Hypomagnesemia in a department of internal medicine.

BACKGROUND: Hypomagnesemia is frequently encountered in hospitalized patients. The aim of this study was to determine the underlying causes of hypomagnesemia as well as the clinical and biochemical characteristics, and concomitant electrolyte and acid-base abnormalities in patients with decreased serum magnesium (Mg(2+)) levels in an internal medicine clinic. METHODS: We prospectively studied adult patients who, either on admission to our clinic or during their hospitalization, were found to have hypomagnesemia (serum Mg(2+) concentration <1.3 mEq/L). RESULTS: One hundred and seven patients out of 2284 patients had hypomagnesemia. The incidence of hypomagnesemia was 4.7%. Malnutrition, drugs (mainly diuretics and aminoglycosides), respiratory alkalosis, diabetes mellitus, acute tubular necrosis, alcohol consumption and gastrointestinal losses were the main causes of the hypomagnesemia. In the majority of patients (80%), more than one condition may have contributed to the development of hypomagnesemia. Seventy-one patients (66.3%) exhibited at least one additional electrolyte disorder. Hypophosphatemia was the most frequent electrolyte abnormality (31.1%), followed by hypokalemia (26.1%), hyponatremia (21.5%), and hypocalcemia (22%). Seventy-eight patients (72.9%) exhibited pure or mixed acid-base disorders, mainly respiratory alkalosis (20.6%), metabolic acidosis (15.8%), and mixed metabolic alkalosis and respiratory alkalosis (18.7%). CONCLUSIONS: Hypomagnesemia in patients hospitalized in an internal medicine clinic was of multifactorial origin. A wide array of concurrent acid-base and electrolyte disorders was evident in this population.

Uric acid homeostasis in the evaluation of diuretic-induced hyponatremia.

BACKGROUND: Diuretics are one of the most common causes of severe hyponatremia. The responsible pathogenetic mechanisms remain unclear. Serum uric acid concentration has been proposed as an index of differentiating between two pathophysiologic constructs of diuretic-induced hyponatremia-extracellular volume depletion and syndrome of inappropriate antidiuretic hormone secretion (SIADH)-like state-but its discriminating value has not been verified in large series of patients. Here we attempt to illuminate the pathophysiology of diuretic-induced hyponatremia by focusing on uric acid homeostasis. Additionally, we analyze the epidemiology and clinical characteristics of the disorder. METHODS: We studied prospectively 158 adult patients with hyponatremia on admission to our internal medicine clinic. Here we report on those with diuretic-induced hyponatremia. RESULTS: Forty patients (13 male and 27 female) had diuretic-induced hyponatremia, rendering it the most common cause of the disorder (25.3%). These patients had lower mean ([Na+]) (121.2 +/- 7.2 vs 126.4 +/- 4.1 mEq/L, p = .0001) than the remaining hyponatremic patients. Patients with serum uric acid levels < 4 mg/dL (n = 14) exhibited a biochemical profile consistent with a SIADH-like state, whereas patients with serum uric acid levels > or = 4 mg/d (n = 26) were consistent with extracellular volume depletion. CONCLUSIONS: Diuretics are the most common cause of community-developed hyponatremia. The serum uric acid level effectively discriminates between two biochemical profiles of diuretic-induced hyponatremia, one consistent with extracellular volume depletion and another that simulates SIADH.

Aminoglycoside-induced reversible tubular dysfunction.

Nonoliguric renal insufficiency is a well-known nephrotoxic consequence of aminoglycosides, although reversible tubular damage in the absence of any change in the renal function has been occasionally found. Reported herein are 2 representative cases of a reversible tubular damage due to prolonged aminoglycoside administration: a patient with a Fanconi-like syndrome of proximal tubular dysfunction and a patient with a syndrome of hypokalemic metabolic alkalosis associated with hypomagnesemia.

A tumor lysis-like syndrome during therapy of visceral leishmaniasis.

Reported herein for the first time in the literature is the case of a 41-yr-old woman who developed a tumor lysis-like syndrome, consisting of hyperkalemia, hyperphosphatemia, hyperuricemia, and acute renal insufficiency, soon after the initiation of chemotherapy for severe visceral leishmaniasis with liposomal amphotericin B. Allopurinol therapy, together with iv fluid administration and urine alkalization, resulted in full recovery of the metabolic abnormalities. Awareness of this condition can lead to prophylactic treatment as well as the early recognition and management of susceptible patients.

Severe hypocholesterolemia with reduced serum lipoprotein(a) in a patient with visceral leishmaniasis.

We report the case of a 36-yr-old man with visceral leishmaniasis who presented with marked hypocholesterolemia, mild hypertriglyceridemia, severely decreased serum levels of HDL-cholesterol, LDL-cholesterol, apolipoproteins AI and B, and increased serum level of apolipoprotein E. Moreover, serum Lp(a) level was markedly reduced on presentation, which is the first published report on Lp(a) levels in kala-azar. Possible mechanisms for the observed alterations of the serum lipid profile are discussed.

SIADH and hyponatremia with theophylline.

OBJECTIVE: To report a case of possible theophylline-induced hyponatremia due to the syndrome of inappropriate antidiuretic hormone (SIADH). CASE SUMMARY: An 88-year-old man developed severe symptomatic hyponatremia (serum sodium 112 mEq/L) associated with inappropriate natriuresis (urinary sodium 58 mEq/L) temporally related to the initiation of theophylline. The patient fulfilled the criteria for the diagnosis of SIADH after all other causes of hyponatremia were excluded. Furthermore, no other drugs or conditions that could have evoked SIADH were found. DISCUSSION: Theophylline has rarely been associated with hyponatremia. A thiazide-like action of the drug on the stimulation of SIADH could be the underlying mechanism for SIADH. CONCLUSIONS: Theophylline should be considered as a possible cause of hyponatremia.