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A 75-year-old woman presents with effort intolerance, progressive dyspnea on exertion to minimal activity, and progressive feet, ankle, and lower leg swelling. She has a 3-year history of idiopathic nonischemic cardiomyopathy with a left ventricular ejection fraction (LVEF) of 35% measured within the last year. She also has a history of obesity, type 2 diabetes mellitus for 15 years with diabetic nephropathy, and hypertension (HTN) for 25 years. The medication profile includes: furosemide 40 mg orally twice a day, carvedilol 25 mg orally twice a day, enalapril 10 mg orally twice a day, and glargine insulin 60 units subcutaneously every night at bedtime. Vital signs were blood pressure of 105/70 mm Hg, heart rate 95 beats per minute, respiration rate 20 breaths per minute, weight 82 kg, and body mass index 33 kg/m2, temperature 98.4°F. Her physical examination reveals jugular venous distention, rales one-half of the way up posteriorly, cardiac enlargement, an S3, 2/6 murmur consistent with mitral regurgitation, hepatomegaly with hepatojugular reflux, and 4+ pitting edema to the midtibia bilaterally, and no visible rashes. The chest x-ray demonstrated cardiomegaly and pulmonary edema and the electrocardiogram revealed normal sinus rhythm, left axis deviation, left bundle branch block, and QRS duration of 120 ms. Laboratory testing was notable for: Na = 133 mEq/L, K = 5.0 mEq/L, creatinine 1.7 mg/dL (estimated glomerular filtration rate [eGFR] = 29 mL/min/1.73 m2), BUN = 48 mg/dL, glucose = 235 mg/dL, glycohemoglobin = 7.2% and B-type natriuretic peptide = 2765 pg/mL. The urine albumin to creatinine ratio was 315 mg/g. The patient initially received furosemide 80 mg intravenously twice a day with a good diuresis, but on the third hospital day the creatinine rose to 2.9 mg/dL and the urine output dropped to 4 mL/kg for 12 hours. The patient’s pulmonary examination improved somewhat; however, the S3 and peripheral edema were essentially unchanged. The managing team was confronted with a series of questions regarding the differential diagnosis, prognosis, and next management steps.


The differential diagnosis includes type 1 cardiorenal syndrome, interstitial nephritis, subclinical sepsis, and prerenal azotemia. Because the patient has considerable evidence of volume expansion, it is unlikely that there has been enough volume loss to have caused prerenal azotemia. The presence of jugular venous distention suggests she has elevated central venous pressure, which is the strongest hemodynamic determinant of type 1 cardiorenal syndrome. While the kidneys may not be receiving enough forward output and there may transiently be a slowed plasma refill from the extravascular space, the patient is very unlikely to be truly volume depleted. There was no evidence of fever or focal infection; hence the overlap between infection and heart failure (HF), while common, is probably not the issue in this patient. Interstitial nephritis generally presents with rash, fever, and urinary eosinophils, all of which are absent in this patient. Additionally, she has not ...

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