# Ancillary Urine Tests: Ask a Focused Physiologic Question

Choose the urine test for a specific physiologic question, then integrate volume, medicines, sediment, and timing before treating the number.

![Infographic: Ancillary Urine Tests: Ask a Focused Physiologic Question](https://urinenephrology.org/visual-reference/images/ancillary-urine-tests.png?v=20261003c)

## Begin with blood, protein, and microscopy

Heme-positive urine with few RBCs prompts pigment/hemolysis evaluation; RBC casts or acanthocytes plus protein raise glomerular disease. Quantify albumin with ACR and total protein when needed. A dipstick or specific-gravity result alone cannot assign the cause of AKI.

## Hyponatremia: is water being excreted?

After confirming hypotonicity, urine osmolality ≤100 mOsm/kg suggests suppressed antidiuresis, as with high water intake or low solute intake. Above 100, assess urine sodium and clinical volume. Urine sodium ≤30 mmol/L supports low effective arterial volume, including congested states.

## Alkalosis: branch on urine chloride

Urine chloride <20 mEq/L suggests chloride depletion, such as vomiting or remote diuretic exposure. At ≥20, ask about active diuretics, BP, potassium, mineralocorticoid effects, or salt-wasting tubulopathy. Current/recent diuretics and advanced CKD limit this distinction; repeat when interpretable.

## Then decide whether chloride fluid fits

Low urine chloride plus true depletion can support isotonic chloride replacement and potassium correction. A congested heart-failure patient can also be chloride depleted: do not automatically give saline. Address congestion, diuretic strategy, potassium, and the cause of ongoing losses.

## AKI: fractional excretion is supportive

FeNa = 100 × (urine Na × plasma creatinine)/(plasma Na × urine creatinine). A value <1% suggests sodium avidity, not necessarily intact tubules. Diuretics, CKD, sepsis, glomerular disease, and obstruction can confound interpretation; FeUrea <35% is also imperfect.

## Pair the result with a decision

Use simultaneous blood/urine samples and record recent fluids or diuretics. In hypokalemia, excessive urine K suggests renal loss and prompts acid–base/BP review. Urine eosinophils cannot rule AIN in or out. Recheck physiology when the course contradicts the initial hypothesis.

## Supporting evidence

- [Clinical evidence and guidance](https://www.ccjm.org/content/91/6/345)
- [Official clinical guidance](https://kdigo.org/wp-content/uploads/2016/10/KDIGO-2012-AKI-Guideline-English.pdf)
- [Official clinical guidance](https://kdigo.org/wp-content/uploads/2026/04/KDIGO-2024-CKD-Guideline.pdf)
- [PubMed 35525634](https://pubmed.ncbi.nlm.nih.gov/35525634/)
- [PubMed 24569496](https://pubmed.ncbi.nlm.nih.gov/24569496/)
- [PubMed 24052222](https://pubmed.ncbi.nlm.nih.gov/24052222/)

## Source lessons

- [microscopic](https://urinenephrology.org/2025_UDPA_Lectures_Live/urinalysis/microscopic.html)
- [interpretation](https://urinenephrology.org/2025_UDPA_Lectures_Live/urinalysis/interpretation.html)
- [urinalysis master diagnostic algorithm](https://urinenephrology.org/student-resources/foundations/urinalysis-master-diagnostic-algorithm.html)

Read alongside the full lessons; the findings and decisions shown here require the stated clinical context.