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Published on: July 3, 2013
High altitude renal syndrome: four elements or one source?
Lei Zhang1, Erchao Feng2, Sezhen Baima2
1The First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei, Anhui Province, China.
High Altitude Renal Syndrome (HARS) is driven by High Altitude Polycythemia (HAPC). This review highlights HAPC
Area of Science:
- High Altitude Physiology
- Nephrology
- Hematology
Background:
- High Altitude Renal Syndrome (HARS) presents with polycythemia, hyperuricemia, hypertension, and albuminuria.
- Hypoxia-induced High Altitude Polycythemia (HAPC) is identified as the central etiological factor in HARS.
- Established diagnostic criteria for HAPC exist, defined by elevated hemoglobin levels at high altitudes.
Purpose of the Study:
- To review the pathophysiology of HARS, focusing on HAPC as the primary driver.
- To discuss current and emerging treatment strategies for HAPC and its renal manifestations.
- To advocate for revised diagnostic criteria and treatment prioritization for HARS.
Main Methods:
- Literature review of studies on HARS and HAPC.
- Analysis of pathological mechanisms, including HIF-2α involvement in glomerular damage.
- Evaluation of therapeutic interventions for HAPC and associated symptoms.
Main Results:
- HAPC leads to systemic hypoxia, hyperuricemia, hypertension, and glomerular injury.
- Pathological mechanisms involve HIF-2α-mediated glomerular hypertrophy and podocyte damage.
- Various treatments exist, including carbonic anhydrase inhibitors, antihypertensives, urate-lowering drugs, and experimental therapies.
Conclusions:
- HAPC is the principal cause of HARS.
- Current treatment strategies address HAPC and its downstream effects.
- Revised diagnostic criteria and treatment prioritization are recommended for HARS.
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