KEY POINTS

1. The renal medulla receives less than 10% of RBF, and metabolically active structures in the juxtamedullary zone and medulla are at constant risk of hypoxia.
2. Increases in efferent arteriolar tone mediated by angiotensin, catecholamines, and vasopressin provide an important compensatory mechanism to maintain glomerular filtration pressure in the face of mild to moderate hypotension.
3. Over a wide range of blood pressure, renal autoregulation maintains GFR and RBF, but not urine flow, which is pressure dependent.
4. The kidney regulates a constant balance between vasoconstrictor, salt-retaining systems that protect against hypovolemia and hypotension and vasodilator, salt-excreting systems that protect against hypervolemia and hypertension.
5. The most metabolically active sites in the renal tubule are the proximal tubule and the medullary thick ascending limb, which play an important role in the pathogenesis of ischemic and nephrotoxic acute tubular necrosis, respectively.
6. Renal clearance estimates the virtual volume of plasma cleared of substance "x" per unit time, which allows us to estimate effective RPF and GFR, depending on how substance "x" is handled by the kidney.
7. A doubling of serum creatinine implies a halving of the GFR.
8. Serum creatinine does not increase above normal levels until the GFR is less than 50 mL/min; in cachectic individuals, it may still be in the normal range when the estimated GFR is between 20 and 30 mL/min.
9. ANP is released in response to increases in atrial volume and induces increases in urine flow and sodium excretion (natriuresis), which could be considered "endogenous renal protection."
10. Renal autoregulation is lost or impaired during acute renal failure, sepsis, and CPB, and vasoconstrictor drugs that maintain or restore renal perfusion pressure improve RBF.