Relationship between serum albumin concentration and tubular reabsorption of glucose in renal disease.

Micropuncture studies in rats and dogs have provided evidence for a cause-and-effect relationship between peritubular protein concentration and proximal tubular reabsorption (PTR). If this effect is obtained in man, hypoalbuminemia in nephrotic syndrome should lead to a fall in PTR. Sodium excretion, however, is very low in nephrotic patients; but this sodium retention may be due to distal over-reabsorption. Glucose may be used as a marker of PTR. Because of the linkage between glucose and sodium, glucose reabsorption is expected to be suppressed when PTR of sodium is suppressed. Glucose titration studies were performed in 21 patients with chronic glomerulonephritis without renal failure divided in three groups: I (six patients) with serum albumin greater than 3 g/100 ml; II (five patients) with serum albumin of 2 to 3 g/100 ml; and III (10 patients with edema and nephrotic syndrome) with serum albumin less than 2 g/100 ml. The minimum threshold for glucose decreased in nephrotic patients (group III), and its fall was related directly to hypoalbuminemia. The splay of titration curve was markedly increased in group III when compared to the titration curves of patients without nephrotic syndrome (groups I and II). The splay point was 0.78 in group I, 0.52 in group II, and 0.37 in group III. These data provide evidence that glucose reabsorption is decreased in nephrotic syndrome and are consistent with a fall in PTR in nephrotic syndrome.