Urinary Anion Gap

In a patient with non-anion gap metabolic acidosis, calculating the urine anion gap can help differentiate between diarrhea and renal tubular acidosis (RTA) as the etiology.

 

A. What is the urine anion gap and how is it calculated?

 

B. In the following case, please determine if the patient has a non-anion gap metabolic acidosis due to diarrhea or RTA:

 

A 24 year old male dancer comes to attention due to a low serum bicarbonate on routine blood work. Additional results include:
Serum: Na 140 meq/L, K 3 meq/L, HCO3 14 meq/L, Cl 116 meq/L
Urine: Na 50 meq/L, K 30 meq/L, Cl 40 meq/L.


Answere:

Urine anion gap is calculated by subtracting the urine concentration of chloride(anions) from the concentrations of sodium plus potassium (cations):

= Na⁺ + K⁺ − Cl⁻

where the concentrations are expressed in units of milliequivalents/liter (mEq/L).

In contrast to the serum anion gap equation, the bicarbonate is excluded. This is because urine is acidic, so the bicarbonate level would be negligible.

Urine anion gap is an 'artificial' and calculated measure that is representative of the unmeasured ions in urine. Usually the most important unmeasured ion in urine isNH₄⁺.

• A positive urine anion gap suggests a low urinary NH₄⁺ (e.g. renal tubular acidosis).
• A negative urine anion gap suggests a high urinary NH₄⁺ (e.g. diarrhea).

Case Discussion

56 year male , ex smoker with significant history of Ischemic heart disease

Presented in emergency with the complaint of Generalized weakness, Short

Of breath and decreased urine output for last 2 weeks.

He was already investigated outside in cardiology services which he often

Visisted for his chronic heart ailment. His serum creatinine jumped from 0.7

Mg/dl to 4.1 mg/dl in 1 week period.

His past history entails stent placement 8 year back after angiography. Since  then

He was on heart medication including anti hypertensive agent s whose is prescription

Was not brought by him and he does not  know the names for all medications.

On examination he was conscious , well oriented and mobile with regular pulse

96 bpm and BP 80/6o with diminished perepheral pulses. He pale , not icteric

Not cyanosed with dry peripheries and flat neck veins.

Systemically he was ok except slight tenderness on right hypochondrial region.

Discussion:

Now this middle age guy has developed acute kidney injury. And the reason for

This is quit well infromed for his low blood pressure with significand heart disease

With medication whose names are not described. Well we can presume medication

In this scenario would be diuretic , ace inhibitors, anti platelets, Beta blockers etc.

This could cause volume depletion and AKI. ACE inhibitors can cause AKI.

He might have developed unstabel angina/MI which has cused AKI. He may have atherembolic disease.

Case Discussion

30 year male admited through emergency in a severe metabolic acidosis state and drowsy.

He had outside s.creatine of 15mg/dl, and xray showing homogenous opacity involving right

Apex of lung. There was recent history of taking ATT, which he soon gave up after using few

Days as he became more nauseated and had vomiting too. There was an aditional history of

Difficulty in passing urine since many years, and also required once catheterization suprapubically.

We got him inserted Double lumen cather and dialysed , later on Ultrasound kidneys and bladder

Showed markly dillated PC system leaving no cortex bilatteraly and thick wall , mild trabeculated

Bladder.

We concluded that he would be having stricture urethra by his tory which was substaciated with

The fact  when he was tried to pass cather but failed to proceed and subsequently suprabubic cathe

Erization done as he was in retention of urine.

Regarding his homogenous opacity in lung we would work him up for tuberculosis by Blood CP, ESR

Mauntox test, Sputum AFB or moring gastric lavage for AFB or BAL. Urine Dr and C/s.