A 65-year-old man comes to the emergency department due to lower extremity swelling and a 9.1-kg (20.1-lb) weight gain over the last month. He also reports some shortness of breath at night. The patient has a history of hypertension and coronary artery disease and underwent coronary artery bypass graft surgery 10 years ago. The patient does not smoke or use recreational drugs. Temperature is 36.7 C (98.1 F), blood pressure is 140/92 mm Hg, pulse is 98/min, and respirations are 18/min. Examination shows jugular venous distension. Breath sounds are decreased at the bilateral bases. The point of maximal impulse is laterally displaced. S1 and S2 are normal, and a II/VI holosystolic murmur is present at the apex. There is 3+ pretibial edema bilaterally. Laboratory results are as follows: Chest x-ray reveals an enlarged cardiac silhouette and pulmonary vascular congestion. The patient is treated with intravenous furosemide for 4 days, with a return to his baseline weight and resolution of his edema. Serum chemistry shows an improvement in creatinine to 1.1 mg/dL. Which of the following is the most likely mechanism for this improvement in renal function?

Question

A 65-year-old man comes to the emergency department due to lower extremity swelling and a 9.1-kg (20.1-lb) weight gain over the last month.  He also reports some shortness of breath at night.  The patient has a history of hypertension and coronary artery disease and underwent coronary artery bypass graft surgery 10 years ago.  The patient does not smoke or use recreational drugs.  Temperature is 36.7 C (98.1 F), blood pressure is 140/92 mm Hg, pulse is 98/min, and respirations are 18/min.  Examination shows jugular venous distension.  Breath sounds are decreased at the bilateral bases.  The point of maximal impulse is laterally displaced.  S1 and S2 are normal, and a II/VI holosystolic murmur is present at the apex.  There is 3+ pretibial edema bilaterally.  Laboratory results are as follows:  Chest x-ray reveals an enlarged cardiac silhouette and pulmonary vascular congestion.  The patient is treated with intravenous furosemide for 4 days, with a return to his baseline weight and resolution of his edema.  Serum chemistry shows an improvement in creatinine to 1.1 mg/dL.  Which of the following is the most likely mechanism for this improvement in renal function?

Quizplus · Accepted Answer

11ec25c8_d328_8e89_bc81_c9763d157537_MD0003_00 This patient's initial presentation is consistent with an acute heart failure exacerbation (eg, jugular venous distension, laterally displaced point of maximal impulse, 3+ lower extremity edema). Initial laboratory results show an elevated serum creatinine with a blood urea nitrogen (BUN)/creatinine ratio >20:1 and an unremarkable urinalysis consistent with acute kidney injury (AKI) of prerenal etiology. Prerenal AKI in the setting of an acute heart failure exacerbation is most likely due to cardiorenal syndrome. The pathogenesis of decompensated heart failure involves reduced cardiac output leading to decreased renal perfusion and the consequent activation of maladaptive neurohormonal mechanisms (eg, renin-angiotensin-aldosterone-system [RAAS], sympathetic nervous system) that create a vicious cycle of decompensation. Cardiorenal syndrome represents further perpetuation of this cycle of mutually detrimental interactions between the heart and the kidneys. vicious cycle The accumulation of back pressure from the failing heart leads to increased central venous and renal venous pressure to the point that the glomerular capillary filtration gradient substantially drops and decreases glomerular filtration rate (GFR). Reduced forward flow from the failing left ventricle decreases renal arterial perfusion and further contributes to decreased GFR. Treatment with intravenous diuretics (eg, furosemide) reduces central venous and renal venous pressure and improves cardiac output. This increases GFR and improves the AKI, as seen in this patient. filtration gradient (Choice A) Filtration fraction is the ratio of GFR to renal plasma flow (ie, percentage of renal plasma flow filtered by glomeruli). By decreasing renal venous pressure, diuretics help restore the glomerular capillary filtration gradient, therefore increasing (rather than decreasing) filtration fraction. (Choice B) Diuretic therapy helps improve cardiac output and increase renal perfusion, which lessens RAAS and sympathetic nervous system activity. This alleviates renal afferent arteriole vasoconstriction (ie, decreases resistance). (Choice C) Acute tubular necrosis (ATN) typically involves ischemic or toxic injury to the renal tubular epithelium, with the recovery phase, if it occurs, starting 7-10 days after initial insult. At the time of initial ATN injury, BUN/creatinine ratio is typically 10-15 (consistent with intrinsic renal injury), and muddy brown casts are expected on urinalysis. (Choice E) Vasodilation of renal efferent arterioles occurs with ACE inhibitors (eg, lisinopril) but not with diuretics. Such efferent arteriole vasodilation tends to decrease, rather than increase, GFR. Educational objective: Cardiorenal syndrome involves a reduction in glomerular filtration rate (GFR) that results from elevated renal venous pressure and reduced cardiac output in the setting of an acute exacerbation of heart failure. Intravenous diuretics reduce renal venous pressure and improve cardiac output to help restore the glomerular capillary filtration gradient and increase GFR. References: Cardiorenal syndrome in acute decompensated heart failure. (http://www.ncbi.nlm.nih.gov/pubmed/19965544) Acute cardio-renal syndrome: progression from congestive heart failure to congestive kidney failure. (http://www.ncbi.nlm.nih.gov/pubmed/17883988)

A 65-Year-Old Man Comes to the Emergency Department Due to Lower