High Altitude Renal Syndrome (HARS)

Aréstegui, Abdías Hurtado; Fuquay, Richard; Sirota, Jeffrey C.; Swenson, Erik R.; Schoene, Robert B.; Jefferson, J. Ashley; Chen, Wei; Yu, Xue; Kelly, Jackeline Pando; Johnson, Richard J.; Escudero, Elizabeth

doi:10.1681/asn.2010121316

Cited by 77 publications

(57 citation statements)

References 66 publications

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“…An increased filtration fraction due to a substantial reduction in renal plasma flow with relative preservation of GFR has been described both in individuals living at high altitude 73 and in children and young adults with congenital cyanotic heart disease. 74 In both circumstances, kidney biopsy samples have shown glomerulomegaly; proteinuria and decreased GFR can also develop over time, particularly in individuals with very high hematocrit levels.…”

Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

“…74 In both circumstances, kidney biopsy samples have shown glomerulomegaly; proteinuria and decreased GFR can also develop over time, particularly in individuals with very high hematocrit levels. 73,74 Therefore the terms 'high altitude renal syndrome' and 'cyanotic nephropathy' have been coined to describe these renal pathologies. 73,74 Obesity Another important condition that leads to glomerular hyperfiltration at the whole-kidney level is obesity.…”

Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

“…73,74 Therefore the terms 'high altitude renal syndrome' and 'cyanotic nephropathy' have been coined to describe these renal pathologies. 73,74 Obesity Another important condition that leads to glomerular hyperfiltration at the whole-kidney level is obesity. In an animal model, the induction of obesity was associated with significantly increased GFR and renal plasma flow.…”

Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

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Glomerular hyperfiltration: definitions, mechanisms and clinical implications

et al. 2012

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Glomerular hyperfiltration is a phenomenon that can occur in various clinical conditions including kidney disease. No single definition of glomerular hyperfiltration has been agreed upon, and the pathophysiological mechanisms, which are likely to vary with the underlying disease, are not well explored. Glomerular hyperfiltration can be caused by afferent arteriolar vasodilation as seen in patients with diabetes or after a high-protein meal, and/or by efferent arteriolar vasoconstriction owing to activation of the renin-angiotensin-aldosterone system, thus leading to glomerular hypertension. Glomerular hypertrophy and increased glomerular pressure might be both a cause and a consequence of renal injury; understanding the renal adaptations to injury is therefore important to prevent further damage. In this Review, we discuss the current concepts of glomerular hyperfiltration and the renal hemodynamic changes associated with this condition. A physiological state of glomerular hyperfiltration occurs during pregnancy and after consumption of high-protein meals. The various diseases that have been associated with glomerular hyperfiltration, either per nephron or per total kidney, include diabetes mellitus, polycystic kidney disease, secondary focal segmental glomerulosclerosis caused by a reduction in renal mass, sickle cell anemia, high altitude renal syndrome and obesity. A better understanding of the mechanisms involved in glomerular hyperfiltration could enable the development of new strategies to prevent progression of kidney disease.

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Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

Section: Glomerular Hyperfiltration In Fsgsmentioning

confidence: 99%

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Glomerular hyperfiltration: definitions, mechanisms and clinical implications

et al. 2012

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“…Although acute changes in renal pO 2 are frequently encountered in hospitalized patients and often result in AKI, not infrequently requiring renal replacement therapy, the cellular and molecular consequences of chronic or intermittent hypoxia on the kidney are less obvious. Some insights into the effects of subacute or chronic hypoxic signaling on healthy and diseased kidneys can be gained from studies of humans living at high altitude (see Arestegui for a review 22 ) and from patients with renal tumors caused by mutations in the O 2 sensing machinery, such as patients with mutations in the von Hippel-Lindau tumor suppressor that result in constitutive HIF activation. 23 In the noncancerous kidney, HIF-a stabilization is found in both acute and chronic kidney diseases.…”

Section: Therapeutic Opportunities Beyond Renal Anemiamentioning

confidence: 99%

Mechanisms of Hypoxia Responses in Renal Tissue

Haase

2013

Journal of the American Society of Nephrology

133

120

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pO 2 in the kidney is maintained at relatively stable levels by a unique and complex functional interplay between renal blood flow, GFR, O 2 consumption, and arteriovenous O 2 shunting. The fragility of this interplay makes the kidney susceptible to hypoxic injury. Cells in the kidney utilize various molecular pathways that allow them to respond and adapt to changes in renal oxygenation. This review provides an integrative perspective on the role of molecular hypoxia responses in normal kidney physiology and pathophysiology, and discusses their therapeutic potential for the treatment of renal diseases.

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“…Once oxygen is reintroduced in the tissues during reperfusion, accumulated hypoxanthine is then oxidized to uric acid; therefore, a high level of these substances is eventually released through the circulation into urine (Papezikova et al, 2006;Zhu et al, 2007;Basu et al, 2008;Sinha et al, 2009). Similarly, subjects living at high altitude frequently have hyperuricemia due to an analogous process with constant yet low levels of hypoxia (Arestegui et al, 2011). In addition, histidine metabolites increase with the introduction of hypoxia, but glutamate metabolites decrease because of hypoxia.…”

Section: Metabolic Pathways Change With Hypoxiamentioning

confidence: 99%

Effects of Acute Systematic Hypoxia on Human Urinary Metabolites Using LC-MS-Based Metabolomics

Lou

Wu²,

Liu³

2014

High Altitude Medicine & Biology

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Lou, Bih-Show, Pei-Shan Wu, Yitong Liu, and Jong-Shyan Wang. Effects of acute systematic hypoxia on human urinary metabolites using LC-MS-based metabolomics. High Alt Med Biol 15:00-00, 2014.-Aims: The metabolic variability and response to acute systematic hypoxia have been characterized by the high resolution of liquid chromatography/time-of-flight/mass spectrometry (LC-TOF/MS) in this study. Specifically, we compared the urinary metabolic profiles of six healthy sedentary men under normoxia (21% O 2 ) with acute systematic hypoxic conditions of 12% (equivalent to about 4500 m in altitude) and 15% O 2 (equivalent to about 3000 m in altitude) for 2 h in a normobaric hypoxia chamber. Results: A clear separation of dose-dependent responses was visualized by Partial Least Squares Discriminant Analysis (PLS-DA) between normoxic and hypoxic conditions. Over one thousand features were found in this study, about 10% of which showed significant change from hypoxia treatment and 26 metabolites were identified; however, there is great variability in metabolite concentrations among the 6 subjects, which reflects the diversity of human systems. Within the variability, we found that 1-methyladenosine and 5-methylthioadenosine are conspicuously upregulated; on the other hand, 3-inodoleacetic acid and L-glutamic acid were downregulated. Conclusion: The increase in purine metabolic products (uric acid, xanthine, and hypoxathine) results from hypoxia; this increase can be used as a marker for the hypoxic condition. 1-Methyladenosine was also highly upregulated from MH to SH and may be a very sensitive biomarker that reflects cellular hypoxia, due to its potential connection to HIF-1. The increase of free carnitine and acetyl carnitines, on the other hand, signals a change in the pathway of energy, or lipid, metabolism.

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High Altitude Renal Syndrome (HARS)

Cited by 77 publications

References 66 publications

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

Glomerular hyperfiltration: definitions, mechanisms and clinical implications

Mechanisms of Hypoxia Responses in Renal Tissue

Effects of Acute Systematic Hypoxia on Human Urinary Metabolites Using LC-MS-Based Metabolomics

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