Calculate the Serum-Ascites Albumin Gradient to differentiate portal-hypertensive from non-portal ascites. Includes ANC screening context, LDH analysis, and a reference pattern table.
The Serum-Ascites Albumin Gradient (SAAG) is a widely used test for classifying the etiology of ascites. By subtracting the ascites albumin concentration from the serum albumin, SAAG reflects the portal-sinusoidal pressure gradient — the driving force behind portal-hypertensive ascites.
A SAAG ≥ 1.1 g/dL identifies portal hypertension with high accuracy and largely replaced the older transudate/exudate classification, which had substantial overlap. This threshold divides ascites into two broad pathophysiologic categories: high-SAAG (portal hypertension from cirrhosis, cardiac failure, or hepatic vein obstruction) and low-SAAG (peritoneal disease from malignancy, tuberculosis, nephrotic syndrome, or pancreatitis).
This calculator extends basic SAAG with ascites fluid cell-count context for spontaneous bacterial peritonitis (SBP) screening, LDH ratio for secondary-peritonitis discussion, and a four-quadrant reference table combining SAAG with ascites total protein for differential-diagnosis context. An ANC of ≥250/µL is shown as a screening threshold, not as a stand-alone treatment directive.
Ascites has many possible causes, and the clinical presentation alone is often insufficient for classification. SAAG narrows the differential into two broad categories — portal-hypertensive versus non-portal patterns — and the added ANC and protein context help refine the worksheet without turning it into a treatment engine.
SAAG = Serum Albumin (g/dL) − Ascites Albumin (g/dL) ≥ 1.1 g/dL = Portal-hypertensive reference pattern < 1.1 g/dL = Non-portal reference pattern Ascites ANC = WBC × (Neutrophil % / 100) ANC ≥ 250 cells/µL = common SBP screening threshold
Result: SAAG = 2.2 g/dL (High), Low protein → Portal hypertension (cirrhosis)
SAAG = 3.2 − 1.0 = 2.2 g/dL, well above the 1.1 threshold confirming portal hypertension. Ascites protein < 2.5 g/dL suggests cirrhosis as the cause rather than cardiac ascites (which typically has high ascites protein). This is the most common clinical scenario.
The practical strength of SAAG is that it quickly separates ascites related to portal hypertension from ascites caused by peritoneal disease. That first split narrows the differential dramatically and changes how the broader picture is framed, especially when cirrhosis, heart failure, malignancy, tuberculosis, or pancreatitis are competing possibilities.
A high SAAG points toward portal hypertension, but the total protein level helps distinguish low-protein cirrhotic ascites from higher-protein cardiac or post-sinusoidal causes. The cell count adds another layer of context, because a neutrophil-predominant sample may raise the possibility of SBP even before culture results return.
The gradient is only reliable when the serum and ascites albumin values come from the same clinical moment. Mixing samples from different days, ignoring marked hypoalbuminemia, or forgetting to calculate the absolute neutrophil count can make a technically correct number clinically misleading.
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This calculator subtracts ascites albumin from serum albumin to compute the serum-ascites albumin gradient, then shows the result beside ascites protein, ANC, and the supporting pattern table on the page. The additional fields are there to help organize the fluid-analysis worksheet rather than to create a stand-alone management rule.
The SAAG threshold is used here to split portal-hypertensive and non-portal patterns, while reminding the reader that symptoms, culture data, imaging, and the rest of the ascites workup still matter.
The old transudate/exudate classification (Light's criteria adapted from pleural fluid) misclassified 15–20% of ascites samples. SAAG has 97% accuracy for identifying portal hypertension because it directly reflects the portal pressure gradient, regardless of diuretic use or albumin infusions.
A SAAG ≥ 1.1 (portal hypertension) with ascites protein ≥ 2.5 g/dL suggests cardiac ascites (CHF, constrictive pericarditis) or acute Budd-Chiari syndrome. In cardiac ascites, the hepatic sinusoidal pressure is elevated by right heart failure rather than liver disease.
An ascites ANC ≥ 250/µL is the common screening threshold used in SBP discussions. It is one important data point, but symptoms, culture data, and the broader clinical picture still matter.
Yes. Severe hypoalbuminemia (serum albumin < 1.0 g/dL) can compress the SAAG, making it falsely low even with portal hypertension. In such cases, clinical context and imaging (splenomegaly, varices) should guide diagnosis.
Commonly reviewed studies include cell count with differential, albumin, and total protein. Depending on the clinical question, clinicians may also review culture data, cytology, LDH, or tuberculosis-focused studies such as ADA.
SAAG is often interpreted alongside repeat clinical assessments, imaging, and the broader laboratory picture. This worksheet helps organize the fluid-analysis pattern, but it does not set the timing of paracentesis or follow-up on its own.