Hyponatremia with Persistent Elevated Urinary Fractional Uric Acid Excretion: Evidence for Proximal Tubular Injury?

Lee, S-M Kurt; Lanaspa, Miguel A.; Sánchez‐Lozada, Laura G.; Johnson, Richard J.

doi:10.1159/000447928

Cited by 7 publications

(6 citation statements)

References 25 publications

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“…In turn, we have shown in a model of diabetic nephropathy that fructokinase-mediated tubular injury is also associated with worse albuminuria and glomerular injury (22), suggesting this might represent the link between vasopressin and glomerular injury. Consistent with this cross talk, we have recently reported evidence for tubular injury in patients with chronic hyponatremia, and in these patients urinary fructose levels are elevated (24). In addition, fructose also stimulates vasopressin release (11,35), thereby leading to a positive feedback system (18).…”

Section: Discussionsupporting

confidence: 62%

Effects of exogenous desmopressin on a model of heat stress nephropathy in mice

Roncal-Jiménez

Milagres

Andrés-Hernando

et al. 2017

American Journal of Physiology-Renal Physiology

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Recurrent heat stress and dehydration have recently been shown experimentally to cause chronic kidney disease (CKD). One potential mediator may be vasopressin, acting via the type 2 vasopressin receptor (V receptor). We tested the hypothesis that desmopressin accelerates CKD in mice subjected to heat stress and recurrent dehydration. Recurrent exposure to heat with limited water availability was performed in male mice over a 5-wk period, with one group receiving desmopressin two times daily and the other group receiving vehicle. Two additional control groups were not exposed to heat or dehydration and received vehicle or desmopressin. The effects of the treatment on renal injury were assessed. Heat stress and recurrent dehydration induced functional changes (albuminuria, elevated urinary neutrophil gelatinase-associated protein), glomerular changes (mesangiolysis, matrix expansion), and tubulointerstitial changes (fibrosis, inflammation). Desmopressin also induced albuminuria, glomerular changes, and tubulointerstitial fibrosis in normal animals and also exacerbated injury in mice with heat stress nephropathy. Both heat stress and/or desmopressin were also associated with activation of the polyol pathway in the renal cortex, likely due to increased interstitial osmolarity. Our studies document both glomerular and tubulointerstitial injury and inflammation in heat stress nephropathy and may be clinically relevant to the pathogenesis of Mesoamerican nephropathy. Our data also suggest that vasopressin may play a role in the pathogenesis of the renal injury of heat stress nephropathy, likely via a V receptor-dependent pathway.

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Section: Discussionsupporting

confidence: 62%

Effects of exogenous desmopressin on a model of heat stress nephropathy in mice

Roncal-Jiménez

Milagres

Andrés-Hernando

et al. 2017

American Journal of Physiology-Renal Physiology

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“…-Finally, the association between high FE urate and enhanced sodium excretion over time may comfort previous studies that hypothesized a defect in sodium transport in the proximal tubule [4]. In this respect, Maesaka et al first suggested the increased excretion fraction of solutes exclusively transported in the proximal tubule such as lithium, urate and eventually phosphate in patients with SWS [15][16][17]. Moreover, proximal renal tubular dysfunction has recently been described in brain-damaged patients [18].…”

Section: Discussionmentioning

confidence: 75%

Salt wasting syndrome in brain trauma patients: a pathophysiologic approach using sodium balance and urinary biochemical analysis

Lannou

Carrié

Rubin³

et al. 2020

BMC Neurol

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Background: To explore the underlying mechanisms leading to the occurrence of hyponatremia and enhanced urinary sodium excretion in brain trauma patients using sodium balance and urinary biochemical analysis. Methods: We conducted a retrospective analysis of a local database prospectively collected in 60 brain trauma patients without chronic renal dysfunction. Metabolic and hemodynamic parameters were averaged over three consecutive periods over the first seven days after admission. The main outcome investigated in this study was the occurrence of at least one episode of hyponatremia. Results: Over the study period, there was a prompt decrease in sodium balance (163 ± 193 vs.-12 ± 154 mmol/day, p < 0.0001) and free water clearance (− 0.7 ± 0.7 vs.-1.8 ± 2.3 ml/min, p < 0.0001). The area under the ROC curves for sodium balance in predicting the occurrence of hyponatremia during the next period was 0.81 [95% CI: 0.64-0.97]. Variables associated with averaged urinary sodium excretion were sodium intake (R 2 = 0.26, p < 0.0001) and fractional excretion of urate (R 2 = 0.15, p = 0.009). Urinary sodium excretion was also higher in patients with sustained augmented renal clearance over the study period (318 ± 106 vs. 255 ± 135 mmol/day, p = 0.034). Conclusion: The decreased vascular volume resulting from a negative sodium balance is a major precipitating factor of hyponatremia in brain trauma patients. Predisposing factors for enhanced urinary sodium excretion were high sodium intake, high fractional excretion of urate and augmented renal clearance over the first seven days after ICU admission.

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“…Basic biochemistry parameters (including lipid profiles, fasting serum glucose, serum creatinine, serum uric acid, urinary creatinine and urinary uric acid) were analysed using a Hitachi 7600-110 Chemistry Autoanalyzer (Hitachi, Ltd., Tokyo, Japan). FEUA was calculated as the ratio of urinary uric acid in umol/L to serum uric acid in umol/L divided by the ratio of urinary creatinine in umol/L to serum creatinine in umol/L [15]. Estimated glomerular filtration rate (eGFR) was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation as shown in Table 1.…”

Section: Methodsmentioning

confidence: 99%

The Relationships of the Fractional Excretion of Uric Acid with Brachial-Ankle Pulse Wave Velocity and Ankle Brachial Index in Chinese Young Adults

Wang

Chu

et al. 2018

Kidney Blood Press Res

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Background/Aims: Elevated serum uric acid (UA) was intimately correlated with vascular stiffness and abnormal ankle brachial index (ABI) in various populations. These correlations lost significance after adjustment for estimated glomerular filtration rate (eGFR), indicating that the association of UA and brachial-ankle pulse wave velocity (baPWV) or ABI might be driven by kidney function. UA is predominantly eliminated through the kidneys, and metabolic disorders can influence the clearance of UA. In this study, we aimed to explore the putative correlation between FEUA and baPWV or ABI to determine to what extent the associations with UA were affected by renal function. Methods: This cross-sectional study enrolled 2351 participants, who underwent general health screening in Hanzhong people’s hospital from March to June of 2017. BaPWV and ABI were measured using a volume-plethysmographic apparatus (BP-203RPEII; Nihon Colin, Tokyo, Japan). FEUA was divided into quartiles: Q1:FEUA≤3.07; Q2: 3.07 9.19. Results: Lower FEUA predicted a higher prevalence of high baPWV and low ABI (p for trend <0.001). The respective ORs for high baPWV from the first to the third quartiles of FEUA were 1.777(1.323, 2.387); 1.561(1.158, 2.104); and 1.680 (1.250, 2.259). The prevalence of low ABI was greatly elevated with the decrement of FEUA [ORs for the first to third FEUA quartiles were 6.977(2.062, 23.610); 5.123(1.475, 17.790); and 2.685(0.709, 10.171), respectively]. The association of FEUA and ABI was independent of related confounding factors. However, the association between FEUA and baPWV was greatly influenced by corresponding confounders, especially gender. The efficacy of FEUA in the prediction of low ABI was stronger than that of serum UA. However, serum UA was more powerful in the prediction of high baPWV. Conclusion: Kidney function exerted a profound influence on the relationship between UA and baPWV or ABI, revealing complex interactions among cardiovascular risk factors.

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Hyponatremia with Persistent Elevated Urinary Fractional Uric Acid Excretion: Evidence for Proximal Tubular Injury?

Cited by 7 publications

References 25 publications

Effects of exogenous desmopressin on a model of heat stress nephropathy in mice

Effects of exogenous desmopressin on a model of heat stress nephropathy in mice

Salt wasting syndrome in brain trauma patients: a pathophysiologic approach using sodium balance and urinary biochemical analysis

The Relationships of the Fractional Excretion of Uric Acid with Brachial-Ankle Pulse Wave Velocity and Ankle Brachial Index in Chinese Young Adults

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