RESUMO
A patient with Bartter's syndrome manifested hypomagnesemia in addition to hypokalemia. Under conditions of maximal free water production, he had a fractional distal solute reabsorption of 0.65, a value consistent with a renal defect in sodium chloride reabsorption in the thick ascending limb of the loop of Henle. This is also the site of 65% to 70% of urinary magnesium reabsorption. With magnesium supplementation and amiloride, the urinary potassium decreased and the serum potassium increased. Atrial natriuretic peptide concentrations in the plasma were low. Evaluation of family members showed five of nine offspring had hypokalemia with no disorder in the parents, an apparent autosomal recessive mode of inheritance. This is a US government work. There are no restrictions on its use.
Assuntos
Síndrome de Bartter/complicações , Hipopotassemia/etiologia , Deficiência de Magnésio/complicações , Adulto , Síndrome de Bartter/genética , Genes Recessivos , Humanos , Hipopotassemia/genética , Túbulos Renais/fisiopatologia , Masculino , LinhagemRESUMO
Type II pseudohypoaldosteronism is an uncommonly reported disorder. The authors recently evaluated a patient who in many respects appeared to have this syndrome. He had hyperkalemia, a normal glomerular filtration rate, "normal" serum and urinary aldosterone levels, and low plasma renin activity. In addition, he had a hyperchloremic metabolic acidosis and hypertension. Fractional excretion of potassium was reduced in response to sodium chloride loading. However, renal potassium excretion in response to administration of sodium sulfate was normal. Thiazide diuretic restored the serum potassium, the low bicarbonate, and blood pressure to normal. He developed marked natriuresis and kaliuresis in response to high-dose exogenous mineralocorticoid. The magnitude of the kaliuretic response achieved to exogenous mineralocorticoid has been reported only once previously.
Assuntos
Aldosterona/deficiência , Mineralocorticoides/farmacologia , Potássio/urina , Acidose/complicações , Adulto , Benzotiadiazinas , Desoxicorticosterona/farmacologia , Diuréticos , Humanos , Hiperpotassemia/complicações , Hipertensão/complicações , Hipertensão/tratamento farmacológico , Masculino , Renina/sangue , Sistema Renina-Angiotensina , Inibidores de Simportadores de Cloreto de Sódio/uso terapêuticoRESUMO
Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
Assuntos
Distúrbio Mineral e Ósseo na Doença Renal Crônica , Alumínio/efeitos adversos , Osso e Ossos/anatomia & histologia , Osso e Ossos/patologia , Calcitriol/uso terapêutico , Cálcio/metabolismo , Cálcio da Dieta/administração & dosagem , Distúrbio Mineral e Ósseo na Doença Renal Crônica/etiologia , Distúrbio Mineral e Ósseo na Doença Renal Crônica/metabolismo , Distúrbio Mineral e Ósseo na Doença Renal Crônica/terapia , Humanos , Falência Renal Crônica/metabolismo , Osteíte Fibrosa Cística/etiologia , Osteíte Fibrosa Cística/patologia , Osteomalacia/etiologia , Osteomalacia/patologia , Osteomalacia/terapia , Hormônio Paratireóideo/metabolismo , Fósforo/metabolismo , Diálise Renal , Vitamina D/metabolismoRESUMO
Histologic bone changes of osteitis fibrosa and osteomalacia are commonly present in patients with end-stage renal disease. Although many patients are not symptomatic from these bone changes, some patients are severely disabled. Altered metabolism of vitamin D, calcium, phosphorus, and parathyroid hormone occurs in renal failure and contributes to the development of uremic bone disease. This article reviews the current theories of pathogenesis and treatment of renal osteodystrophy. In addition, the clinical presentation, pathogenesis, and treatment of the various aluminum-associated osteomalacic syndromes in uremia are discussed.
Assuntos
Distúrbio Mineral e Ósseo na Doença Renal Crônica , Alumínio/efeitos adversos , Osso e Ossos/anatomia & histologia , Osso e Ossos/patologia , Calcitriol/uso terapêutico , Cálcio/metabolismo , Cálcio da Dieta/administração & dosagem , Distúrbio Mineral e Ósseo na Doença Renal Crônica/etiologia , Distúrbio Mineral e Ósseo na Doença Renal Crônica/metabolismo , Distúrbio Mineral e Ósseo na Doença Renal Crônica/terapia , Humanos , Falência Renal Crônica/metabolismo , Osteíte Fibrosa Cística/etiologia , Osteíte Fibrosa Cística/patologia , Osteomalacia/etiologia , Osteomalacia/patologia , Osteomalacia/terapia , Hormônio Paratireóideo/metabolismo , Fósforo/metabolismo , Diálise Renal , Vitamina D/metabolismoRESUMO
Two patients developed acute interstitial nephritis (AIN) following treatment with mezlocillin sodium. Diagnosis was made by renal biopsy. Gallium 67 citrate scanning was abnormal in both. All patients were receiving multiple-drug therapy, but AIN has either not been described with the other drugs, or the temporal relationship between the AIN and termination of other drug therapy makes a causative relationship unlikely. All were infected with Pseudomonas aeruginosa. A role for the infecting organism or drug synergism in contributing to the renal disease cannot be excluded.