Normokalaemic pseudohypoaldosteronism is present in children with acute pyelonephritis.

The present study demonstrates that renal tubular unresponsiveness to aldosterone, without associated hyperkalaemia, is present in children with acute pyelonephritis. We studied 32 children with a diagnosis of acute pyelonephritis established by high fever, flank pain/tenderness, increased blood levels of C-reactive protein and significant Escherichia coli growth in the urine culture. Renal tubular function tests and determinations of plasma renin activity and aldosterone concentration were performed at diagnosis (study 1), after three days of iv gentamycin (study 2) and after 21 days of antibiotic therapy (study 3). Findings were compared to those present in 32 normal children of similar age. Despite normal plasma potassium concentration, fractional potassium excretion and transtubular potassium concentration gradient were significantly decreased in studies 1 and 2, becoming normal in study 3. Decreased renal potassium excretion coexisted with increased values for plasma renin activity and aldosterone concentration. In study 3 these hormones remained elevated only in patients with scarred kidneys. The functional alteration present in acute pyelonephritis may be directly caused by the interstitial inflammation or be mediated by some E. coli endotoxin.