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hyporeninemic hypoaldosteronism

Naziha Chelaghma, Samson O Oyibo
A 58-year-old man presented with a 3-year history of chronic and intermittent hyperkalemia requiring recurrent attendances to the emergency department for urgent treatment. His medical history included secondary diabetes mellitus following a bout of acute pancreatitis and a previous splenectomy for a spontaneous splenic rupture. He also had a history of prolonged use of non-steroidal anti-inflammatory drugs for back pain and painful neuropathy. He was not on any medication or diet that would cause a raised serum potassium level and his renal function was normal...
2018: International Medical Case Reports Journal
Carlos Henrique Pires Ratto Tavares Bello, João Sequeira Duarte, Carlos Vasconcelos
Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible...
October 2017: Jornal Brasileiro de Nefrologia: ʹorgão Oficial de Sociedades Brasileira e Latino-Americana de Nefrologia
Jane Jackie David, Preeti Shanbag
Branchio-oto-renal (BOR) syndrome is an autosomal dominant, clinically heterogeneous disorder characterized by branchial arch anomalies, hearing impairment, and renal malformations. We report the case of a 10-year-old boy with BOR syndrome who presented with hyperkalemic hyperchloremic metabolic acidosis due to hyporeninemic hypoaldosteronism. The child also had mental retardation and spastic diplegia which have hitherto not been described in BOR syndrome.
September 2017: Saudi Journal of Kidney Diseases and Transplantation
André Gustavo P Sousa, João Victor de Sousa Cabral, William Batah El-Feghaly, Luísa Silva de Sousa, Adriana Bezerra Nunes
Patients with diabetes mellitus (DM) frequently develop electrolyte disorders, including hyperkalemia. The most important causal factor of chronic hyperkalemia in patients with diabetes is the syndrome of hyporeninemic hypoaldosteronism (HH), but other conditions may also contribute. Moreover, as hyperkalemia is related to the blockage of the renin-angiotensin-aldosterone system (RAAS) and HH is most common among patients with mild to moderate renal insufficiency due to diabetic nephropathy (DN), the proper evaluation and management of these patients is quite complex...
March 10, 2016: World Journal of Diabetes
Maryam Razzaghy-Azar, Mabel Yau, Ahmed Khattab, Maria I New
Apparent mineralocorticoid excess (AME) is a genetic disorder causing severe hypertension, hypokalemia, and hyporeninemic hypoaldosteronism owing to deficient 11 beta-hydroxysteroid dehydrogenase type-2 (11βHSD2) enzyme activity. The 11βHSD2 enzyme confers mineralocorticoid receptor specificity for aldosterone by converting cortisol to its inactive metabolite, cortisone and inactivating the cortisol-mineralocorticoid receptor complex. The 20year follow-up of a consanguineous Iranian family with three sibs affected with AME shows the successes and pitfalls of medical therapy with spironolactone...
January 2017: Journal of Steroid Biochemistry and Molecular Biology
Meta Phoojaroenchanachai, Peera Buranakitjaroen, Chanin Limwongse
A thirty-eight years old female presented with frequent proximal weakness, severe hypertension, and persistent kaliuresis despite hypokalemia. After normalized serum potassium level, hyporeninemic hypoaldosteronism was detected Pedigree study supported an autosomal dominant inherited disease. A causative mutation for Liddle's syndrome (LS) in this patient was identified to be a novel frameshift mutation. DNA sequencing resulted in exon 13 of SCNN1B gene: SCNN1B NM_000336.2:c.1 724_1730dupGGCCCAC [p.Pro5 75Argfs*17]...
October 2015: Journal of the Medical Association of Thailand, Chotmaihet Thangphaet
C Sánchez-Marcos, V Hoffman, S Prieto-González, J Hernández-Rodríguez, G Espinosa
Renal tubular acidosis (RTA) is a rare complication of renal involvement of systemic lupus erythematosus (SLE). We describe a 24-year-old male with type IV lupus nephropathy as a presenting manifestation of SLE. He presented with improvement of renal function following induction therapy with three pulses of methylprednisolone and 500 mg biweekly pulses of cyclophosphamide. However, a week after the first pulse of cyclophosphamide, the patient presented with a significant increase in legs edema and severe hyperkalemia...
March 2016: Lupus
George Liamis, Evangelos Liberopoulos, Fotios Barkas, Moses Elisaf
Diabetic patients frequently develop a constellation of electrolyte disorders. These disturbances are particularly common in decompensated diabetics, especially in the context of diabetic ketoacidosis or nonketotic hyperglycemic hyperosmolar syndrome. These patients are markedly potassium-, magnesium- and phosphate-depleted. Diabetes mellitus (DM) is linked to both hypo- and hyper-natremia reflecting the coexistence of hyperglycemia-related mechanisms, which tend to change serum sodium to opposite directions...
October 16, 2014: World Journal of Clinical Cases
Robert Krysiak, Bogusław Okopień
Hypoaldosteronism is a clinical condition resulting from inadequate stimulation of aIdosterone secretion (hyporeninemic hypoaIdosteronism), defects in adrenal synthesis of aldosterone (hyperreninemic hypoaldosteronism), or resistance to the peripheral action of this hormone (pseudohypoaldosteronism). The disease is characterized by a wide spectrum of clinical manifestations, ranging from asymptomatic hyperkalemia to life-threatening volume depletion, and, if unrecognized and untreated, it increases morbidity and mortality rates...
2012: Wiadomości Lekarskie: Organ Polskiego Towarzystwa Lekarskiego
Patricia B Mory, Marcia C dos Santos, Claudio E Kater, Regina S Moisés
Maternally-inherited diabetes with deafness (MIDD) is a rare form of monogenic diabetes that results, in most cases, from an A-to-G transition at position 3243 of mitochondrial DNA (m.3243A>G) in the mitochondrial-encoded tRNA leucine (UUA/G) gene. As the name suggests, this condition is characterized by maternally-inherited diabetes and bilateral neurosensory hearing impairment. A characteristic of mitochondrial cytopathies is the progressive multisystemic involvement with the development of more symptoms during the course of the disease...
November 2012: Arquivos Brasileiros de Endocrinologia e Metabologia
Musab Hommos, Christine Sinkey, William G Haynes, Bradley S Dixon
The role of neurohumoral factors in the sodium retention of nephrotic syndrome is controversial. We report a case with abrupt onset of severe nephrotic-range proteinuria and hypoalbuminemia due to membranous glomerulonephritis that was associated with renal salt wasting and hypovolemia without edema. Further evaluation showed hypoaldosteronism, hyporeninemia, and primary autonomic failure principally affecting the sympathetic nervous system, determined by the Valsalva maneuver. Administration of exogenous mineralocorticoid and oral salt caused edema and accelerated hypertension...
September 2012: American Journal of Kidney Diseases: the Official Journal of the National Kidney Foundation
Nicole Gröger, Helga Vitzthum, Henning Fröhlich, Marcus Krüger, Heimo Ehmke, Thomas Braun, Thomas Boettger
The human SLC4A5 gene has been identified as a hypertension susceptibility gene based on the association of single nucleotide polymorphisms with blood pressure (BP) levels and hypertension status. The biochemical basis of this association is unknown particularly since no single gene variant was linked to hypertension in humans. SLC4A5 (NBCe2, NBC4) is expressed in the collecting duct of the kidney and acts as an electrogenic ion-transporter that transports sodium and bicarbonate with a 1:2 or 1:3 stoichiometry allowing bicarbonate reabsorption with relatively minor concurrent sodium uptake...
March 1, 2012: Human Molecular Genetics
J J Kreissler, C E Langston
No abstract text is available yet for this article.
July 2011: Journal of Veterinary Internal Medicine
J Shimizu, A Inatsu, S Oshima, E Shimizu, H Hirata, H Yasuda, T Kubota
AIM: To contribute to understanding the pathogenesis of hyperkalemia that often occurs in patients with diabetes. MATERIALS AND METHODS: We describe 3 familial cases of mitochondrial diabetes mellitus. The mitochondrial A3243G point mutation was confirmed in a mother and her 2 children. We examined their clinical features and pathological findings, and assessed heteroplasmy of mutant mitochondria DNA (mtDNA) by molecular analysis. RESULTS: The second son had spontaneous hyperkalemia and hyporeninemic hypoaldosteronism...
October 2008: Clinical Nephrology
Fumi Takemoto, Yoshifumi Ubara, Shinya Kaname, Hideyuki Katori, Naoki Sawa, Junichi Hoshino, Tatsuya Suwabe, Yasushi Higa, Shohei Nakanishi, Michio Nagata, Kenichi Ohashi, Kenmei Takaichi
No abstract text is available yet for this article.
August 2008: Kidney International
I Pela, S Gasperini, E Pasquini, M A Donati
The patients affected by vitamin B12-unresponsive methylmalonic acidemia (MMA) on the long run develop chronic renal disease with interstitial nephropathy and progressive renal insufficiency. The mechanism of nephrotoxicity in vitamin B12-unresponsive MMA is not yet known. Chronic hyporeninemic hypoaldosteronism has been found in many cases of methylmalonic acidemia, hyperkalemia and renal tubular acidosis type 4. We report 2 patients affected by B12-unresponsive methylmalonic acidemia diagnosed at the age of 23 months and 5 years, respectively, with normal glomerular filtration and function...
July 2006: Clinical Nephrology
Joyce C Hollander-Rodriguez, James F Calvert
Hyperkalemia is a potentially life-threatening metabolic problem caused by inability of the kidneys to excrete potassium, impairment of the mechanisms that move potassium from the circulation into the cells, or a combination of these factors. Acute episodes of hyperkalemia commonly are triggered by the introduction of a medication affecting potassium homeostasis; illness or dehydration also can be triggers. In patients with diabetic nephropathy, hyperkalemia may be caused by the syndrome of hyporeninemic hypoaldosteronism...
January 15, 2006: American Family Physician
E Wainer, G Boner, J Rosenfeld
No abstract text is available yet for this article.
1982: Medicina
Ludwik K Malendowicz, Raffaella Spinazzi, Gastone G Nussdorfer, Marcin Trejter
Many lines of evidence have shown that preproglucagon-derived peptides affect steroid secretion from dispersed adrenocortical cells, and that streptozotocin (STZ)-induced experimental diabetes alters adrenocortical-cell function. Hence, we compared the effects of glucagon, glucagon-like peptide (GLP)-1 and GLP-2 on basal and ACTH-stimulated secretion of dispersed adrenocortical cells from normal and STZ-induced diabetic rats. We also examined the effects of exendins (EX) 3 and 4, because EX4 is known to be a potent and long-lasting agonist of GLP-1 receptors...
July 2003: International Journal of Molecular Medicine
Toru Watanabe, Koju Nitta
While hyporeninemic hypoaldosteronism (HH) has been well described in relation to chronic renal diseases, transient HH has rarely been reported. Here we present a 9-year-old boy with acute glomerulonephritis who developed hyperkalemia, which persisted for a period of 3 weeks despite normal values of creatinine clearance and an absence of acidosis. He was diagnosed as having HH because of low basal plasma renin activity and serum aldosterone level. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis...
November 2002: Pediatric Nephrology: Journal of the International Pediatric Nephrology Association
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