Red blood cell sodium transport in patients with cirrhosis.

Patients with advanced cirrhosis have abnormal sodium homoeostasis. The study was undertaken to quantify the sodium transport across the plasma membrane of red blood cells (RBC) in patients with cirrhosis. RBC efflux and influx of sodium were studied in vitro with tracer (22) Na(+) according to linear kinetics in 24 patients with cirrhosis and 14 healthy controls. The sodium efflux was modified by ouabain (O), furosemide (F) and a combination of O and F (O + F). RBC sodium was significantly decreased (4·6 versus control 6·3 mmol l(-1) , P<0·001) and directly related to serum sodium (r = 0·57, P<0·05). The RBC fractional sodium efflux was higher in patients with cirrhosis (+46%, P<0·01) compared to controls. Inhibition in both high (145 mmol l(-1) )- and low (120 mmol l(-1) )-sodium buffers showed that the F-insensitive sodium efflux was twice as high in cirrhosis as in controls (P = 0·03-0·007), especially the O-sensitive, F-insensitive efflux was increased (+ 225%, P = 0·01-0·006). Fractional F-sensitive transport was normal in cirrhosis. RBC sodium influx was largely normal in cirrhosis. In conclusion, RBC sodium content is reduced in patients with cirrhosis with a direct relation to serum sodium. Increased RBC sodium efflux is especially related to ouabain-sensitive, furosemide-insensitive transport and thus most likely due to upregulated activity of the sodium-potassium pump. The study gives no evidence to an altered intracellular/extracellular sodium ratio or to a reduced fractional furosemide-sensitive sodium transport in cirrhosis.

(99m) Tc-labelled human serum albumin cannot replace (125) I-labelled human serum albumin to determine plasma volume in patients with liver disease.

BACKGROUND AND AIMS: Determination of plasma volume (PV) is important in several clinical situations. Thus, patients with liver disease often have augmented PV as part of their sodium-water retention. This study was undertaken to compare PV determination by two indicators: technetium-labelled human serum albumin ((99m) Tc-HSA) and iodine-labelled human serum albumin ((125) I-HSA), as the former may have advantages at repeated measurements and the latter is the classical gold standard. STUDY POPULATION AND METHODS: In 88 patients, (64 with liver disease, mainly cirrhosis, and 24 patients without liver disease), simultaneous measurements of PV were taken with (99m) Tc-HSA and (125) I-HSA after 1 h in the supine position. Blood samples were obtained before and 10 min after quantitative injection of the two indicators. In a subset of patients (n = 32), the measurements were repeated within 1 h. RESULTS: In all patients, a close correlation was present between PV determined by the two indicators (r = 0·89, P<0·0001). In all, but twelve patients, a higher PV was obtained with (99m) Tc-HSA compared with (125) I-HSA (P<0·0001). PV determined with (99m) Tc-HSA exceeded PV determined with (125) I-HSA by 367 ml (5·2 ml kg(-1) ) in liver patients as compared to 260 ml (3·5 ml kg(-1) ) in patients without liver disease (P<0·05). The precision of repeated PV determination was 1·75% (coefficient of variation) with (99m) Tc-HSA and 1·71% with (125) I-HSA (ns), and similar values were found in patients with and without liver disease. CONCLUSION: The study demonstrates that (99m) Tc-HSA has the same precision as that of (125) I-HSA. However, especially in patients with liver disease, (99m) Tc-HSA consistently overestimates the PV, most likely owing to indicator heterogeneity with subsequent fast removal from the circulating medium with a higher volume of distribution as the outcome.