ArticlePhysiological reports2018
Amiloride resolves resistant edema and hypertension in a patient with nephrotic syndrome; a case report.
Article in Physiological reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 32 citations in OpenAlex.
- Article
- Epithelial NaComprehensive Physiology · 2024Review
- Nephrotic Syndrome: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2024Review
- Oral Furosemide and Hydrochlorothiazide/Amiloride versus Intravenous Furosemide for the Treatment of Resistant Nephrotic Syndrome.Journal of clinical medicine · 2023Article
- Albumin is an interface between blood plasma and cell membrane, and not just a sponge.Clinical kidney journal · 2022Article
- Mechanisms and management of edema in pediatric nephrotic syndrome.Pediatric nephrology (Berlin, Germany) · 2021Review
- Regulating ENaC's gate.American journal of physiology. Cell physiology · 2020Review
- New insights regarding epithelial Na+ channel regulation and its role in the kidney, immune system and vasculature.Current opinion in nephrology and hypertension · 2019Review
- ENaC blockade in proteinuria-associated extracellular fluid volume overload - effective but risky.Physiological reports · 2018Article
- Amiloride resolves resistant edema and hypertension in a patient with nephrotic syndrome; a case report.Physiological reports · 2018Article
- Nephrotic Syndrome: Oedema Formation and Its Treatment With Diuretics.Frontiers in physiology · 2018Review
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Sodium and fluid retention is a hallmark and a therapeutic challenge of the nephrotic syndrome (NS). Studies support the "overfill" theory of NS with pathophysiological proteolytic activation of the epithelial sodium channel (ENaC) which explains the common observation of suppressed renin -angiotensin system and poor therapeutic response to ACE inhibitors. Blockade of ENaC by the diuretic amiloride would be a rational intervention compared to the traditionally used loop diuretics. We describe a 38-year-old male patient with type1 diabetes who developed severe hypertension (200/140 mmHg), progressive edema (of at least 10 L), and overt proteinuria (18.5 g/24 h), despite combined administration of five antihypertensive drugs. Addition of amiloride (5 mg/day) to treatment resulted in resolution of edema, weight loss of 7 kg, reduction in blood pressure (150/100-125/81 mmHg), increased 24 h urinary sodium excretion (127-165 mmol/day), decreased eGFR (41-29 mL/min), and increased plasma potassium concentration (4.6-7.8 mmol/L). Blocking of ENaC mobilizes nephrotic edema and lowers blood pressure in NS. However, acute kidney injury and dangerous hyperkalemia is a potential risk if amiloride is added to multiple other antihypertensive medications as ACEi and spironolactone. The findings support that ENaC is active in NS and is a relevant target in adult NS patients.
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