RESUMO
A patient with profound hypokalemia satisfied the criteria for Bartter's syndrome, including hyperreninemia, aldosteronism, normal blood pressure, and hyperplasia of the juxtaglomerular apparatus. Two screening tests of urine and one of plasma for diuretic agents gave negative results. A third urinary sample gave negative results for thiazide but positive for furosemide; the fourth and fifth samples gave negative results for furosemide but positive for thiazide. Urinary prostaglandin excretion was normal. We conclude that this apparent case of Bartter's syndrome was caused by long term surreptitious diuretic ingestion and suggest this may occur more frequently than is generally appreciated.
Assuntos
Síndrome de Bartter/etiologia , Diuréticos/efeitos adversos , Hiperaldosteronismo/etiologia , Transtornos Relacionados ao Uso de Substâncias , Adulto , Síndrome de Bartter/diagnóstico , Benzotiadiazinas , Biópsia , Diagnóstico Diferencial , Diuréticos/urina , Relação Dose-Resposta a Droga , Feminino , Furosemida/efeitos adversos , Furosemida/urina , Humanos , Hiperplasia/patologia , Sistema Justaglomerular/patologia , Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos , Inibidores de Simportadores de Cloreto de Sódio/urina , Fatores de TempoRESUMO
Rats fed a low potassium diet were studied before and after KCl infusion to determine whether potassium recycling in the renal medulla accelerates potassium excretion by increasing delivery of sodium, water, and potassium to the distal tubule. Fluid samples were obtained from the end-proximal and beginning-distal tubule before and at the same sites after KCl loading by re-collection micropuncture and were compared with samples obtained from similarly fed control animals not infused with KCl. Potassium excretion increased in the KCl group from 3 to 48% but remained low in the controls. Fractional sodium and water delivery to end-proximal and beginning-distal tubule increased with time equally in both groups. Potassium reabsorption in Henle's loop fell from 75 to 58% (P less than 0.005) after KCl infusion but not significantly in the controls (from 77 to 75%). Fractional potassium delivery to the distal tubule increased from 12 to 26% (P less than 0.005) in the KCl group, which could account for over half the potassium excreted. The increase in controls from 12 to 17% was significantly less (P less than 0.02). These findings suggest that potassium recycling reduces potassium reabsorption in Henle's loop, enabling the loop to participate with the distal and collecting tubule in accelerating urinary excretion of an acute potassium load.