Multiple Metabolic Abnormalities in a Patient with the Syndrome of Inappropriate Antidiuresis

Rizos, Evangelos C.; Liamis, Georgé; Elisaf, Moses

doi:10.1159/000058416

Cited by 6 publications

(3 citation statements)

References 3 publications

(3 reference statements)

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“…Similarly, findings have been described in patients with different pathologies associated to the syndrome of inappropriate antidiuretic hormone secretion 16,35 .…”

Section: Discussionsupporting

confidence: 59%

Hyponatremia in visceral leishmaniasis

Verde

Veronese

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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SUMMARYThere are few reports linking hyponatremia and visceral leishmaniasis (kala-azar). This is a study of 55 consecutive kala-azar patients and 20 normal individuals as a control group. Hyponatremia and serum hypo-osmolality were detected in 100% of kalaazar patients. High first morning urine osmolality (750.0 ± 52.0 vs. 894.5 ± 30.0mOsm/kg H 2 O, p < 0.05), and high 24-hour urine osmolality (426.0 ± 167.0 vs. 514.6 ± 132.0 mOsm/kg H 2 O, p < 0.05) demonstrated persistent antidiuretic hormone secretion. Urinary sodium was high (82.3 ± 44.2 vs.110.3 ± 34.7 mEq/L, p < 0.05). Low seric uric acid occurred in 61.8% of patients and increased fractional urinary uric acid excretion was detected in 74.5% of them. Increased glomerular filtration rate was present in 25.4% of patients. There was no evidence of extracellular volume depletion. Normal plasma ADH levels were observed in kala-azar patients. No endocrine or renal dysfunction was detected. It is possible that most hyponatremic kala-azar patients present the syndrome of inappropriate antidiuretic hormone secretion.

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“…Similarly, findings have been described in patients with different pathologies associated to the syndrome of inappropriate antidiuretic hormone secretion 16,35 .…”

Section: Discussionsupporting

confidence: 59%

Hyponatremia in visceral leishmaniasis

Verde

Veronese

et al. 2010

Rev. Inst. Med. trop. S. Paulo

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“…24 These patients present some aspects that contribute to intensifying the hypomagnesemia and body magnesium depletion: 1) the inflammatory parasitic process at the jejunum and ileum and frequent diarrheic episodes 24 ; 2) the presence of interstitial nephritis with an inflammatory infiltrate of the renal cortex and medulla reducing the tubular reabsorption of magnesium 25 ; and 3) the volume expansion state with a reduction of the reabsorption of sodium, potassium, calcium, and magnesium at the thick ascendant loop. 25,26 Hypocalcemia is mainly caused by a reduction in the fraction of albumin bound to calcium in Kala-azar patients . Low PTH levels may be responsible for the decreased ionic calcium concentrations found in the plasma of these patients.…”

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confidence: 99%

Hormonal Disturbances in Visceral Leishmaniasis (Kala-Azar)

Verde¹,

Verde²,

Neto³

et al. 2011

The American Society of Tropical Medicine and Hygiene

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This study presents a cross-sectional analysis of the hormonal alterations of patients with visceral leishmaniasis. The diagnosis was established by the bone marrow aspiration and polymerase chain reaction test. Primary adrenal insufficiency was observed in 45.8% of patients; low aldosterone/renin plasma ratio in 69.4%; low daily urinary aldosterone excretion in 61.1%; and low transtubular potassium gradient in 68.0%. All patients had normal plasma antidiuretic hormone (ADH) concentrations, hyponatremia, and high urinary osmolality. Plasma parathyroid hormone was low in 63%; hypomagnesemia was present in 46.4%, and increased Mg++EF in 100%. Primary thyroid insufficiency was observed in 24.6%, and secondary thyroid insufficiency in 14.1%. Normal follicle-stimulating hormone plasma levels were present in 81.4%; high luteinizing hormone and low testosterone plasma levels in 58.2% of men. There are evidences of hypothalamus-pituitary-adrenal axis abnormalities, inappropriate aldosterone and ADH secretions, and presence of hypoparathyroidism, magnesium depletion, thyroid and testicular insufficiencies.

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“…However, normal plasma aldosterone level and absence of metabolic alkalosis made hyperaldosteronism unlikely. Reviewing the literature, only one case report associating SIADH with multiple electrolyte disturbances was found 4 . The authors speculated that the multiple electrolyte depletion was related to increased renal excretion as a result of relative volume expansion, but the cause of SIADH was not specified in that case report.…”

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confidence: 99%