Five patients with pseudo-Bartter's syndrome from surreptitious diuretic abuse 
were compared with six patients with true Bartter's syndrome, diagnosed as a 
normotensive, hyperreninaemic, hypokalaemic metabolic alkalosis with normal 
urine chloride excretion, low CH2O/(CH2O+CCl) ratio during maximal water 
diuresis and negative urine screen for diuretics. The latter was positive for 
frusemide in four and for hydrochlorothiazide in the remaining pseudo-Bartter's 
patients. The two groups of patients did not differ as for plasma Na+, Cl-, K+, 
HCO3-, renin, and aldosterone, while uric acid and Mg2+ were greater in 
pseudo-Bartter's patients. Daily and fasting urine Na+, Cl- and K+ excretion 
were less in pseudo-Bartter's patients; however, there was substantial overlap 
of values between the two groups. Fractional distal solute reabsorption during 
maximal water diuresis was low in the six patients with Bartter's syndrome and 
in two pseudo-Bartter's patients; thus, this parameter could not be taken as a 
specific diagnostic marker of Bartter's syndrome. Frusemide administration, 40 
mg i.v., induced a brisk increase of urine flow (11.7-21.8 ml/min), UOsm 
(148-186 mOsm/kg H2O) and FENa (14.6-24%) in Bartter's syndrome, but not 
pseudo-Bartter's patients; in all pseudo-Bartter's patients frusemide-induced 
changes of UOsm (13-97) and FENa (-0.5 to 10.2) were markedly less than in 
Bartter's syndrome patients. Frusemide resistance in pseudo-Bartter's patients 
was most probably related to diuretic-induced ECF volume contraction and 
increased proximal tubule solute reabsorption; in fact fractional lithium 
clearance (FELi, a marker of post-proximal solute delivery) was low in 
pseudo-Bartter's, but not in Bartter's syndrome patients.(ABSTRACT TRUNCATED AT 
250 WORDS)