Two cases of transient pseudohypoaldosteronism due to group B streptococcus pyelonephritis.
Department of Pediatrics and Developmental Biology, Tokyo Medical and Dental University, 1-5-45, Bunkyo-ku, Yushima, Tokyo, 103-0034, Japan.Pediatric Nephrology (Impact Factor: 2.94). 10/2008; 23(9):1569-70. DOI:10.1007/s00467-008-0843-9
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ABSTRACT: Obstructive uropathy causes tubular resistance to aldosterone and severe metabolic imbalance may be precipitated by an episode of pyelonephritis. In the last 3 years we investigated 52 episodes of pyelonephritis (positive urine culture, elevated C reactive protein, fever, elevated neutrophil count) in 50 children between 15 days and 15 months of age. Ultrasonography voiding cystography and renal scintiscan were performed in all cases and i.v. urography in some. A salt-losing syndrome with hyponatremia and hyperkalemia (Na < 125 meq/liter; K > 6.3 meq/liter) was observed in 17 infants < 3 months, accompanied by plasma aldosterone concentration of 5000 to 23,000 pg/ml (normal value, < 1000 pg/ml). All these children had a severe urinary tract (UT) malformation (ureteropelvic junction stenosis in 7 cases, vesicoureteral reflux in 7, posterior urethral valves in 2, double system in 1). Thirteen infants < 3 months, 7 with no urinary tract malformations, did not have electrolyte imbalance. Pyelonephritis was diagnosed in 20 other patients ages 4 to 15 months, including 16 with severe UT malformations; 4 had normal UTs. We conclude that a salt-losing syndrome with tubular resistance to aldosterone can occur during pyelonephritis in young infants with congenital UT malformation, that the risk diminishes considerably or disappears after 3 months of age and that in the absence of UT malformation pyelonephritis does not cause acute sodium loss of clinical relevance.The Pediatric Infectious Disease Journal 01/1995; 14(1):56-9. · 3.57 Impact Factor
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ABSTRACT: A syndrome of renal tubular resistance to aldosterone has been identified in infants with obstructive uropathy and urinary tract infection. Six infants (ages 9 days to 7 months) were seen with fever, vomiting, polyuria, dehydration, or failure to thrive. Urine cultures were positive for Escherichia coli. Radiologic studies demonstrated bilateral ureterohydronephrosis (four patients), left ureteral duplication with upper pole hydronephrosis (one), and left vesicoureteral reflux (one). The infants had hyponatremia, hyperkalemia, and metabolic acidosis. Plasma aldosterone concentration was markedly elevated, and plasma renin activity was similar to or higher than that reported in normal infants of comparable age. Fractional excretion of potassium was not significantly different from control values, both in absolute terms or when related to glomerular filtration rate, but fractional sodium excretion was significantly increased. The UK/UNa ratio was significantly lower in the patients. After medical or surgical therapy (when appropriate), all blood and urine determinations returned to normal, except for UK/UNa values, which although higher, remained significantly diminished. Our data indicate that a hyperkalemic salt-losing state can arise in infants with obstructive uropathy and urinary tract infection as a consequence of tubular unresponsiveness to aldosterone, and that the clinician should rule out such cause before establishing the diagnosis of primary pseudohypoaldosteronism.Journal of Pediatrics 10/1983; 103(3):375-80. · 4.04 Impact Factor
- Pediatric Nephrology 06/2003; 18(5):486. · 2.94 Impact Factor
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