ACUTE KIDNEY INJURY- MECHANISM AND TYPES

AKI FOR TECHNICIANS

1. AKI

2. Acute kidney injury - Definition Abrupt decline in GFR resulting in accumulation of nitrogenous waste products and other uremic toxins.

3. Pathophysiology of AKI Impaired renal perfusion with decrease in GFR. GFR is maintained by afferent arteriolar vasodilation (mediated by vasodilatory eicosanoids) and efferent arteriolar vasoconstriction (mediated by angiotensin II [Ang II]) Gastrointestinal losses ( diarrhea , vomiting, prolonged nasogastric drainage ), renal losses (diuretics, osmotic diuresis in hyperglycemia ), dermal losses (burns, extensive sweating), or sequestration of fluid, sometimes known as third-spacing (e.g., acute pancreatitis, muscle trauma)

4. PRE-RENAL AKI Increased extracellular fluid, when cardiac output is reduced (heart failure), or when there is systemic arterial vasodilation with redistribution of cardiac output to extrarenal vascular beds (e.g., sepsis, liver cirrhosis). Infusion of large quantities of osmotically active substances such as mannitol, dextran, or protein, which can increase the glomerular oncotic pressure enough to exceed the capillary hydrostatic pressure stopping filtration.

5. Post renal injury Obstruction at any level (renal pelvis, ureters, bladder, or urethra) can increase intratubular pressure, which opposes glomerular filtration pressure and decreases GFR) Prostatic disease, single kidney, intraabdominal or pelvic cancer. Ureteral obstruction without hydronephrosis can occur with retroperitoneal fibrosis

6. ACUTE TUBULAR NECROSIS Most common cause of AKI in hospital settings. In patients with trauma, vascular and cardiac surgery, severe burns, pancreatitis, sepsis, and chronic liver disease. Vacuolization and loss of brush border in proximal tubular cells. Sloughing of tubular cells.

7. Mechanisms of ATN Site of tubular injury – Medulla.

8. Impaired Renal Autoregulation- Autoregulation between SBP of 80 and 150 mm Hg allows maintenance of RBF, glomerular pressures, and GFR in a stable range. Below 80 mm Hg, this autoregulation fails, and ischemic injury results. Intrarenal Vasoconstriction - RBF is decreased by 30% to 50%, mediated by increased cytosolic calcium content in afferent arterioles as a result of ischemia. Mediators - Ang II, endothelin-1, adenosine, thromboxane A2 , prostaglandin H2 , leukotrienes C4 and D4 , sympathetic nerve stimulation. Endothelial and tubular cell injury