Nephrology
Clinical discussions on kidney disease management, dialysis, transplantation, and electrolyte disorders.
Recent Discussions
Do you check a fractional excretion of sodium in nonoliguric patients with AKI?
The FENa is diagnostically less useful in non-oliguric AKI. However, FENa can still be checked, but it has to be interpreted in conjunction with the patient's clinical and other laboratory data.
What is your approach to managing AKI secondary to intravenous acyclovir?
First and foremost, obviously, is to stop the acyclovir and switch to something different if indicated. Second, fluid therapy is important if the patient is still urinating. With oliguria, significant saline administration is not possible due to the risk of fluid overload. Of course, like all causes...
Do you recommend captopril for patients with cystine nephrolithiasis given mixed data on its effectiveness?
No. Newer drugs are superior.
Do you avoid peritoneal dialysis in cirrhotic patients with ascites?
There are two major concerns regarding the performance of PD in patients with ascites: the potential for fluid leakage at the site of the newly placed catheter and the perceived increased potential for peritonitis. In my experience, neither of these is a compelling reason to shy away from PD in a pa...
What is your approach to the management of patients with recurrent nephrolithiasis who continue to have elevated stone risk parameters in the setting of dietary factors despite receiving education from a dedicated stone clinic dietician?
Diets are notoriously difficult to follow. Once it is apparent that the patient is not going to get satisfactory control of metabolic stone disease (an increase in stone number or size as opposed to the passage of pre-existing stones, unchanged in size or number), it is time to start preventative me...
Do you taper steroids more aggressively to decrease the risk of developing new-onset diabetes after transplantation in kidney transplant recipients who had pretransplant impaired fasting glucose?
Steroids are given after any transplant (kidney, heart, lung, bone marrow, etc.,) to reduce risk of rejection of the transplanted organ. Preservation of organ function is the number one concern for the transplant team. Steroid free regimens for anti-rejection are always a goal but the transition to ...
Would you consider making a diagnosis of hepatorenal syndrome-associated acute kidney injury with a one-day diagnostic fluid challenge instead of a two-day challenge to expedite vasoconstrictor therapy if needed?
Depending on the circumstances, of course. If the patient is already significantly fluid overloaded, even one day of fluids may not be necessary. The main issue is renal vasoconstriction, as these patients are never truly total-body fluid depleted. The key question is whether the renal vasoconstrict...
In older adults with chronic mild hyponatremia (Na 128–132) attributed to SSRIs but good psychiatric response, do you tolerate persistent hyponatremia, reduce the dose, or switch agents?
In my practice, I generally tolerate mild hyponatremia, Na>130, if asymptomatic and mood symptoms have good control. If there’s moderate hyponatremia, Na 125-130, I generally consider either changing the dose or the agent. If severe, Na<125, I would change the agent and likely avoid the entire class...
Do you plan to initiate combination therapy with an SGLT-2 inhibitor and finerenone, instead of an SGLT-2 inhibitor alone, when treating patients with proteinuric chronic kidney disease and type 2 diabetes in light of the CONFIDENCE trial findings?
I would start one (typically the SGLT-2 inhibitor), then add finerenone potentially later. If both are started simultaneously and there is an AE, then both may have to be stopped. I prefer to see that one is tolerated, then start another.
What is your calcium level threshold for initiating targeted calcium lowering therapies for patients with an acute kidney injury believed secondary to renal vasoconstriction and volume depletion?
Treatment of hypercalcemia should be based on the severity of the symptoms rather than any arbitrary calcium level threshold. Therefore, if the AKI is due to hypercalcemia-induced renal vasoconstriction and volume depletion, then the hypercalcemia should be treated.