- Draw same-day serum and diagnostic-paracentesis ascitic-fluid samples. Enter the serum albumin (g/dL).
- Enter the ascitic-fluid albumin (g/dL). The SAAG and its interpretation update automatically.
- Optionally enter the ascitic-fluid total protein (g/dL). When the SAAG is high (≥ 1.1), this sub-classifies a high-SAAG ascites as cardiac (total protein ≥ 2.5) versus cirrhotic (< 2.5).
- SAAG ≥ 1.1 g/dL → portal hypertension present; < 1.1 g/dL → portal hypertension absent.
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When to Use
Use the SAAG on every new-onset ascites and whenever the cause of ascites is uncertain. It is computed from albumin in same-day serum and ascitic-fluid samples obtained at diagnostic paracentesis. The SAAG sorts ascites into two physiologic categories — portal-hypertensive (high SAAG, ≥ 1.1 g/dL) and non-portal-hypertensive (low SAAG, < 1.1 g/dL) — with roughly 97% accuracy, which is more reliable than the older transudate/exudate classification.
Appropriate use
Adults with new or undiagnosed ascites. High SAAG (≥ 1.1) points to portal hypertension — cirrhosis, alcoholic hepatitis, cardiac ascites, Budd-Chiari syndrome, massive hepatic metastases, or portal-vein thrombosis. Low SAAG (< 1.1) points to a non-portal cause — peritoneal carcinomatosis, tuberculous peritonitis, pancreatic ascites, nephrotic syndrome, or serositis. Relevant to the hepatorenal-syndrome and the nephrotic-syndrome (low-SAAG) differentials.
Caveats
The gradient requires same-day samples; serum and ascitic albumin drawn days apart can mislead. The SAAG categorizes the mechanism (portal hypertension yes/no) — it does not identify the specific disease, and mixed ascites (e.g. cirrhosis plus peritoneal carcinomatosis) can blur the gradient. Always send the diagnostic tap for cell count with differential and culture to exclude spontaneous bacterial peritonitis (PMN ≥ 250/µL), regardless of the SAAG.
Pearls & Pitfalls
1.1 g/dL is the line that matters
A SAAG ≥ 1.1 g/dL means portal hypertension is present (≈97% accurate); < 1.1 g/dL means it is absent. The gradient reflects the oncotic–hydrostatic balance across the hepatic sinusoids, so it tracks portal pressure rather than fluid "transudate vs. exudate" — which is why it has supplanted the old classification.
Add ascitic total protein to split high-SAAG ascites
When the SAAG is high (≥ 1.1), the ascitic-fluid total protein distinguishes the level of the block: ≥ 2.5 g/dL suggests a post-sinusoidal / cardiac cause (heart failure, constrictive pericarditis, Budd-Chiari), whereas < 2.5 g/dL suggests a sinusoidal cause (cirrhosis). This sub-split is most useful for separating cardiac ascites from cirrhosis.
Pitfalls
(1) Always send the diagnostic paracentesis for cell count + culture to exclude spontaneous bacterial peritonitis (PMN ≥ 250/µL) — the SAAG never substitutes for this. (2) Use same-day serum and ascitic samples; non-contemporaneous albumins distort the gradient. (3) The SAAG categorizes the mechanism, not the disease — confirm the specific cause clinically. (4) Mixed ascites (e.g. cirrhosis with superimposed peritoneal carcinomatosis or infection) can produce an intermediate or misleading gradient.
Why Use It
The SAAG turns the first decision in any ascites workup — is portal hypertension present? — into a single subtraction with about 97% accuracy. In the landmark Runyon study it outperformed the long-standing transudate/exudate (total-protein) classification, and it is now the AASLD- and EASL-endorsed first step in characterizing ascites. For the nephrologist it matters twice: a low-SAAG ascites belongs to the nephrotic-syndrome and serositis differential, while a high-SAAG cirrhotic ascites frames the assessment of acute kidney injury and hepatorenal syndrome. Adding the ascitic total protein to a high SAAG further separates cardiac ascites from cirrhosis, refining management before more invasive testing.
Serum-Ascites Albumin Gradient (SAAG)
Enter the serum albumin and ascitic-fluid albumin (same-day samples) to get the SAAG and whether portal hypertension is present. Optionally add the ascitic-fluid total protein to sub-classify a high-SAAG ascites as cardiac versus cirrhotic.
⚕ Runyon BA, et al. Ann Intern Med. 1992;117(3):215–220. The SAAG classifies ascites by the presence (≥ 1.1 g/dL) or absence (< 1.1 g/dL) of portal hypertension; it does not identify the specific disease and assumes same-day serum and ascitic samples. Always send the diagnostic paracentesis for cell count and culture to exclude SBP (PMN ≥ 250/µL). For licensed clinicians; not a substitute for individualized assessment.
Next Steps
Use the SAAG to set the direction of the ascites workup, then characterize the specific cause.
- SAAG ≥ 1.1 g/dL (portal hypertension present): pursue cirrhosis, alcoholic hepatitis, cardiac ascites, Budd-Chiari, massive hepatic metastases, or portal-vein thrombosis. If ascitic total protein ≥ 2.5 → favor a cardiac/post-sinusoidal cause (echocardiogram, BNP); if < 2.5 → favor cirrhosis (liver imaging, hepatology).
- SAAG < 1.1 g/dL (portal hypertension absent): pursue peritoneal carcinomatosis, tuberculous peritonitis, pancreatic ascites, nephrotic syndrome, or serositis — order ascitic cytology, fluid amylase, adenosine deaminase / mycobacterial studies, and assess for proteinuria.
- Always send the diagnostic tap for cell count with differential and culture to exclude spontaneous bacterial peritonitis (PMN ≥ 250/µL), independent of the SAAG.
- In cirrhotic ascites, assess kidney function and the hepatorenal-syndrome differential; score severity with the Child-Pugh score and the MELD & MELD-Na.
Evidence & References
Formula
| Quantity | Formula |
|---|---|
| SAAG (g/dL) | Serum albumin − ascitic-fluid albumin (same-day samples) |
| Cutoff | ≥ 1.1 → portal hypertension present · < 1.1 → absent |
| High-SAAG sub-split | Ascitic total protein ≥ 2.5 → cardiac · < 2.5 → cirrhotic |
Interpretation of the SAAG
| Result | Interpretation & causes |
|---|---|
| SAAG ≥ 1.1 g/dL | Portal hypertension present (≈97% accurate) — cirrhosis, alcoholic hepatitis, cardiac ascites, Budd-Chiari, massive hepatic metastases, portal-vein thrombosis |
| ↳ total protein ≥ 2.5 | Suggests a cardiac / post-sinusoidal cause |
| ↳ total protein < 2.5 | Suggests cirrhosis (sinusoidal) |
| SAAG < 1.1 g/dL | Portal hypertension absent — peritoneal carcinomatosis, TB peritonitis, pancreatic ascites, nephrotic syndrome, serositis |
Runyon and colleagues showed the SAAG classifies ascites by portal pressure with about 97% accuracy, outperforming the older transudate/exudate (total-protein) concept; it is the AASLD- and EASL-endorsed first step in characterizing ascites.
References
- Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117(3):215–220.
- Runyon BA; AASLD. Management of adult patients with ascites due to cirrhosis: update 2012. Hepatology. 2013;57(4):1651–1653.
- European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018;69(2):406–460.
