cells. Normal responses of immune cells can be reduced, leading to infectious diseases or pre-activated/primed, giving rise to inflammation and subsequently to cardiovascular disease. This review summarizes the impact of kidney dysfunction on the immune system. Renal failure results in disturbed renal metabolic activities with reduced renin, erythropoietin, and vitamin D production, which adversely affects the immune system. Decreased kidney function also leads to reduced glomerular filtration and the retention of uremic toxins. A large number of uremic toxins with detrimental effects on immune cells have been identified. Besides small water-soluble and protein-bound compounds originating from the intestinal microbiome, several molecules in the middle molecular range, e.g., immunoglobulin light chains, retinol-binding protein, the neuropeptides Met-enkephalin and neuropeptide Y, endothelin-1, and the adipokines leptin and resistin, adversely affect immune cells. Posttranslational modifications such as carbamoylation, advanced glycation products, and oxidative modifications contribute to uremic toxicity. Furthermore, high-density lipoprotein from uremic patients has an altered protein profile and thereby loses its anti-inflammatory properties.

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Section: Erythropoietin and Ironmentioning

confidence: 94%