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Nephrol Dial Transplant (1992) 7: 896-901
© 1992 European Renal Association-European Dialysis and Transplant Association

research-article

Pseudo-Bartter's syndrome from surreptitious diuretic intake: differential diagnosis with true Bartter's syndrome

G. Colussi, G. Rombolà, C. Airaghi, M. E. De Ferrari and L. Minetti

Division of Nephrology and Dialysis Niguarda-Ca'Granda Hospital Milan, Italy

Correspondence and offprint requests to: Correspondence and offprint requests to: Dr Giacomo Colussi, Divisione di Nefrologia e Dialisi, Ospedale Niguarda-Ca'Granda, Piazza Ospedale Maggiore 3, 20162 Milan, Italy.

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 (148–186mOsm/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 diureticinduced 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. Accordingly, fractional uric acid clearance (FEUa.) was low in pseudo-Bartter's, but not Bartter's syndrome patients. Thus, tubular effects of ECF volume contraction (i.e. reduced FELi and FEUa, and renal resistance to frusemide) could be detected in pseudo-Bartter's but not in Bartter's syndrome patients. These biochemical parameters, particularly renal resistance to frusemide, may be of diagnostic value in the evaluation of normotensive, hypokalaemic metabolic alkalosis, if a direct diuretic screen is not routinely available.

Keywords: Bartter's syndrome; diuretic abuse; frusemide; hypokalaemic metabolic alkalosis


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