Fig. 1 Proposed pathogenetic mechanisms involved in the initiation and progression of chronic kidney disease in cats. In this widely accepted model of the course of chronic kidney disease, one or more factors initiate the renal injury (initiation), leading to changes in renal structure and function (consequences). If the disease progresses unabated, disruption of homeostasis coupled with maladaptive renal responses further contributes to renal damage and nephron loss (sequelae). These consequences and sequelae operate synergistically as a positive feedback loop that, absent therapeutic intervention, eventually leads to end-stage renal failure. GFR, glomerular filtration rate.
Fig. 2 Tubular hypoxia and chronic kidney disease. Tubular hypoxia acting alone or in concert with other factors may cause tubular epithelial cell injury, interstitial inflammation, and eventual fibrosis and tubular atrophy. Potential mechanisms of tubular hypoxia include extrarenal factors (hypotension, anemia) and intrarenal factors (arteriolar constriction, glomerulosclerosis, pericyte contraction) resulting in decreased blood flow (or oxygenation) through peritubular capillaries and vasa recta, causing transient or continued tubular injury from hypoxia. Disruption of the normal close association of capillaries and tubules by an expanded interstitium perpetuates tubular hypoxia
