Anemia and Hypoxia Impact on Chronic Kidney Disease Onset and Progression: Review and Updates

Abstract

Chronic kidney disease (CKD) is caused by hypoxia in the renal tissue, leading to inflammation and increased migration of pathogenic cells. Studies showed that leukocytes directly sense hypoxia and respond by initiating gene transcription, encoding the 2-integrin adhesion molecules. Moreover, other mechanisms participate in hypoxia, including anemia. CKD-associated anemia is common, which induces and worsens hypoxia, contributing to CKD progression. Anemia correction can slow CKD progression, but it should be cautiously approached.In this comprehensive review, the underlying pathophysiology mechanisms and the impact of renal tissue hypoxia and anemia in CKD onset and progression will be reviewed and discussed in detail. Searching for the latest updates in PubMed Central, Medline, PubMed database, Google Scholar, and Google search engines were conducted for original studies, including cross-sectional studies, cohort studies, clinical trials, and review articles using different keywords, phrases, and texts such as "CKD progression, anemia in CKD, CKD, anemia effect on CKD progression, anemia effect on CKD progression, and hypoxia and CKD progression". Kidney tissue hypoxia and anemia have an impact on CKD onset and progression. Hypoxia causes nephron cell death, enhancing fibrosis by increasing interstitium protein deposition, inflammatory cell activation, and apoptosis. Severe anemia correction improves life quality and may delay CKD progression. Detection and avoidance of the risk factors of hypoxia prevent recurrent acute kidney injury (AKI) and reduce the CKD rate. A better understanding of kidney hypoxia would prevent AKI and CKD and lead to new therapeutic strategies.

Progression of chronic kidney disease among adults attending tertiary hospitals in Dodoma, Tanzania

“…Similar to ndings from other studies that reported proteinuria is traditionally regarded as single most important risk factor for developing CKD and CKD progression (55,56). Anaemia is a signi cant risk factor for CKD and CKD progression; correction of anaemia improves quality of life and may slow down CKD progression (57,58) (70,71). Electrolyte imbalances and hyperkalemia are life threatening conditions that often occur in patients with CKD and CKD progression (72,73).…”

Modified Zhenwu Tang delays chronic renal failure progression by modulating oxidative stress and hypoxic responses in renal proximal tubular epithelial cells

“…During the progression of CKD, activation of the Renin-Angiotensin-Aldosterone System leads to tubular atrophy, alterations in tubular sodium ion concentration, and changes in filtrate flow rate. Angiotensin II (Ang II) induces afferent arteriolar contractions, reducing peritubular capillary perfusion and causing tubulointerstitial hypoxia [ 14 ]. Additionally, Ang II directly harms endothelial cells by inducing OS through NADPH oxidase activation, leading to peritubular capillary loss and subsequent cellular hypoxia due to inefficient respiration in tubular epithelial cells.…”