Renal Pathophysiology



dogs occurs over a certain range of renal perfusion pressures; reducing the pressure below this level will lower the GFR even in the presence of angiotensin II. Nonsteroidal Anti-Inflammatory Drugs Effective volume depletion of any cause leads to enhanced secretion of angio tensin II and norepinephrine, both of which are potent renal vasoconstric tors. Angiotensin II and norepinephrine also stimulate the renal production of vasodilator prostaglandins, particularly prostacyclin and prostaglandin E 2 (PGE 2 ) by the glomeruli. As a result of these hormonal interactions, excessive vasoconstriction (with consequent reductions in renal blood flow and GFR) is generally prevented. This relationship assumes clinical importance because of the wide spread use of NSAIDs, which reduce prostaglandin synthesis by inhibiting the enzyme cyclooxygenase. NSAIDs have little effect on renal function in normal subjects in whom angiotensin II, norepinephrine, and renal prosta glandin production are relatively low. However, NSAID can lead to AKI when given to patients with true volume depletion (as with diuretic therapy), con gestive heart failure, or hepatic cirrhosis. In these settings, exaggerated renal vasoconstriction occurs as the compensatory prostaglandin response to in creased release of angiotensin II and norepinephrine is blocked. The selective cyclooxygenase-2 inhibitors have been shown to result in fewer gastrointestinal side effects, but the consequences on renal hemody namics and renal function are similar to traditional NSAIDs. Therefore, these drugs should also be avoided in patients with renal insufficiency, volume de pletion, congestive heart failure, or hepatic cirrhosis. CASE PRESENTATION-2 A 63-year-old man is admitted for elective removal of an infrarenal abdominal aortic aneurysm. Routine preoperative laboratory findings include a blood urea nitrogen (BUN) of 20 mg/dL, a plasma creatinine concentration of 1.4 mg/dL, and a normal urinalysis. The surgery is complicated by intermittent periods of hypotension, which are reversed by fluid and blood administration. Postopera tively, the patient is hemodynamically stable, but it is noted that the urine output is averaging only 10 mL/h. The following blood and urine values are noted 12 hours after surgery: BUN = 33 mg/dL (9-25) Creatinine = 2.5 mg/dL (0.8-1.4) Urine Na = 61 mEq/L Urine osmolality = 320 mOsm/kg FENa = 3.4% The urine sediment reveals many muddy-brown granular casts (see Chapter 8; Plate 8.1 panel F). Intravenous furosemide (a loop diuretic) is be gun, and the urine output increases to 60 to 80 mL/h.

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