Transient hyporeninemic hypoaldosteronism in acute glomerulonephritis

Abstract

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.

Hypothesis: A simple algorithm to distinguish between hypoaldosteronism and renal aldosterone resistance in patients with persistent hyperkalemia

“… HA.14 reports, 33 patients, plus an unreported case of our own 8–21 . Twenty‐two of these patients had associated renal impairment and two also had PHA.…”

A Case of Hyporeninemic Hypoaldosteronism in the Dog

“…The magnitude of proteinuria in this dog was substantial and the proteinuria was thought to be glomerular 19 . Proteinuria may have been an indication of functional or structural damage to the JGA 5,20 . Kidney biopsy specimens may have provided useful diagnostic information, but the owner declined renal biopsy specimens because of the risk of complications of percutaneous renal biopsy in small dogs, and postmortem samples were not made available 21 .…”

“…Kidney biopsy specimens may have provided useful diagnostic information, but the owner declined renal biopsy specimens because of the risk of complications of percutaneous renal biopsy in small dogs, and postmortem samples were not made available 21 . HH associated with functional or structural damage to the JGA has been reported in humans with diseases such as lupus nephritis, 22 amyloidosis, 23 monoclonal gammopathy, 24 and acute glomerulonephritis 20,25 . Reports of treatment of HH with concurrent proteinuria showed improvement or resolution with therapy targeted at the primary etiology.…”

“…19 Proteinuria may have been an indication of functional or structural damage to the JGA. 5,20 Kidney biopsy specimens may have provided useful diagnostic information, but the owner declined renal biopsy specimens because of the risk of complications of percutaneous renal biopsy in small dogs, and postmortem samples were not made available. 21 HH associated with functional or structural damage to the JGA has been reported in humans with diseases such as lupus nephritis, 22 amyloidosis, 23 monoclonal gammopathy, 24 and acute glomerulonephritis.…”

“…21 HH associated with functional or structural damage to the JGA has been reported in humans with diseases such as lupus nephritis, 22 amyloidosis, 23 monoclonal gammopathy, 24 and acute glomerulonephritis. 20,25 Reports of treatment of HH with concurrent proteinuria showed improvement or resolution with therapy targeted at the primary etiology.…”