Fluids Mismanaged

"Well I gave her some fluid for the blood pressure but the urine output was still low so I followed it with some furosemide." the FY1 doctor explained to me, my eyebrow slowly raising.

He had asked me to review an 85-year-old with pneumonia who he had been managing during a ward cover shift.

"Did you assess her volume status?" I probed.

"No I didn't." My heart sank.

"So how do you know if she needs more fluid or fluid removal?"

"I figured that if her kidneys weren't responding to the fluid, she's going to go into overload so the furosemide should help to kick them into action."

“Why do her kidneys need ‘kicking along’?” I asked, trying to stifle my frustration. The FY1 looked at me, slightly puzzled. “The outreach nurse was worried about the urine output, so I thought…”

I interrupted him gently. “Urine output is a just number, not a disease,” I said, before launching into a well-worn explanation. I’ve found myself having this conversation with many of my junior colleagues. Too often, the idea persists that low urine output is itself inherently pathological—that it demands a swift intervention to correct it.

But urine output is more nuanced. It’s the endpoint of finely tuned renal processes involving solute load, water balance, and concentrating ability. Trying to “fix” low urine output with fluids and diuretics ignores the underlying physiology, which is often functioning perfectly well, even when the numbers appear low.

First in my arsenal is a thought experiment one of my professors gave me when I entered his renal clinic as a medical student.

"Once you understand this," the don had told me "you'll be ahead of most of my SHOs!"

I turn back to my FY1; "Imagine I lock you in a room with nothing but a tap, a drinking glass and a bucket. What is the maximum volume of urine you could produce in 24 hours?"

The FY1 returns a perplexed look. "Well urine output is determined by lots of factors: renal blood flow, glomerular filtration, tubular function…"

I can see this turning into a hand-waving response, so I cut him short. "Thinking about this in really simple terms, what's the main role of the kidney?"

"Well, to get rid of waste I guess."

"Right. Now is it possible for one to excrete pure water?"

"Obvious not. You'd be dead of water intoxication before then!"

So far, so good. I offer him a clue: "Great, so would you agree that in the most basic terms, urine comprises a solute load - waste - which is diluted in a given volume of water? We can't excrete pure waste because some water is kept in the tubules by osmosis, and conversely we can't excrete pure water."

"I suppose that makes some sense, but what has that got to do with the maximum I would be able to pee out?"

“Well,” I said, “let’s start with the mechanics. The kidneys concentrate urine via the Loop of Henle, where the filtrate is refined into a solution that can range from as concentrated as 1200 mosmol/L to as dilute as 50 mosmol/L. This range allows the kidneys to adapt fluid excretion to our body’s needs. Now, an adult has an obligate solute load of around 600 mosmol/day—this is the minimum amount of waste solute, mainly urea, that needs to be excreted to maintain metabolic balance. This amount is largely determined by factors like muscle mass and protein intake.”

I continued, “So if we know that the kidneys can dilute urine down to a minimum concentration of 50 mosmol/L, what would be the theoretical maximum urine output for a healthy adult with an obligate solute load of 600 mosmol/day?”

He hesitated, then ventured, “So… if you divide the solute load by the minimum concentration, I suppose…”

“Precisely,” I encouraged. “At maximum dilution, the kidneys would need around 12 litres of water to excrete the 600 mosmol of solute, because:

So if you were drinking excessively, in theory, your kidneys could produce up to 12 litres of urine in a day. But under normal conditions, this high output is unusual.”

The FY1 seemed to be following, so I pressed on. “Now, let’s consider the opposite extreme: the theoretical minimum urine output. When the kidneys are working to conserve water, they can concentrate urine up to 1200 mosmol/L. With a solute load of 600 mosmol/day, the minimum volume required to excrete this would be:

This translates to about 20-21 mL/hour—the lowest physiological urine output for a healthy adult with adequate renal concentrating function.”

I paused to let this sink in, then added, “But here’s the crux. In older, frail patients with decreased muscle mass, like your patient, the obligate solute load is often lower—say around 300 mosmol/day. In such cases, the kidneys would only need to produce around 10 mL/hr at maximum concentration to maintain solute balance. So, a low urine output in this scenario isn’t necessarily abnormal; it’s just physiology adapting to a lower solute load. More fluid won’t change this fundamentally, and giving diuretics will only increase urine volume by ‘switching off’ the Loop of Henle’s concentrating function. But the amount of solute excreted won’t increase. The kidneys are not designed to ‘kick along’ on demand.”

The FY1 seemed contemplative. “So… her low urine output could just be normal?”

“Exactly. Low output alone doesn’t imply a pathological state. It’s about understanding the patient’s physiology, not just treating numbers. In this case, rather than forcing a response from the kidneys, we need to evaluate her fluid status, solute load, and overall clinical picture. Sometimes, less intervention is better.”

Why is this Turtle Crying?

The answer: renal physiology. No, this reptile is not overwhelmed by the complexity of nephron dynamics, rather, I would argue these tears illustrate the point further.

While humans rely on the kidneys’ ability to concentrate urine, not all animals are equipped with this structure. Turtles, for instance, lack a Loop of Henle, which means they cannot concentrate their urine to conserve water the way mammals can. Without the loop, turtles face the challenge of managing their solute load in environments where fresh water isn’t readily available. Humans are unable to survive on sea water due to its high salinity, even with the ability to excrete excess solute whilst minimising water loss.

As disucussed above, the Loop of Henle creates a medullary concentration gradient that allows the kidneys to produce urine of variable concentration, up to 1200 mosmol/L in humans. This flexibility is essential for terrestrial mammals, as it conserves water whilst allowing efficient excretion of solutes. Without a Loop of Henle, turtles cannot generate such a high medullary gradient, and thus their kidneys produce a relatively dilute urine, close to the osmolality of their plasma. This means that, without other adaptations, turtles would need large amounts of water to excrete even a modest solute load, which is impractical, especially given that they live an environment with high salinity. The high salt intake from seawater would simply overwhelm their renal system.

Turtles and other reptiles have evolved an alternative strategy to handle excess solutes: specialised salt glands. Located near their eyes or nostrils, these glands actively secrete concentrated salt solutions, independently of urine. They are also favourites of environmental campaigners as they make for quite good pictures for posters about not dumping stuff in the ocean.

Salt glands operate by actively pumping out excess sodium and chloride ions, often at concentrations much higher than can be achieved through urine alone. For instance, marine turtles can secrete a salt solution with an osmolality well above that of seawater, removing the burden of high salt loads without relying on the kidneys. This mechanism conserves water while efficiently managing solute excretion.

Beyond Fluid Volume: Treating the Patient, Not the Number

As we’ve seen, a true understanding of renal physiology goes far beyond simply measuring absolute volumes or trying to “boost” urine output. At its core, the kidney’s primary role is solute handling—the precise excretion of metabolic waste products, electrolytes and toxins. After all, in renal failure, it is not the lack of urine volume that directly threatens life but rather the accumulation of solutes and toxins leading to uraemia.

By viewing the kidneys’ function through the perspective of solute load, rather than fluid volume alone, we can avoid some common misconceptions and unnecessary interventions that often arise in critically unwell patients. In the case of an elderly or frail ill patient, a lower urine output is not always a pathological sign. Rather, it may simply reflect a lower obligate solute load, and therefore a lower urine volume requirement. Forcing an increase in urine volume, such as by use of loop diuretics, without considering solute load doesn’t enhance the kidneys’ filtering ability or reduce toxin buildup. It merely dilutes the excretion process without addressing the underlying physiology. Thus, in a patient with normal or reduced solute load, diuretics can lead to volume depletion without aiding in the removal of waste products. In cases of acute renal failure, there is no evidence that shows that diuretics do prevent or mitigate uraemia; they simply create the illusion of improved renal function by generating a higher urine output.

The lessons from solute handling underscore the importance of treating patients based on their physiological needs, rather than trying to “correct” numbers in isolation. Just as turtles evolved salt glands to handle solute excretion independently of water, the human kidney has evolved highly specialised mechanisms for solute excretion and water balance, both of which deserve equal consideration.

In critically ill patients, a thoughtful approach to renal function means evaluating the broader clinical context rather than reacting solely to urine output metrics. Assessing volume status, identifying and managing nephrotoxic exposures, and addressing underlying metabolic or infectious issues are often more beneficial than administering diuretics to “boost” urine flow.

In summary, interpreting renal function in terms of solute handling provides a clearer, more physiologically-based approach to managing oliguria. By focusing on the kidney’s role in balancing solutes and excreting toxins, we can make better-informed decisions that align with renal physiology rather than forcing interventions that may do more harm than good.