Single nephron study of intrarenal urea handling in experimental pyelonephritis

Armsen, T.; Joppich, R.; Schubert, G; Edel, H. H.

doi:10.1007/bf01854840

Cited by 5 publications

(2 citation statements)

References 16 publications

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“…Fractional urea excretion, tubular urea reabsorption, and the urine-to-plasma ratio for osmolality, all indicators of tubular function in this study, decreased after LPS injection, indicating renal tubular damage consistent with the findings of previous studies (4,21,25). Notably, it has been shown in our and other investigations that LPS administration led to a fourfold decrease in both urea concentration and osmolality in the renal IM, indicating that urea may be crucial for the production of a hyperosmolar medullary interstitium (21, 25).…”

Section: Discussionsupporting

confidence: 92%

Cytokine-mediated regulation of urea transporters during experimental endotoxemia

Schmidt¹,

Höcherl²,

Bucher³

2007

American Journal of Physiology-Renal Physiology

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Acute renal failure (ARF) is a frequent complication of sepsis and has a high mortality. Sepsis-induced ARF is known to be associated with significant impairment of tubular capacity. However, the pathogenesis of endotoxemic tubular dysfunction with failure of urine concentration is poorly understood. Urea plays an important role in the urinary concentrating mechanism and expression of the urea transporters UT-A1, UT-A2, UT-A3, UT-A4, and UT-B is essential for tubular urea reabsorption. The present study attempts to assess the regulation of renal urea transporters during severe inflammation in vivo. Lipopolysaccharide-(LPS)-injected mice presented with reduced glomerular filtration rate, fractional urea excretion, and inner medulla osmolality associated with a marked decrease in expression of all renal urea transporters. Similar alterations were observed after application of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, interferon (IFN)-gamma, or IL-6. LPS-induced downregulation of urea transporters was not affected in knockout mice with deficient TNF-alpha, IL-receptor-1, IFN-gamma, or IL-6. Glucocorticoid treatment inhibited LPS-induced increases of tissue TNF-alpha, IL-1beta, IFN-gamma, or IL-6 concentration, diminished LPS-induced renal dysfunction, and attenuated the downregulation of renal urea transporters. Renal ischemia induced by renal artery clipping did not influence the expression of urea transporters. Our data demonstrate that renal urea transporters are downregulated by severe inflammation, which likely accounts for tubular dysfunction. Furthermore, they suggest that the downregulation of renal urea transporters during LPS-induced ARF is mediated by proinflammatory cytokines and is independent from renal ischemia because of sepsis-induced hypotension.

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Section: Discussionsupporting

confidence: 92%

Cytokine-mediated regulation of urea transporters during experimental endotoxemia

Schmidt¹,

Höcherl²,

Bucher³

2007

American Journal of Physiology-Renal Physiology

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“…A decrease in interstitial osmolality of renal medullary tissue may contribute to the impaired water reabsorption. A decrease in solute and urea concentration in the renal medulla, diminished corticopapillary concentration gradients, and inhibited urea recycling have been demonstrated in animals with acute and chronic pyelonephritis [23,25,26]. The dilution of interstitial solutes may be a result of increased renal blood flow in response to inflammation.…”

Section: Discussionmentioning

confidence: 99%

Urinary aquaporin-2 in children with acute pyelonephritis

Rodionova

et al. 2005

Pediatr Nephrol

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Children with acute pyelonephritis develop polyuria and have reduced maximum urinary concentration capacity. We studied whether these abnormalities are associated with altered urinary excretion of the water channel aquaporin-2 (AQP2) in the renal collecting duct. AQP2 is the main target for antidiuretic action of arginine vasopressin (AVP), and the urinary excretion of this protein is believed to be an index of AVP signaling activity in the kidney. Children with acute pyelonephritis, aged 5-14 years, were examined for urinary flow rate, creatinine clearance, unchallenged urine osmolality, and urinary ion excretion. Urinary excretion of AQP2 was measured by dot immunoblotting technique. Studies were performed in the acute phase of pyelonephritis, in the same children after treatment, and in control patients. At the onset of pyelonephritis, urinary flow rate and solute excretion were increased, but the urinary osmolality was unchanged. The urinary level and urinary excretion of AQP2 was increased in acute pyelonephritis and decreased after treatment. Excretion of aquaporin-3 was unchanged, suggesting that the increase in AQP2 urinary excretion was not due to a shedding of collecting duct cells. The results suggest that a mechanism proximal to the collecting duct may be responsible for the polyuria observed in children with acute pyelonephritis. Increased urinary AQP2 levels suggest that a compensatory activation of apical plasma membrane targeting of AQP2 may occur in pyelonephritis.

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Renal Transport of Urea

Roch-Ramel¹,

Peters

1981

Proceedings in Life Sciences

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Single nephron study of intrarenal urea handling in experimental pyelonephritis

Cited by 5 publications

References 16 publications

Cytokine-mediated regulation of urea transporters during experimental endotoxemia

Cytokine-mediated regulation of urea transporters during experimental endotoxemia

Urinary aquaporin-2 in children with acute pyelonephritis

Renal Transport of Urea

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