Table 3.
Consequences of metabolic acidosis
| Consequences of metabolic acidosis | Pathomechanism | References |
|---|---|---|
| MIA syndrome | Increased protein catabolism (stimulation of proteolytic mechanisms) | [31, 32] |
|
| ||
| Inflammation | Increase in TNF-α secretion by macrophages | [33] |
|
| ||
| Impaired growth in children | Reduction of GH secretion and impairment of its peripheral activity | [34, 35] |
|
| ||
| Loss of muscle mass in adults | Abnormalities in the GH-IGF-1 axis | |
|
| ||
| Hypercalcemia | Decreased calcium receptor sensitivity | [7, 36] |
|
| ||
| Osteodystrophy Osteoporosis | Increased PTH secretion | |
|
| ||
| β2−microglobulin myloidosis | Increased plasma concentration of β2−microglobulin | [37] |
|
| ||
| Insulin resistance | Insulin sensitivity reduction | [38–40] |
| Increased liver gluconeogenesis | ||
| Decrease in insulin-dependent glucose uptake by muscles | ||
|
| ||
| Hypothyroidism | Disorder of thyroxine conversion to triiodothyronine | [42] |
|
| ||
| Anemia of chronic diseases | Increased hepcidin plasma concentration | [43–45] |
|
| ||
| Dysfunction of cardiovascular system | Increased stiffness of the vessel wall | [46, 47] |
| Endothelial cell dysfunction | ||
|
| ||
| Progression of CKD | Stimulation of the renin-angiotensin system | [48–54] |
| Increased production of ROS | ||
| Increase in plasma ET-1 concentration | ||
| Local increase in ammonium ion concentration in the renal interstitium, leading to stimulation of the complement system | ||
| Kidney interstitial fibrosis | ||
MIA, malnutrition-inflammation-atherosclerosis; TNF-α, tumor necrosis factor alpha; GH, growth hormone; IGF-1, insulin-like growth factor 1; PTH, parathyroid hormone; ROS, reactive oxygen species; ET-1, endothelin-1.