During medical school, I noticed that many patients who presented with heart failure or end-stage renal disease had both conditions simultaneously. My simplistic mind chalked this up to “all the bad things happen to the sickest patients,” but it turns out there is a relationship between heart failure and kidney failure, and it is called the cardiorenal syndrome.
Patients with cardiorenal syndrome have kidney disease that is worsened by heart function. When someone’s heart doesn’t pump as well, transrenal perfusion decreases, causing a rise in creatinine and other things we associate with AKI. Neurohumoral stimulation due to decreased renal perfusion pressure also feeds back to the heart and causes increased fluid retention.
Patients with cardiorenal syndrome are at risk for diuretic resistance–when they stop responding to 240 mg of furosemide/day or the equivalent (a practical measure on physical exam is pulmonary congestion: look at the JVP or listen for crackles on exam).
Predisposing factors for diuretic resistance are commonsensical: being old, history of CHF, pre-existing CKD, diabetes, hypertension.
The first go-to for diuretics in CHF exacerbations is furosemide, or Lasix. However, it is especially likely to cause diuretic resistance because it is poorly absorbed through the gut when the gut is hypoperfused/edematous. Furthermore, IV furosemide boluses have large salt loads which can cause rebound resorption of sodium, rendering moot the goals of diuresis.
In these cases, furosemide drips, or slow infusions over 2-4 hours, may be more efficacious. However, alternatives such as bumetanide (Bumex) or torsemide are also available. Torsemide in particular has much better bioavailability. Using metolazone, a thiazide diuretic, in combination with a loop diuretic, can help inhibit distal resorption of sodium.