Extreme hypomagnesemia: characteristics of 119 consecutive inpatients.

Extreme hypomagnesemia (hypoMg) can be encountered in many situations, but little data currently exist. Our aim is to describe the epidemiological, clinical, etiological characteristics, and the biological abnormalities of consecutive inpatients with extreme hypomagnesemia. In our observational monocentric study, between 1st July 2000 and April 2015, all inpatients with extreme hypomagnesemia, defined by at least one plasma magnesium concentration (PMg) below 0.3 mmol/L, were included. Demographic, clinical, biological characteristics and the drugs prescribed before the qualifying PMg measurement were retrospectively collected. 41,069 patients had at least one PMg assessment. The prevalence of extreme hypomagnesemia is 0.3% (119 inpatients). The median age is 70 years, 52% are women. The patients were mainly hospitalized in intensive care (n = 37, 31.1%), oncology (n = 21, 17.6%), gastroenterology (n = 18, 15.1%) and internal medicine (n = 16, 13.4%) departments. One hundred patients (84%) had a medical history of gastrointestinal disease (39% with bowel resections, 24% with stoma), and 50 (42%) had a cancer history. The drugs most commonly prescribed (known to induce hypoMg) are proton pump inhibitors (PPI) (n = 77, 70%), immunosuppressive regimens (n = 25, 22.5%), platinum salt-based chemotherapies (n = 19, 17.1%), and diuretics (n = 22, 19.8%). The suspected causes of hypomagnesemia are often multiple, but drugs (46%, including PPI in 19%) and chronic gastrointestinal disorders (37%) are prominent. Associated electrolyte disturbances include hypocalcemia (77%) and mild hypokalemia (51%). The 1-month mortality from all causes is 16%. Extreme hypomagnesemia is rare in inpatients, and is frequently associated with severe hypocalcemia. Digestive disorders and drugs are the main contributory causes.

Uso de las concentraciones urinarias en mg/dl en relación a los valores absolutos en 24 h para la evaluación de factores litogénicos en pacientes litiásicos / Use of urinary concentrations in mg/dl in relation to absolute values in 24-hour samples for the evaluation of lithogenic factors in stone forming patients

OBJETIVO: El objetivo de este estudio es analizar las concentraciones en orina (mg/dl) de diferentes factores litogénicos en una muestra de 24 h como predictor de estas alteraciones en lugar de valores absolutos que dependen del volumen de diuresis. MÉTODOS: Desde junio 2014 a mayo 2015 se incluyen un total de 131 pacientes, pertenecientes al Área de Gestión Sanitaria Norte de Almería, con litiasis a los que se indica estudio metabólico. Se realiza estudio de concentraciones de calcio, oxalato, úrico y citrato en orina, junto con cociente calcio/citrato. Se tiene en cuenta la clasificación de hipercalciuria (> 260 mg/24h), hiperuricosuria (> 750 mg/24 h), hiperoxaluria (> 40 mg/24h), hipocitraturia (< 320 mg/24h), hipomagnesuria (< 35 mg/24h). Análisis estadístico con SPSS 17.0. RESULTADOS: Para la concentración de calcio en orina se estima un punto de corte de 12,55 mg/dl con sensibilidad 90% y especificidad 85% con RR de 51,2 (13,9-188,4). En relación a la concentración de oxalato se estima un punto de corte de 1,86 mg/dl con sensibilidad del 91% y especificidad del 84%, con un RR estimado de 67,2 (8,3-540,6). En cuanto a la concentración de úrico en orina se estima un punto de corte de 31,2 mg/dl con una sensibilidad 85% y especificidad 70%, con un RR estimado de 12 (3,8-37,6). En cuanto al citrato, el punto de corte estimado para su concentración fue de 18,8 mg/dl con una sensibilidad y especificidad del 82% y 74% respectivamente, estimando un RR de 13,7 (4,4-42,6). El punto de corte para el magnesio fue de 2,26 mg/dl con sensibilidad 95% y especificidad 78% y RR de 67,6 (11,4-398,3). CONCLUSION: La determinación de concentraciones en orina, en lugar de valores absolutos que dependen en gran medida de la diuresis, parece ser útil a la hora de estimar alteraciones metabólicas clásicas, por lo que deben ser tenidos en cuenta en la evaluación de los pacientes con litiasis

OBJECTIVE: The aim of this study is to analyze urine concentrations (mg/dl) of different lithogenic factors in a sample of 24 h as a predictor of these changes rather than absolute values depend on the volume of diuresis. METHODS: A total of 131 patients from the North Almeria Health Management Area (Spain) with urinary stone disease in whom a metabolic study was indicated were included from June 2014 to May 2015. The concentrations of calcium, oxalate, uric acid, citrate and magnesium were measured in the urine, and the calcium/citrate ratio was calculated. The classifications used were: hypercalciuria (> 260 mg/24h), hyperuricosuria (> 750 mg/24h), hyperoxaluria (> 40 mg/24h), hypocitraturia (> 320 mg/24h) and hypomagnesuria (< 35 mg/24h). The statistical analysis was performed using SPSS 17.0. RESULTS: A cut-off point of 12.55 mg/dl, with a sensitivity of 90% and a specificity of 85% and a relative risk (RR) of 51.2 (13.9-188.4), was estimated for urinary calcium. For oxalate the cut-off point was 1.86 mg/dl, with a sensitivity of 91% and a specificity of 84% with an estimated RR of 67.2 (8.3-540.6). As regards the uric acid concentration in urine, a cut-off point of 31.2 mg/dl was estimated, with a sensitivity of 85% and a specificity of 70% and a RR of 12 (3.8-37.6). For citrate the cut-off point was 18.8 mg/dl, with a sensitivity and specificity of 82% and 74%, respectively, with a RR of 13.7 (4.4- 42.6). The cut-off point for magnesium was 2.26mg/dl with a sensitivity of 95% and specificity of 78%, with a RR of 67.6 (11.4-398.3). CONCLUSION: The determination of urine concentrations, instead of absolute values, depends to a large extent on urine output, appears to be useful when estimating classic metabolic alterations and should be taken into account in the evaluation of patients with urinary stone disease

Detection of absorptive hypercalciuria type I without the oral calcium load test.

PURPOSE: We retrospectively analyzed the validity of a simple method of detecting absorptive hypercalciuria type I, a common stone forming condition with hypercalciuria that is believed to be due to high intestinal calcium absorption. The method is based on urinary calcium derived from 24-hour urine collections while on random and restricted diets rather than on a calciuric response to an oral calcium load. MATERIALS AND METHODS: A group of 916 well characterized patients with idiopathic calcium oxalate urolithiasis comprised the study group. We also analyzed a subgroup of 695 patients, excluding 221 with dietary abuse, defined as urinary sodium greater than 150 mEq daily and/or sulfate greater than 35 mmol daily, to eliminate potential confounding dietary factors affecting the diagnosis. In each group absorptive hypercalciuria type I was detected by the old criteria, requiring an exaggerated calciuric response to an oral calcium load test, and by the new criteria, based on 24-hour urinary calcium 200 mg or greater daily while on random and restricted diets. RESULTS: Using the old criteria as the gold standard the positive and negative predictive values, sensitivity and specificity of the new criteria were 80.1%, 95.9%, 90.8% and 90.5%, respectively. When excluding patients with dietary abuse the values were 85.9%, 97.2%, 92.4% and 94.5%, respectively. CONCLUSIONS: Absorptive hypercalciuria type I may be reliably detected by a simple method based on high 24-hour urinary calcium while on random and restricted diets, especially when excluding patients with evidence of dietary abuse during the restricted diet.

Evidence for metabolic origin of absorptive hypercalciuria Type II.

The objective of this retrospective data analysis was to test the hypothesis that absorptive hypercalciuria Type II (AH-II) is a less severe variant of absorptive hypercalciuria Type I (AH-I), a common cause of calcareous stones. 24-h urinary calcium obtained on constant metabolic diets was retrieved from several data sources, including those of the authors and another group. On a low calcium diet (10 mmol calcium), 35 patients with AH-II were compared with 70 non-stone formers (NSF) and 76 patients with AH-I. On a high calcium diet (25 mmol calcium/day), 10 patients with AH-II were compared with 35 NSF and 32 with AH-I. On a low calcium diet for all participants, 24-h urinary calcium in AH-II (4.13 ± 0.63 mmol/day) was significantly higher than in NSF (3.06 ± 1.17 mmol/day), but significantly lower than in AH-I (6.11 ± 1.14 mmol/day) (p < 0.001). In a smaller subset, fractional intestinal calcium absorption in AH-II (65.0 ± 11.1%) was intermediate between NSF (50.0 ± 6.4%) and AH-I (71.0 ± 6.7%) (p < 0.001 between AH-II and other groups). On a high calcium diet, the rise in urinary calcium in AH-II was significantly higher than in NSF, but not as marked as in AH-I. Estimated calcium balance in AH-II was similar to NSF, but significantly more positive than AH-I. In conclusion, AH-II shares with AH-I the same metabolic disturbance(s) stimulating intestinal absorption and renal excretion of calcium but to a lesser degree. Bone might be spared in AH-II.

Complications of hypercalciuria.

Idiopathic hypercalciuria is a common disorder in children and can present with a range of clinical presentations such as hematuria, voiding dysfunction, flank pain, abdominal pain, nephrolithiasis, urinary tract infection and decreased bone mineral density. In the review below we provide a brief overview of calcium metabolism, types and clinical consequences of hypercalciuria and a brief approach to evaluation and management of hypercalciuria.

Diagnosis and management of hypercalciuria in children.

PURPOSE OF REVIEW: In this review, recent advances in the epidemiology, genetics, clinical associations and management of idiopathic hypercalciuria will be discussed. RECENT FINDINGS: A significant genetic contribution exists in the pathophysiology of hypercalciuria. Although several candidate genes and genetic alterations have been proposed, identification of precise gene(s) responsible remains elusive. Decreased bone density has been increasingly associated with hypercalciuria. Recent publications have suggested that bisphosphonates may play a role in the management in patients in whom both hypercalciuria and decreased bone density are present. SUMMARY: Idiopathic hypercalciuria is a common disorder in children and can present with a range of clinical presentations such as hematuria, voiding dysfunction, flank pain, abdominal pain, nephrolithiasis, urinary tract infection and decreased bone mineral density. Dietary modifications are often sufficient in the management of hypercalciuria. If the symptoms persist or a rare monogenic disorder is present, consideration should be given to medical treatment with a thiazide diuretic and/or citrate therapy.

Hypercalciuria revisited: one or many conditions?

Idiopathic hypercalciuria is a defect occurring in 5-10% of the general population and most commonly detected in patients with calcium kidney stones or osteoporosis. Although high-penetrance autosomal dominant inheritance cannot be ruled out, hypercalciuria is probably a polygenic phenomenon. Findings obtained in monogenic disorders characterized by renal calcium stones, and/or hypercalciuria, and/or nephrocalcinosis, have suggested a number of genes as candidate genes in the pathogenesis of idiopathic hypercalciuria, i.e. soluble adenylate cyclase, calcium sensing receptor, vitamin D receptor and 1-alpha hydroxylase, sodium-phosphate co-transporter-2, claudin-16, chloride channel 5, etc. All the genetic findings obtained so far do not support the idea of different types of idiopathic hypercalciuria, i.e. absorptive, renal, and resorptive. On the contrary, they support clinical observations, which suggest idiopathic hypercalciuria as a single disorder characterized by altered calcium transport in the intestine, kidney and bone, due to various different combinations of multiple genetic and dietary players.