Antinatriuretic phenomena seen in children with acute pyelonephritis may be related to the activation of intrarenal RAAS

Abstract

We investigated whether antinatriuretic phenomena [decreases in urinary sodium (uNa) and fractional excretion of sodium (FENa)] seen in children with acute pyelonephritis (APN) are associated with the renin–angiotensin–aldosterone system (RAAS).We examined 114 children experiencing their first episode of febrile urinary tract infection (fUTI) consecutively admitted to our hospital from July 2012 to June 2014. Blood tests [C-reactive protein, white blood cell count, erythrocyte sedimentation rate, and aldosterone (Aldo)] and urine tests [uNa, urine potassium (uK) and FENa] were performed upon admission. All enrolled children underwent a 99m-dimercaptosuccinic acid renal scanning (DMSA) at admission. Areas with cortical defects (AreaCD) and uptake counts (UptakeCD) on their DMSA scans were calculated. Data were compared between children with positive DMSA results (APN), lower urinary tract infection (L-UTI), and controls; and between children with high and low Aldo levels.uNa, uNa/K, and FENa negatively correlated with AreaCD%, UptakeCD, and Aldo; were significantly lower in APN patients than in LUTIs and controls regardless of Aldo level; were lower in the high Aldo group than in the low Aldo group. However, there is no difference in AreaCD% and UptakeCD between APN children with the high and low Aldo level.Decreases in uNa, uNa/K, and FENa in children with APN may result from an antinatriuretic effect of RAAS and be related to the activation of the intrarenal RAAS.

Association of Electrolyte Changes and Inflammatory Markers with Renal Involvement in Children with Febrile UTI

“…The first mechanism is secondary pseudohypoaldosteronism as a result of pyelonephritis. This results in the inability of tubules to respond to aldosterone due to severe tubular inflammation and a high intrarenal pressure (8,13,14). Second increased secretion of ADH may be induced by inflammatory cytokines such as IL-18, IL-6, and TNF-α as was proposed by Watanabe et al and Shin et al (15,16).…”

<p>COVID’s Razor: RAS Imbalance, the Common Denominator Across Disparate, Unexpected Aspects of COVID-19</p>

“…Circulating pressure/volume regulation within the vascular system is not the only function of RAS. 29 After much debate, 30,31 there is now widespread agreement that local tissue-level RAS systems administer paracrine and autocrine effects in various structures including adipose tissue, the pancreas, vascular walls, and the heart, kidneys, and brain. 19,32 Evidence suggests that locally produced RAS components affect physiology independently of blood pressure.…”

“…96 Kidneys locally express all ACE axis components. 29,106 Additionally, the renal glomeruli filter most circulating RAS proteins, which are then reabsorbed by the proximal tubule. 106 Combined resorption and local production result in renal AII levels 100 to 1000 times higher than in plasma.…”

“…106 Combined resorption and local production result in renal AII levels 100 to 1000 times higher than in plasma. 29,106 Dysregulated tissue RAS, as occurs in hypertension, results in significant renal inflammatory damage, with progressive destruction of nephrons amid RASmediated remodeling and fibrosis. 49 Similarly, the heart has significant local RAS, which mediates inflammatory remodeling in conditions such as hypertension and infarction.…”

Reconsideration of urine culture for the diagnosis of acute pyelonephritis in children: a new challenging method for diagnosing acute pyelonephritis

“…Therefore, the former would be a better choice for discriminating APN. CRP is positively correlated with the area of cortical defects on their DMSA results [9]. Procalcitonin is more sensitive for detecting APN and renal scarring than CRP but is expensive; in practice, the combination of CRP, ESR, and WBC is not worse than procalcitonin [10].…”