Polyuria

Pathophysiology and classification

The daily urine output is determined predominantly by the daily intake of fluids, daily solute excretion, and the urine-concentrating ability of the nephrons. The average person excretes about 600–800 mOsm of solutes per day, and average urine output is about 1.5–2.5 L/day. Polyuria happens usually because of one or more of the following mechanisms:

• Increased fluid intake, necessitating excretion of a large volume of urine (primary polydipsia)

• Increased glomerular filtration rate (rare)

• Increased solute excretion (solute or osmotic diuresis)

• Inability of the kidney to reabsorb water (central or nephrogenic diabetes insipidus [DI])

Polyuria is hence broadly classified into solute diuresis or water diuresis . When increased solute excretion drives the polyuria, it is termed solute diuresis. Increased urine output secondary to increased water intake or impaired water reabsorption is termed water diuresis. However, some patients have mixed water and solute diuresis.

Recognition of polyuria

In critically ill patients, polyuria is usually easy to identify in patients with an indwelling urinary catheter. Careful measurement of urine volume passed or placement of a urinary catheter should be undertaken in patients who have increased urinary frequency; who are passing large volumes of urine; and who are severely hyperglycemic, hypercalcemic, or hypokalemic. Importantly, because intensive care unit (ICU) patients frequently receive in excess of 3 L a day in total input, urine output may exceed 3 L without pathology. Therefore clinical context and clinical judgement are required. ^,

Solute diuresis

Total daily urinary solute excretion varies widely varies different ethnicities, cultures, and dietary habits. The average urinary solute excretion in a healthy American adult is between 500 and 1000 mOsm/d. Solute or osmotic diuresis causing polyuria is due to solute excretion in excess of the usual excretory rate. The primary abnormality in such conditions is the inability for the kidney to reabsorb a large proportion of the solute filtered. Increased solute load can be secondary to excess solute intake or increased generation of solutes because of metabolism. Increased solute intake can occur after administration of intravenous fluids (saline, dextrose, or bicarbonate); enteral or parenteral nutrition; or ingestion of exogenous proteins, sugars, or alcohols. Increased solute generation from metabolism is seen in hyperglycemia and azotemia.

Solute excretion increases urine output in a linear fashion, and solute diuresis impairs the ability of the kidney to concentrate the urine. Solute diuresis can be quite severe and can be caused by more than one solute concurrently. Unless there is an adequate replacement of solute and water, a persistent solute diuresis contracts extracellular volume, leading to severe dehydration and hypernatremia.

Multiplying urine osmolality by the 24-hour urine volume gives an estimate of total urine solute concentration. If urinary total solute concentration is abnormally large, a solute diuresis is present. Solute diuresis is caused by either excessive electrolyte excretion or excessive nonelectrolyte solute excretion. If the total urinary electrolyte excretion exceeds 600 mOsm/d, then an electrolyte diuresis is present. The total urinary electrolyte excretion (in mOsm/d) can be estimated as 2 × (urine [Na ⁺ ] + urine [K ⁺ ]) × total urine volume. Electrolyte diuresis is generally driven by a sodium salt, usually because of iatrogenic administration of excessive normal saline or sodium bicarbonate solutions, excessive salt ingestion, and repetitive administration of loop diuretics. However, salt-losing nephropathies usually do not cause polyuria because the increased delivery of chloride to the macula densa cells triggers tubuloglomerular feedback, causing afferent arteriolar constriction and resulting in decreased glomerular filtration rate (GFR) and an overall decrease in sodium excretion.

Cerebral salt wasting (CSW) is a clinical syndrome characterized by excess renal sodium excretion, polyuria, hypovolemia, and hyponatremia. Although most often seen in patients with aneurysmal subarachnoid hemorrhage (SAH), it can occur in any primary neurologic illness, including central nervous system (CNS) tumors, infectious or carcinomatous meningoencephalitis, and after neurosurgical procedures. Normally, the sympathetic nervous system promotes reabsorption of sodium directly at the proximal tubule. During CSW, increased sodium excretion occurs possibly because of impaired sympathetic neural input to the kidney related to the brain injury. Another putative mechanism involves release of brain natriuretic peptide (BNP) leading to decreased sodium reabsorption and renin release. The resulting solute diuresis and polyuria cause hypovolemia, which then stimulates antidiuretic hormone (ADH) release via a baroreceptor-mediated mechanism, leading to water retention and hyponatremia. Often CSW and syndrome of inappropriate ADH secretion (SIADH) overlap and are difficult to distinguish biochemically. Clinical evidence of volume contraction suggests a diagnosis of CSW, whereas patients with SIADH are usually euvolemic.

A clearly excessive value for urine nonelectrolyte excretion (i.e., >600 mOsm/d) implies that nonelectrolytes are the predominant solutes contributing to the diuresis. The urinary nonelectrolyte excretion can be calculated by subtracting urine electrolyte excretion from the total urine solute excretion. The most common nonelectrolyte solute causing excessive diuresis is glucose, although its incidence is decreasing in critically ill patients because of tighter glycemic control practices. Conditions associated with glucose-induced diuresis include diabetic ketoacidosis or hyperosmolar state. Excessive excretion of urea is another important cause of solute diuresis. This problem can occur after relief of urinary tract obstruction, as a consequence of enteral nutrition using a high-protein tube feeding formula, or during recovery from acute tubular necrosis. Mannitol administration (e.g., as a therapy for intracranial hypertension) also can lead to significant solute diuresis. This issue is pertinent because mannitol is often administered to patients with head trauma, who are at risk for development of nephrogenic DI.

The correct diagnosis of solute diuresis depends on a clear systematic approach as discussed earlier. Management usually involves treatment of the underlying disorder and repletion of extracellular volume by hydration.

Water diuresis