Bill Whittier @TWhittier_RUSH
Bill Whittier is a Professor of Medicine practicing Nephrology at Rush University Medical Center in Chicago, IL. His main research area involves the adequacy and safety of the renal biopsy. Other research publications are in the realm of lupus nephritis, glomerulonephritis, and diabetic nephropathy. He has also written on topics of acid-base disorders and hyponatremia.
Competitors for the Cardiorenal Region
Treatment of diuretic resistance for the win! The reason, quite simply, that this powerful team will go all the way is that finally the Blue Ribbon Panel (BRP) should recognize and give credit to what nephrologists actually do on a day-to-day basis. So far, for nine years in a row, the BRP (#BlueRibbonFail) has missed the final shot:
Now, I love a good story about a futuristic implantable kidney, how well a camel can concentrate urine, or what really goes on during bear hibernation – these are all great conversation topics at a party. And clearly guidelines, genetics, and health-related disparities are important on a global scale, but no team has ever been considered by the BRP which highlights what a nephrologist actually does every day. On rounds, in the medical floors, in the ER, in the ICU, in clinic, and in dialysis units. Seeing patients, teaching about it, mesmerizing colleagues with physiology and results, and actually doing: directly helping patients, every hour of the day. The clinical nephrologists are leading the way in patient care, inspiring future generations to go into nephrology, and doing so with results everyone sees.
Enter a nephrologist’s favorite realm: making some urine (or ultrafiltration) – when others can’t.
Amlodipine strikes again. pic.twitter.com/XNSQGfkM8v
— Bill Whittier (@TWhittier_RUSH) February 4, 2022
First and foremost, assessment of the cause of edema is paramount. Refractory or non-recruitable edema can be the culprit, e.g. in the case of venous obstruction, or arterial vasodilation, as is often seen with dihydropyridine calcium channel blockers. Diuresis in this setting typically results only in progressive azotemia, without recruitment of the edema. How many times have we stopped/reduced the dose of amlodipine, or added renin-angiotensin aldosterone blockade and watched the edema melt away, without the use of diuretics?
But when this type of edema isn’t overlooked, and the patient truly needs diuresis, cardiologists around the world reluctantly pick up the phone and call the ones who get it done: the nephrologists. Some cardiologists just ask outright for ultrafiltration directly. We quietly think yes, we may need that, but let’s roll up our sleeves and see if we can make some urine.
First, maximizing the efficiency of loop diuretics. Finding the appropriate type of loop diuretic, route, dose, and/or frequency to hit the threshold should be tried, especially in the setting of CKD. Often, when in the congestive phase of cardiorenal kidney injury, adding inotropic diuresis with dobutamine or milrinone can be helpful. But frequently diuresis is still resistant, because the kidney (via autoregulation and tubuloglomerular feedback) is doing exactly what it is being told to do: hang on to volume when threatened by non-euvolemic states. Despite improving perfusion and using loop diuretics efficiently, the vicious cardiorenal cycle of vascular congestion is perpetuated by reabsorption of sodium at every potential downstream channel in the nephron.
Thus, sequential blockade of all the channels can assist to get the urine “in the bucket.” Use of metolazone with loops is particularly effective, as long as we are watching for hypokalemia/hyponatremia and chloride-depleted metabolic alkalosis. Amiloride, mineralocorticoid antagonists, and acetazolamide can come off the bench to help manage the electrolytes and acid-base status while promoting diuresis, and the vasopressin antagonists can help to reject water reabsorption. There is even a role for the Nephmadness 2020 winner to be a player, as the SGLT inhibitors will promote sodium-glycosuria, and have been shown not only to reduce weight and edema in the CKD trials, but also have significant natriuretic effect when combined with loop diuretics, not to mention the longterm CV benefit in patients with heart failure.
This blockade of autoregulation and tubuloglomerular feedback, to put the full court press on the nephron’s primary function of sodium reabsorption, is often enough to rescue the patient from vascular congestion. In addition to promoting diuresis, the role of the nephrologist should also be one of reassurance for the patient and other providers, who may often be dissuaded from adequate diuresis if the creatinine bumps, or if an electrolyte abnormality such as hyponatremia or hyperkalemia pops up. As I’m often overheard with our renal team on rounds in the cardiac care unit, “We need to treat the patient. We’d rather be able to walk and breathe and have a creatinine of 2.0 mg/dL than be confined to a chair with orthopnea and a have a creatinine of 1.0 mg/dL.”
When these sequential maneuvers fail to move the ball, boluses of 3% saline can be attempted, especially in the setting of sodium or chloride depletion. While many nephrologists are resistant to the concept due to the perception that sodium and volume restriction is necessary in congested states, there may actually be a role for it. Giving bolus(es) of 3% saline with diuresis theoretically can draw interstitial fluid into the vascular space, and through chloride repletion achieve a diuresis. Studies have been mixed, and this may end up being the new (and improved?) version of intravenous albumin boluses, where studies have mostly been negative. However, ongoing trials with 3% boluses may help answer this question for the future.
Ultimately, when all else fails, ultrafiltration is always there for the win. Even though it seems extreme, long-term extracorporeal therapy can still provide relief of vascular congestion and should be considered as an alternative to prolonged hospitalizations or death. In certain cases, once congestion has been unloaded, the patient’s starling curve can reset, and dialysis dependence can be temporary. Conservative and/or palliative care should also be considered, and the nephrologist is essential to participate in this shared decision-making.
So when the game is on the line, and the team is going to live or die, the ball should be in the hands of the person you want to take the final shot: the clinical nephrologist, who will not only take the shot, but make it for the win.
– Guest Post written by Bill Whittier @TWhittier_RUSH
As with all content on the AJKD Blog, the opinions expressed are those of the author of each post, and are not necessarily shared or endorsed by the AJKD Blog, AJKD, the National Kidney Foundation, Elsevier, or any other entity unless explicitly stated.