Transient hyporeninemic hypoaldosteronism in acute glomerulonephritis.
While hyporeninemic hypoaldosteronism (HH) has been well described in relation to chronic renal diseases, transient HH has rarely been reported. Here we present a 9-year-old boy with acute glomerulonephritis who developed hyperkalemia, which persisted for a period of 3 weeks despite normal values of creatinine clearance and an absence of acidosis. He was diagnosed as having HH because of low basal plasma renin activity and serum aldosterone level. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis. There were no apparent pathological changes in the juxtaglomerular apparatus (JGA). Rapid adrenocorticotropic hormone administration increased adequately both serum aldosterone and cortisol levels. Responses of both plasma renin activity and serum aldosterone level following the furosemide upright provocation were blunted in the hyperkalemic acute phase, but recovered in the normokalemic convalescent phase. Serum levels of human atrial natriuretic peptide were within normal range, both in the hyperkalemic and normokalemic phases. These results suggested that a transient dysfunction of the JGA, without volume expansion or structural damage of the JGA, caused HH in this patient.
Watanabe
Toru
T
Department of Pediatrics, Niigata City General Hospital, 2-6-1 Shichikuyama, Niigata 950-8739, Japan. twata@hosp.niigata.niigata.jp
Nitta
Koju
K
D000208:Acute Disease; D000324:Adrenocorticotropic Hormone; D000450:Aldosterone / Q000097:blood; D002648:Child; D004232:Diuretics; D005665:Furosemide; D005921:Glomerulonephritis / Q000097:blood* / Q000150:complications* / Q000473:pathology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D006994:Hypoaldosteronism / Q000097:blood* / Q000209:etiology*; D007668:Kidney / Q000473:pathology; D008297:Male; D012083:Renin / Q000097:blood*
D004232:Diuretics; D000450:Aldosterone; D005665:Furosemide; D000324:Adrenocorticotropic Hormone; D012083:Renin; D006854:Hydrocortisone