Urine Microscopy in Heart Failure: A Key Test for Acute Kidney Injury Diagnosis

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• Clinical Case: Heart Failure and Rising Creatinine
• Urine Sediment Analysis for Kidney Injury
• Interpreting Urine Microscopy Findings
• Treatment Implications from Urine Exam
• Broader Clinical Applications of Urine Microscopy
• Full Transcript

Clinical Case: Heart Failure and Rising Creatinine

Dr. David Ellison, MD, recounts a consult for a patient with acute decompensated heart failure. The patient had known chronic kidney disease with a baseline creatinine of 2.5 mg/dL. Treatment with high-dose loop diuretics like furosemide successfully produced a urine output of 3-4 liters per day. However, the patient's serum creatinine rose from 2.2 to 3.0 mg/dL over three days. This increase alarmed the primary care team, who believed it signaled over-diuresis and impending kidney damage. They demanded the diuretics be stopped, creating a critical treatment dilemma.

Urine Sediment Analysis for Kidney Injury

Instead of relying solely on the creatinine level, Dr. Ellison performed a microscopic urine sediment examination. He obtained a fresh urine sample from the patient's Foley catheter bag. The sample was centrifuged (spun) to concentrate any solid material, or sediment, for analysis. Dr. David Ellison, MD, emphasizes that a nephrologist's direct microscopic exam can be more accurate than automated lab tests or newer biomarkers for determining the type of kidney dysfunction. This hands-on approach provides immediate, actionable data at the bedside.

Interpreting Urine Microscopy Findings

The urine sediment analysis revealed only hyaline casts. Hyaline casts are simple protein structures that indicate a functional decline in kidney perfusion, often due to volume depletion or reduced blood flow from heart failure. Crucially, the sediment was devoid of signs of structural kidney damage. There were no white blood cells, red blood cells, or cellular casts. The absence of muddy brown granular casts, which are classic markers of acute tubular necrosis (ATN) and genuine kidney injury, was the most significant finding. This pattern confirmed a pre-renal state.

Treatment Implications from Urine Exam

Based on the urine microscopy results, Dr. Ellison advised continuing the aggressive diuretic regimen. He reassured the team that the rising creatinine reflected a hemodynamic change, not parenchymal injury. Current guidelines support targeting a diuresis of 3-5 liters per day in acute decompensated heart failure. Achieving full decongestion is paramount for improving outcomes, reducing hospital readmissions, and extending survival. Dr. David Ellison, MD, concluded that the benefits of effective decongestion far outweighed the temporary, functional rise in creatinine in this context.

Broader Clinical Applications of Urine Microscopy

This case underscores the enduring value of urine sediment microscopy in nephrology. It is a rapid, low-cost diagnostic tool that differentiates between pre-renal azotemia and acute kidney injury. Dr. Ellison's approach highlights a key clinical pearl: a rising creatinine during diuresis should not automatically trigger a cessation of therapy. Instead, it should prompt a diagnostic evaluation to determine the cause. For nephrologists and intensivists, mastering urine microscopy remains an essential skill for guiding complex fluid management decisions in critically ill patients.

Full Transcript

Dr. Anton Titov, MD: Could you please discuss a clinical story or vignette that illustrates some of the topics that were talked about?

Dr. David Ellison, MD: Yeah, I think that this is a little bit the vignette we talked about before, but let me just repeat it again. I was on call on a weekend in the hospital about a year ago, during COVID. I was seeing patients on the oncology floor and I got a call from a cardiologist at OHSU who's interested in heart failure.

He asked me to consult on a patient, but before we saw the patient, he sort of wanted to ask me my philosophy about patients with decompensated heart failure, because he was being told that the patient was being given high doses of furosemide. And the creatinine was going up and the primary team was demanding to stop the furosemide because the creatinine had gone from 2.2 to three in three days.

He told me that the patient was responding to the diuretics and was putting out three to four liters of fluid a day. And he told me that the primary care team was also very concerned because they thought the patient was being over-diuresed and it was putting out too much urine.

We ended up going to see the patient, and seeing the patient, how he represented the patient was exactly right. The patient had come in and had severe acute decompensated heart failure. The patient had known chronic kidney disease with a baseline creatinine of about two and a half and the patient was really in extremis when he came in.

They started giving him loop diuretics. The good thing was the patient was urinating three to four liters a day. We used to consider that amount of urine output a day in a patient like this worrisome. We thought we should restrict the fluid excretion to one to two liters a day.

And then when the patient's creatinine started going up, we also thought that was an indication of over-diuresis and time to back off. But because of the new controlled studies, which showed that we should target three to five liters a day of diuresis for acute decompensated heart failure, so that's a pretty good target range for diuresis.

We should target three to five liters a day for diuresis. And as I mentioned earlier, we should not be too worried about the creatinine going up. That said, when we saw that patient, that rising creatinine, we did take note of that, and it is possible that that could potentially lead to a real acute kidney injury.

So we wanted to evaluate the patient to make sure the patient was having a functional decrease in their kidney function that wasn't indicative of kidney damage. So what did we do? We didn't send biomarkers, we didn't send an electrolyte panel laboratory test, or an NGAL.

Instead, we asked what we always do: the nurse gave us a sample of urine from the Foley bag, and we got a fresh sample of urine. We took it to the laboratory. We spun the urine, and we did a microscopic examination.

While we often send the urine to the laboratory, we believe that there's some data to support this, that a microscopic examination by a nephrologist is more accurate in determining kidney injury.

When we looked at the urine, we were very pleased to see that there were some hyaline casts, but there were no other formed elements. There were no white cells, no red cells, and certainly no cellular casts. Hyaline casts indicate just a functional decline in kidney activity.

But if we had seen a lot of muddy brown casts, for example, which are indicative of acute kidney injury, we would have gone back and said, wait, you probably need to back off because this patient is getting genuine acute kidney injury.

Instead, we went back and said, no, the patient is responding to the loop diuretic. Continue, the patient is not fully decongested. If the patient gets fully decongested, they have a much higher chance of leaving the hospital and staying out of the hospital and actually living longer.

We will live with the fact that the creatinine has gone up a bit. And that's okay. So we reassured the team that they were doing the right thing.