Table 1.
Overview of kidney disorders and their pathogenesis.
| Disorder/disease | Causative factor | Pathophysiology |
|---|---|---|
| Diabetic nephropathy | Diabetes (High blood glucose) | An increase of extracellular matrix leads to a thickened glomerular basement membrane and an enlarged mesangium. The portion of the kidneys that filters blood is damaged. Destroyed filters become 'leaky', leading to protein released into the urine. |
| Diabetics insipidus | Inadequate secretions of anti-diuretics hormones | Impaired arginine vasopressin (AVP) secretions from the posterior pituitary gland lead to an imbalance of plasma osmolality and arterial blood volume, resulting in dilute urine, frequent urination and excessive thirst (Kalra et al., 2016). |
| Hyperuricemia nephropathy | Increased serum uric acid concentration | Reduced excretion (underexcretions) or/and increased production (overproducers) of uric acid. |
| Glomerulonephritis | Immune mediated and inflammatory response | The antigen–antibody reaction and cell-mediated immune response lead to inflammatory reactions. The pro-inflammatory cytokines and complement products, in turn, proliferate the glomerular cells (Trachtman et al., 2019). |
| Kidney stones | Supersaturations of minerals constituent in kidney | The imbalance level between the promoter of crystallizations and urinary inhibitors leads to kidney stones. The ion transformation from a liquid into a solid is influenced by the pH and concentration of excess minerals (Alelign and Petros, 2018). |
| Lupus nephritis | Autoimmune disorders | Tolerance to nuclear autoantigens is lost, and autoreactive T and B cells are activated, resulting in the generation of pathogenic autoantibodies and tissue damage. |
| Polycystic kidney disease (PKD) | Inheritance genetic mutations | Decreased amount of PKD protein results in a disturbance of cell homeostasis and signalling pathways. The vascular endothelial growth factor and hippo signalling is impaired (Bastos and Onuchic, 2011). |
| Renal cell carcinoma (RCC) | The cytotoxic immune system failed to distinguish the cancer cell | Genetic alterations of Von Hippel-Lindau (VHL) gene and protein polybromo-1 gene (PBRM-1) leads to renal carcinoma. The cytotoxic immune system unable to recognize, and eliminate and kill the cancer cells (Petejova and Martinek, 2016). |
| Renal fibrosis | Excessive accumulation and deposition of extracellular matrix components | Failure of tissues wound-healing process due to a persistent and prolonged insult to the kidney tissues. |
| Renal injury | Ischemia, nephrotoxicity or hypoxia | Reduction of renal blood flow followed by the decrease in glomerular filtration rate (GFR). |
| Urinary tract infections (UTI) | Bacterial infections | Bacteria spreading and colonizing on the lower or upper urinary tract. The symptoms include fever and pain during urination (Pulipati et al., 2017). |