Urine Osmolality Calculator

How to Use This Calculator

1. Enter urine sodium, potassium, glucose, and urea to calculate urine osmolality.
2. Osmolar Gap tab: compare calculated vs measured osmolality to detect unmeasured solutes.
3. SIADH Workup tab: enter serum osmolality and sodium to assess SIADH criteria.
4. Professional tier adds DI assessment, specific gravity estimate, and integrated AKI classification.

Formula

Example

Frequently Asked Questions

• How is urine osmolality calculated from spot urine values? ▼
  Urine osmolality can be estimated from spot urine electrolytes using the following formula: Calculated Uosm = 2 × (Urine Na + Urine K) + Urine Glucose (mg/dL) / 18 + Urine Urea (mg/dL) / 2.8. The factor of 2 before the electrolyte sum accounts for the counterions (each cation is balanced by an anion contributing to total osmolality). Dividing glucose by 18 and urea by 2.8 converts from mg/dL to mmol/L (the unit of osmolality), using molecular weights of 180 g/mol for glucose and 28 g/mol for the nitrogen portion of urea (BUN). In normal urine without glycosuria, glucose contributes negligibly to calculated osmolality, so the dominant terms are the electrolyte component and urea. Normal urine osmolality ranges from 50–1200 mOsm/kg depending on hydration status, with a random specimen typically 300–900 mOsm/kg. The calculated value correlates well with measured osmolality (by freezing point depression) when glycosuria and unusual solutes are absent. When the measured osmolality significantly exceeds the calculated value (urine osmolar gap >100 mOsm/kg), unmeasured osmoles are present — most commonly ethanol, ketone bodies, or exogenous osmoles (mannitol). This calculated approach is useful when a measured osmolality is unavailable or for rapid bedside estimation.
• What does high versus low urine osmolality indicate? ▼
  Urine osmolality reflects the kidney's concentrating or diluting activity, which is regulated primarily by antidiuretic hormone (ADH, vasopressin). High urine osmolality (>700–800 mOsm/kg) indicates that the kidney is maximally concentrating urine under the influence of high ADH — a response to volume depletion, hyperosmolality, or inappropriate ADH secretion. Moderate to high concentrations (400–700 mOsm/kg) indicate partial ADH stimulation. Low urine osmolality (<100–150 mOsm/kg) indicates maximal water diuresis with suppressed ADH — appropriate in primary polydipsia, low solute intake (beer potomania, tea-and-toast diet), or if the kidney cannot concentrate despite high ADH (nephrogenic DI). Intermediate values (200–400 mOsm/kg) are isosthenuric — approaching the osmolality of plasma (~290 mOsm/kg) — indicating loss of concentrating ability, which is characteristic of acute tubular necrosis (ATN), tubular interstitial diseases, or other intrinsic renal pathology. In the context of AKI: Uosm >500 mOsm/kg suggests an intact concentrating mechanism, consistent with prerenal AKI where tubular function is preserved; Uosm <350 mOsm/kg suggests loss of tubular function, consistent with established ATN. When urine osmolality is used together with FENa or FEUrea, diagnostic accuracy for AKI cause is substantially improved compared to either marker alone.
• How is urine osmolality used in AKI diagnosis? ▼
  In the workup of acute kidney injury (AKI), urine osmolality provides complementary information to FENa and FEUrea about the kidney's tubular function status. The diagnostic principle is the same: in prerenal AKI, intact tubular function drives maximal sodium and water reabsorption in response to volume depletion and high ADH. This produces concentrated urine (high UOsm). In established ATN, tubular damage impairs the ability to concentrate urine, resulting in isosthenuric urine (UOsm approaching plasma osmolality, ~290 mOsm/kg). KDIGO AKI guidelines note: Uosm >500 mOsm/kg in the context of oliguric AKI supports prerenal cause; Uosm <350 mOsm/kg in oliguric AKI is more consistent with ATN. Important caveats: Uosm is less specific than FENa when used alone, particularly in elderly patients who have diminished concentrating ability at baseline. Diuretics, chronic tubulointerstitial disease, and any condition that impairs the medullary gradient (loop diuretics, hypercalcemia, hypokalemia) can reduce Uosm in prerenal states. Uosm should be interpreted with FENa (or FEUrea in diuretic use) and urine sediment (muddy brown casts = ATN, hyaline casts = prerenal). A complementary marker is urine specific gravity (SG): SG 1.020+ generally corresponds to Uosm >600 mOsm/kg; SG ~1.010 corresponds to ~300 mOsm/kg (isosthenuric). Dipstick SG is less precise but can be used when formal osmolality is not yet available.
• What is the role of urine osmolality in SIADH? ▼
  Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a cause of hyponatremia defined by: (1) serum hypo-osmolality (<280 mOsm/kg); (2) inappropriately concentrated urine (UOsm >100 mOsm/kg, and typically >200 or >300 mOsm/kg); (3) urine sodium >40 mEq/L despite hyponatremia; (4) absence of volume depletion, hypothyroidism, and adrenal insufficiency; (5) no diuretic use. The cardinal criterion directly involving urine osmolality is that urine should not be maximally dilute (Uosm >100 mOsm/kg) in the presence of plasma hypo-osmolality. Normally, when plasma osmolality falls below ~280 mOsm/kg, ADH is completely suppressed and the kidney dilutes urine to <100 mOsm/kg to excrete the excess water. In SIADH, ADH is secreted despite low plasma osmolality (due to tumors, CNS pathology, pulmonary disease, medications, nausea, pain), preventing urine dilution. Clinically, Uosm > Serum Osm is a useful screen: if urine is more concentrated than plasma in a hyponatremic patient, SIADH is highly likely after excluding other causes. The Verbalis et al. 2013 Endocrine Society guidelines recommend Uosm measurement as part of the initial hyponatremia workup. Some cases of SIADH have very high Uosm (>500 mOsm/kg) indicating strong inappropriate ADH secretion; others may have Uosm only 100–200 mOsm/kg (partial SIADH or recent water load). All values above 100 mOsm/kg in hypo-osmolar hyponatremia are consistent with SIADH.
• How does urine specific gravity relate to urine osmolality? ▼
  Urine specific gravity (SG) and urine osmolality both measure urine concentration, but by different methods: SG measures the ratio of urine density to water density, while osmolality measures the number of solute particles per kilogram of water. SG is routinely reported on urinalysis (dipstick or refractometer) and provides a rapid, practical estimate of urine concentration. The approximate relationship: SG 1.001 ≈ 50 mOsm/kg (very dilute); SG 1.010 ≈ 290–300 mOsm/kg (isosthenuric, same as plasma); SG 1.020 ≈ 600–700 mOsm/kg (concentrated); SG 1.030 ≈ 1000+ mOsm/kg (maximally concentrated). The practical rule: SG 1.010 = isosthenuric (plasma-equivalent), consistent with ATN pattern. SG >1.018 = good concentrating ability, consistent with prerenal. SG is less accurate than osmolality because large molecules (glucose, protein, contrast dye, radiographic agents) elevate SG disproportionately relative to osmolality. For example, heavy glycosuria raises SG significantly while adding only a modest osmolar contribution per particle weight. In such cases, SG overestimates the kidney's actual concentrating ability. Measured osmolality (freezing point depression method) is the gold standard. Calculated urine osmolality (from electrolytes, glucose, urea) is a reasonable proxy when measurement is unavailable. Dipstick SG is acceptable for quick screening — if SG >1.020, the kidney is concentrating well; if 1.010, tubular function is impaired.

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