Fractional Excretion Of Magnesium Research Articles

Gitelman Syndrome

Gitelman Syndrome

Renal physiology in elderly persons with severe immobility syndrome

The immobility syndrome (IS) is a common condition in the elderly and consists of a reduction in the capacity to perform daily activities because of motor function deterioration. This syndrome leads to characteristic structural and physiological changes in the body, but renal physiology studies have not been conducted on this population. For this reason, we decided to study prospectively changes in renal function in these individuals. We enrolled into this study 17 volunteers over 64 years of age, all of whom lived in the same nursing home. The patients were divided into two groups: nine healthy mobile persons and eight others who suffered from severe IS. Exclusion criteria were the presence of any disease or use of any drug that could induce water and electrolytes alteration. Blood and urine samples were drawn to measure sodium, potassium, creatinine, urea, calcium, phosphorus, magnesium, and uric acid in order to obtain their fractional excretion. Plasma osmolality and vasopressin were also measured. Total body water and lean body mass were obtained by bioelectrical impedance analysis. Statistical analysis was performed applying Student's t-test (P = 0.01) and Pearson's correlation test. A significant difference in body water composition was found between the groups. Thus in the IS group plasma sodium level was slightly lower and total water content was significantly higher than in the mobile subjects: 140 +/- 5 vs. 143 +/- 1 mmol/l (P = 0.01); 61 +/- 8% vs. 50 +/- 10% (P < 0.001), respectively. Despite these differences, plasma osmolality and vasopressin values were within the normal range in both groups. However, there was a good positive correlation between these two variables in the mobile group only: R 0.9 (mobile) vs. R -0.2 (immobile). We found no significant difference in plasma creatinine or fractional excretion of sodium, potassium, calcium, phosphorus, magnesium, urea, and uric acid between the groups. Total body water content was significantly higher in the elderly who suffered from severe immobility syndrome than in healthy mobile elderly. In contrast with the mobile group, for which there was a good positive correlation between plasma osmolality and plasma vasopressin, for individuals with IS there was no correlation between plasma osmolality and plasma vasopressin.

Indication of intracellular magnesium deficiency in lactating dairy cows revealed by magnesium loading and renal fractional excretion

Nine non-pregnant, lactating dairy cows were used to study plasma and urinary magnesium concentrations ([Mg]pl; [Mg]u), and the urinary fractional excretion of magnesium (FE(Mg)) before, during and after an 120 min intravenous magnesium (Mg) administration (2.5 mg/kg body weight). Animals received a total mixed ration, and Mg content of the diet was within recommended range. Basal mean [Mg]pl, [Mg]u and FE(Mg) were 0.89 +/- 0.09 mm, 5.92 +/- 2.99 mm and 8.3 +/- 9.7% respectively. For all parameters, a substantial inter-individual variation was observed. Three cows showed suboptimal [Mg]pl and/or [Mg]u as well as low FE(Mg) values of approximately 2% indicating an insufficient Mg supply to these animals (depressed feed intake, reduced absorption of Mg). The applied Mg challenge induced no significant change of mean [Mg]pl in the cows because part of the excess Mg was excreted in the urine. But in five out of nine cows, a decrease of the FE(Mg), during and after an intravenous Mg load was observed showing that part of the infused Mg is used to replenish intracellular Mg pools. Thus, the existence of an intracellular Mg deficiency in these cows was unmasked by performing the Mg loading test only. Because a reduced free intracellular [Mg] impairs cell and tissue functions, the results highlight the importance of an accurate definition of the intracellular Mg status. The Mg loading test is a suitable procedure, however, for practical purposes less expensive and time consuming methods must be developed.

Hypovitaminosis D and secondary hyperparathyroidism in resident physicians of a general hospital in southern Brazil

To evaluate the prevalence of hypovitaminosis D and secondary hyperparathyroidism in resident physicians of a general hospital in southern Brazil and identify associated factors. Cross-sectional study. Resident physicians of Hospital de Clinicas de Porto Alegre, Porto Alegre, southern Brazil. Seventythree subjects age 26.4+/-1.9. Serum PTH, 25- hydroxyvitamin D [25(OH)D], total calcium, phosphorus, magnesium, creatinine, and alkaline phosphatase were measured. In addition calcium, creatinine, and magnesium were measured in urine. Fractional excretion of calcium and magnesium were calculated. Calcium intake was estimated by a food intake questionnaire. Mean serum levels of 25(OH)D were 17.9+/-8.0 ng/ml and 57.4% presented 25(OH)D below 20 ng/ml. Secondary hyperparathyroidism, defined as serum PTH > or =48 pg/ml and normal or low serum calcium, was identified in 39.7% of the individuals. Mean serum levels of magnesium were higher (p=0.02) and the fractional excretion of calcium was lower (p<0.001) in individuals with secondary hyperparathyroidism. Serum PTH levels were positively correlated with body mass index (r=0.33 and p=0.006) and serum magnesium levels (r=0.33 and p=0.02) and negatively correlated with serum 25(OH)D levels (r=-0.33 and p=0.008), estimated calcium intake (r=-0.25 and p=0.04), and fractional excretion of calcium (r=-0.34 and p=0.009). Vitamin D deficiency and secondary hyperparathyroidism was very common in resident physicians. Therefore, measures to prevent this situation should be recommended.

Familial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC): Compound heterozygous mutation in the claudin 16 (CLDN16) gene

BackgroundFamilial hypomagnesaemia with hypercalciuria and nephrocalcinosis (FHHNC) is an autosomal recessive disorder of renal calcium and magnesium wasting frequently complicated by progressive chronic renal failure in childhood or adolescence.MethodsA 7 year old boy was investigated following the findings of marked renal insufficiency and nephrocalcinosis in his 18-month old sister. He too was found to have extensive nephrocalcinosis with increased fractional excretion of magnesium: 12.4% (<4%) and hypercalciuria: 5.7 mmol (< 2.5/24 hours). He had renal impairment, partial distal renal tubular acidosis and defective urinary concentrating ability. Therapy with thiazide diuretics and magnesium supplements failed to halt the progression of the disorder. Both children subsequently underwent renal transplantation. Both children's parents are unaffected and there is one unaffected sibling.ResultsMutation analysis revealed 2 heterozygous mutations in the claudin 16 gene (CLDN16) in both affected siblings; one missense mutation in exon 4: C646T which results in an amino acid change Arg216Cys in the second extracellular loop of CLDN16 and loss of function of the protein and a donor splice site mutation which changes intron 4 consensus splice site from 'GT' to 'TT' resulting in decreased splice efficiency and the formation of a truncated protein with loss of 64 amino acids in the second extracellular loop.ConclusionThe mutations in CLDN16 in this kindred affect the second extra-cellular loop of claudin 16. The clinical course and molecular findings suggest complete loss of function of the protein in the 2 affected cases and highlight the case for molecular diagnosis in individuals with FHHNC.

Citraturic, alkalinizing and antioxidative effects of limeade-based regimen in nephrolithiasis patients

Potassium citrate has long been used as a prophylactic remedy for nephrolithiasis recurrence. Lemonade consumption is also suggested as an option. We compared the efficacy of consumption of solution containing manufactured lime powder with that of potassium citrate, on the improvement of metabolic risk factors, oxidative stress and renal tubular damage in nephrolithiasis patients. Patients with kidney stone were enrolled and randomly assigned to three treatment programs for 3 month period consisting of consumption of solution containing lime powder (Group 1, n=13), potassium citrate (Group 2, n=11) and lactose as placebo regimen (Group 3, n=7). Lime powder and potassium citrate contained equal amounts of potassium (21 mEq) and citrate (63 mEq). After treatment, there was an increase in urinary pH, potassium and citrate in Group 1 and 2. Increased plasma potassium and red blood cell glutathione (R-GSH) and decreased urinary malondialdehyde were found in Group 1, but not observed in Group 2. R-GSH was decreased in Group 2. Urinary N-acetyl-beta-glucosaminidase activity and fractional excretion of magnesium, as renal tubular damage indicators, were decreased only in Group 1. In Group 3, all measured parameters were unaltered except for an increased urinary chloride. In conclusion, consumption of our in-house lime powder exerted citraturic and alkalinizing actions as efficient as consumption of potassium citrate. In addition, it provided an antioxidative effect and was able to attenuate renal tubular damage. These pharmacological properties may be clinically useful to diminish the stone-forming potential in kidney stone patients and hence for preventing recurrent calculi.

Magnesium Retention in 12 to 48 Month-Old Children

Objectives: In adults, adaptation to changes in magnesium intake is largely due to changes in fractional magnesium absorption and urinary magnesium excretion. We sought to examine whether these homeostatic mechanism also occurred in young children.Methods: Children, 12–48m old were studied (n=30). They were adapted to a home diet representative of their usual magnesium intake for 7d then admitted for a stable isotope study. Children received 5mg Mg-25 intravenously, and 10mg Mg-26 orally (5mg with breakfast and 5mg with lunch). Magnesium absorption was calculated from the relative fractional excretion of the oral and intravenous isotopes in the urine samples. Endogenous fecal magnesium absorption was calculated in a subgroup from the fecal and urinary excretion of the intravenous tracer.Results: Magnesium intake (mean ± SD; 106 ± 25mg/d) was significantly greater than the Estimated Average Requirement (EAR) described by the Institute of Medicine in the US (65 mg/d, p < 0.0001). Across the range of intake studied, fractional magnesium absorption was significantly (P = 0.0383) but weakly (r2 = 0.144) related to magnesium intake. Absolute magnesium absorption (the product of fractional absorption and intake) significantly increased as intake increased (r2 = 0.566, P < 0.0001). Urinary magnesium excretion was unrelated to magnesium intake (r2 = 0.036, P = 0.31). Endogenous fecal magnesium excretion tended to increase as magnesium intake increased (r2 = 0.312, P = 0.12). Magnesium retention (absolute absorption minus urinary and fecal losses) was positive in 26 of the 30 subjects studied, and was linearly related to magnesium intake (r2 = 0.157, P = 0.0304). A magnesium intake of 52–78 mg/d would appear to be required to meet the needs for absorbed magnesium for half the children at this age range, suggesting that the current EAR is broadly appropriate.Conclusions: In young children, consuming magnesium intakes typical of the US population, fractional magnesium absorption is a major site of magnesium homeostasis, but magnesium retention increased linearly across the intake range studied. Our results support at EAR for magnesium of 55–80 mg/d and an RDA of 70–100 mg/d.

Renal Microvascular Disease in an Aging Population: A Reversible Process?

Renal microvascular disease and tubulointerstitial fibrosis are usually demonstrated in aging in humans and animals. It has recently been proposed that renal microvascular disease is the crucial determinant of tubulointerstitial disease or fibrosis. Enhanced circulating endothelial cell loss is a biomarker that reflects glomerular endothelial injury or renal microvascular disease, and fractional excretion of magnesium (FE Mg) is a sensitive biomarker that reflects an early stage of tubulointerstitial fibrosis. In aging in humans, both of these biomarkers are abnormally elevated. In addition, a glomerular endothelial dysfunction determined by altered hemodynamics associated with peritubular capillary flow reduction is substantiated. A correction of such hemodynamic alteration with vasodilators can effectively improve renal perfusion and restore renal function. Thus, anti-aging therapy can reverse the renal microvascular disease and dysfunction associated with the aging process.

Renal function in late survivors of Iranian children with cancer: Single centre experience

One of the side-effects of chemotherapy is nephrotoxicity, whose incidence rate has reportedly been higher in pediatrics. Early diagnosis of renal dysfunction may decrease the morbidity in those with partial or complete remission by avoiding nephrotoxic agents and promoting regular follow-up. We studied the frequency of renal dysfunction in pediatric patients whose therapy was completed regardless of the type of chemotherapy. Prospective cross sectional study in Hematoncology department of children's hospital. 0 One hundred and eight pediatric cancer patients (44 females, 64 males), who were at least one year off therapy, enrolled in the study from 2003 to 2005. Demographic data, mean dosages of anticancer drugs, history of other nephrotoxic agents, nephrectomy, radiotherapy and acute renal failure were recorded. Fasting blood and urine samples were collected to calculate fractional excretion of magnesium, calcium, phosphate, urine protein to urine creatinine ratio, creatinine clearance (using Schwartz formula), urine analysis, urine osmolality and blood gas analysis. T-test, Chi square and binary logistic regression were used to compare means, frequency and correlation respectively. P values Renal dysfunction was seen in 25.2% of cases. These abnormalities included hypercalciuria (7.2%), phosphaturia (13.5%), magnesuria (3.6%), glomerular filtration rate less than 90 ml/min (7.5%), metabolic acidosis (3%), metabolic alkalosis (10%), urinary concentration defect (19%), proteinuria (7.2%), glycosuria (2%), microscopic hematuria (4%), sterile pyuria (6%), and hypertension (8%). We found only Procarbazin as an independent variable of nephrotoxicity (P< 0.05). Mild to moderate tubular dysfunction has been observed in the survivors of cancer disease.

Renal magnesium wasting and tubular dysfunction in leptospirosis

Tubulo-interstitial nephritis is the main cause of acute renal injury in leptospirosis. The aim of this study was to evaluate renal tubular function and excretion of solutes in leptospirosis patients during a recent outbreak of leptospirosis in Nan province, Thailand. Clinical manifestations were recorded and routine laboratory tests were performed upon admission. Renal tubular functions including tubular reabsorption of phosphate (TRP), fractional excretion of magnesium (FE(Mg)), urinary calcium to creatinine ratio (Uca/cr), urine N-acetyl-beta-D glucosaminidase (NAG) and urine beta(2)-microglobulin were serially monitored during 2 weeks after admission. A total of 20 leptospirosis patients were recruited. Nine (45%) patients had acute renal failure (ARF). Increased urine NAG and beta(2)-microglobulin, which indicate proximal tubular dysfunction, were demonstrated in all 20 (100%) patients. Fifteen (75%) patients had hypermagnesuria, whereas 10 (50%) patients had decreased TRP. Renal magnesium (Mg) and phosphate (P) wasting caused hypomagnesaemia and hypophosphataemia in nine and three patients with ARF, respectively. These abnormal findings significantly improved within 2 weeks after admission. We conclude that renal Mg and P wasting commonly occur in patients with leptospirosis. The measurement of Mg and P levels in both serum and urine of leptospirosis patients, especially those with ARF, is therefore highly recommended.

A Biomarker for Detecting Early Tubulointerstitial Disease and Ischemia in Glomerulonephropathy

Present diagnostic tests such as serum creatinine determination and creatinine clearance are unable to reflect early tubulointerstitial disease. Because a kidney biopsy cannot be performed in every single patient, tubular epithelial function (namely, the fractional excretion of magnesium; FE Mg) that correlates directly with the degree of tubulointerstitial fibrosis would serve this purpose. FE Mg is normal in acute post-streptococcal glomerulonephritis and mesangial proliferative nephrosis with intact tubulointerstitial structure, and is abnormally elevated in nephrosis with focal segmental glomerulosclerosis (FSGS) and in chronic kidney diseases in which kidney biopsies have been obtained. FE Mg is useful in the screening of tubulointerstitial disease in patients when indication for kidney biopsy in not fulfilled, such as diabetic patients or patients with microscopic proteinuria, hematuria, and hypertension. Altered FE Mg is usually associated with a reduction in peritubular capillary flow. There is a linear correlation between FE Mg and peritubular capillary flow, which supports the chronic ischemic injury inducing altered tubular function and tubulointerstitial fibrosis.

Improvement of Renal Function in Type 2 Diabetic Nephropathy

Background. Therapeutic failure in preventing renal disease progression in type 2 diabetic nephropathy (DN) is due to a failure in the early detection of DN by microalbuminuria and the inappropriate correction of renal hemodynamic maladjustment secondary to glomerular endothelial dysfunction. Methods. Thirty patients associated with normoalbuminuric type 2 DN were subject to the following studies: tubular function by means of fractional excretion of magnesium (FE Mg), vascular function by means of determining the circulating endothelial cell, VEGF, VEGF/TGF B ratio, and intrarenal hemodynamic studies. Results. FE Mg, circulating endothelial cells, and TGF B were abnormally elevated, and VEGF/TGF B ratio was decreased in these normoalbuminuric patients. The intrarenal hemodynamic study revealed a hemodynamic maladjustment characterized by a preferential constriction at the efferent arteriole and a reduction in peritubular capillary flow. Following treatment with vasodilators, a decrease in efferent arteriolar resistance and increase in peritubular capillary flow as well as glomerular clearance were observed. Conclusion. FE Mg appears to be a more sensitive marker than microalbuminuria for the early detection of DN. Increased endothelial cell injury is reflected by enhanced circulating endothelial cell loss in conjunction with the increased TGF B and the decreased ratio between VEGF and TGF B. This is further supported by the dysfunctioning glomerular endothelium, which is characterized by hemodynamic maladjustment and a reduction in the peritubular capillary flow. A correction of such hemodynamic maladjustment by multidrug vasodilators effectively improves renal perfusion and restores renal function in type 2 DN.

The effect of intrauterine growth retardation on renal function in the first two months of life

Children born with growth retardation (GR) have a smaller nephron number and are at increased risk for the development of renal disease and hypertension in adult life. Data on the immediate post-natal development of renal function in neonates born with GR are limited and data on the effects of aminoglycosides (AGs) on renal function in these infants are lacking. This was a prospective study of 81 preterm neonates with a mean gestational age of 32.5 weeks, 40 born with GR (small for gestational age, SGA) and 41 without GR (appropriate for gestational age, AGA). The infants were classified into 4 groups. Groups A (n = 21) and B (n = 20) consisted of AGA and SGA neonates, respectively, who received AGs, and groups C (n = 20) and D (n = 20) of AGA and SGA neonates, respectively, who did not receive AG treatment. Indices of renal function were: serum creatinine (SeCr), the fractional excretion of sodium (FENa), potassium (FEK), phosphorus (FEP), magnesium and uric acid (FEUA), the urinary calcium/creatinine ratio and the transtubular potassium gradient (TTKG). No differences were observed in the parameters examined between SGA and AGA neonates who did not receive AGs. Conversely, SGA infants who received AGs after birth (group B) exhibited higher values of SeCr 2 months later. Specifically, their mean +/- SD value of SeCr (micromol/l) was 42 +/- 05 compared with 33 +/- 08 in group D, 35 +/- 04 in group A and 33 +/- 04 in group C (P < 0.01). These infants also had significantly higher values of TTKG than SGA infants without AG treatment (22 +/- 9 vs 13 +/- 3 in group D) and FEUA (60 +/- 23 vs 35 +/- 14 in group D). Their FENa and FEP were also inappropriately high despite having lower serum levels of Na and P. Preterm SGA infants who had no need of AG treatment after birth have similar renal functional maturation than AGA preterm infants at 2 months of life, but preterm SGA infants who received AGs had indications of impaired glomerular and tubular function at this age.

Tacrolimus-Associated Hypomagnesemia in Renal Transplant Recipients

Background Since hypomagnesemia occurs frequently in tacrolimus treated patients, we studied the correlation between renal magnesium wasting and tacrolimus blood levels in renal transplant patients. Methods Serum magnesium, fractional excretion of magnesium (FE Mg), and 24-hour urinary excretion of magnesium were measured in 41 transplant patients and 10 healthy volunteers for correlation with tacrolimus level. Results Of tacrolimus-treated patients, 43% displayed hypomagnesemia. FE Mg (7.42 ± 3.59% versus 1.88 ± 0.43%) and 24-hour urinary excretion (112.36 ± 51.43 mg/dL versus 6.7 ± 2.79 mg/dL) were significantly higher among tacrolimus-treated patients than controls. Magnesium replacement did not influence FE Mg or 24-hour urinary magnesium excretion. Tacrolimus level was the best predictor of 24-hour urinary magnesium excretion and FE Mg. Serum magnesium levels correlated inversely with tacrolimus concentrations and creatinine clearance. Conclusion Hypomagnesemia in renal transplant recipients results from renal magnesium wasting. Tacrolimus levels and renal function impact on the excess renal magnesium excretion. Studies of longer duration are warranted to assess the long-term effects of this early posttransplant hypomagnesemia.

Renal tubular function in children with β‐thalassemia minor

beta-thalassemia minor is a common heterozygous haemoglobinopathy that is characterized by both microcytosis and hypochromia. It requires no treatment. It has been postulated that low-grade haemolysis, tubular iron deposition and toxins derived from erythrocytes might cause renal tubular damage in adult patients with beta-thalassemia minor. Our aim was to investigate the renal tubular functions in children with beta-thalassemia minor and to determine its possible harmful effects. The study was conducted on 32 children (14 female and 18 male) at the age of 5.8 +/- 3.1 years (range 2-14 years) with beta-thalassemia minor. The patients were classified as anaemic (haemoglobin (Hb) </= 11 g/dL) (Group 1, n = 14) and non-anaemic (Hb > 11 g/dL) (Group 2, n = 18). A control group was formed with 18 healthy children whose ages and sexes match those in other groups (Group 3, n = 18). Fractional excretion of sodium (FE(Na), %), fractional excretion of magnesium (FE(Mg), %), fractional excretion of uric acid (FE(UA), %) and tubular phosphorus reabsorption (TPR,%) were calculated with standard formulas. Urinary calcium excretion (mg/kg per 24 h), zinc (Zn) (microg/dL), glucosuria (mg/dL), beta-2 microglobulin (mg/dL) and N-acetyl-beta-D-glycosaminidase (NAG, U/mmol creatinine) levels were measured through biochemical methods. There was no statistically significant difference among the three groups in terms of the results of FE(Na) (%), FE(Mg) (%), FE(UA) (%), TPR (%), calciuria (mg/kg per 24 h), NAG, urine Zn, proteinuria, glucosuria or urine beta- 2 microglobulin levels (P > 0.05). On the contrary of children with beta-thalassemia major, renal tubular dysfunction has not been determined in children with beta-thalassemia minor in the present study.

Isolated Idiopathic Hypomagnesemia Presenting as Aphasia and Seizures

Isolated hypomagnesemia of the idiopathic form is a rare condition that is known to present as generalized motor seizures in children. This report describes a 4-year-old African-American male who presented with a predominant symptom of sudden onset aphasia and no clear initial motor seizure activity. An evaluation revealed an isolated and severe hypomagnesemia (initial serum magnesium levels <1.0 mg/dL) and inappropriate renal handling of magnesium (fractional excretion of magnesium >40% under conditions of hypomagnesemia). The child had subsequent generalized tonic-clonic seizures that were brought under control with valproic acid therapy and magnesium supplementation. Six months after the diagnosis, he had regained 50-60% of his speech and had no further staring spells or motor seizure activity after the initial episode. Isolated and idiopathic hypomagnesemia caused by defective renal reabsorption of magnesium is a rare familial condition with variable inheritance. Aphasia as the solitary presenting symptom has not been described before. The exact pathophysiology of hypomagnesemic aphasia and seizures is not known but may relate to disinhibition of specific types of glutamate receptors. In the present case, neuronal depolarization may have been localized to language areas in the temporal lobes.

Hypomagnesemia associated with chemotherapy in patients treated for acute lymphoblastic leukemia: Possible mechanisms

Body weight, height and lumbar spine bone mineral density (BMD) were measured in 40 children (27 male, 13 female, aged 0.3-17.0 years) with acute lymphoblastic leukemia (ALL) at diagnosis and 6 months after initiation of chemotherapy, and in 40 age- and sex-matched local healthy children. Serum and urinary biochemical indices of mineral metabolism were measured in the children with ALL at both time points. From diagnosis to 6 months, a reduction in the fractional excretion of magnesium was found. Serum osteocalcin was low at diagnosis and increased during chemotherapy, whereas 24-h urinary type I collagen cross-linked N-telopeptide was unchanged. The Z-scores for lumbar spine BMD increased and were correlated with the serum osteocalcin at 6 months. The change in serum magnesium was correlated negatively with the change in lumbar spine BMD, and with the lumbar spine BMD Z-score at 6 months. After initiation of treatment for ALL, rapid recovery in bone formation, which results in the movement of extracellular magnesium into the skeleton through bone formation, may be an important contributor to hypomagnesemia.

Fractional excretion of electrolytes during pre- and postpartum periods in cows.

In this study, fractional excretions (Fe) of sodium (Na), potassium (K), chloride (Cl), calcium (Ca), magnesium (Mg) and phosphorus (PO4) were examined with the aim to demonstrate interactions between fractional excretions of these electrolytes within each period and relate them to electrolyte metabolism in clinically normal cows at different stages of lactation and dry period. The material of this study consisted of 20 clinically healthy Holstein-Friesian cows of the same age and milk yield. Blood and urine samples were collected on 190-200th, 240-250th and 270-280th days of pregnancy and on days 1-7th, 35-45th and 75-85th after calving, altogether 6 times. An increase was observed in FeCa and FeMg during the transition from the lactation to the dry period (p < 0.05), and a decrease in FeCa (p < 0.05), FeMg (p < 0.01) in the 2nd month of the dry period. FePO4 and FeMg, respectively, increased on levels of p < 0.01 and p < 0.05, while FeCa decreased on a level of p < 0.05 after gestation compared to the level before gestation. FeNa and FeK showed a decrease of p < 0.001 and p < 0.01, respectively, between the 1st and 2nd months of the dry period, while after gestation this value showed an increase in FeNa (p < 0.05) and FeK (p < 0.01). FeCl increased significantly (p < 0.05) only from postpartum to the 1st month of lactation. There was a strong positive correlation between FeNa and FeCl in all of the periods. It was concluded that there were significant changes in the Fe of Na, K, Cl, Ca, PO4 and Mg before parturition and during lactation; these changes could have an important role in assessing renal function and electrolyte balance.

Tubular function in patients with hypokalemia induced by sirolimus after renal transplantation

FreeText:The tubular function study included 24-hour urinary excretion of sodium, potassium, chloride, phosphorus, uric acid, magnesium, urinary pH in the first micturition in the morning, and urinary culture. Also, the presence of proteinuria, glycosuria, and aminoaciduria were measured. Urinary tubular enzymes, N-acetyl-beta-dextroglucosaminidase (NAG) and alanine aminopeptidase (AAP) were also measured. Fractional excretion of sodium, chloride and magnesium, transtubular potassium gradient (TTKG), and phosphate tubular reabsorption were calculated. Blood determinations of serum creatinine, measured creatinine clearance, plasma renin activity (PRA), aldosterone, sodium, potassium, chloride, bicarbonate, uric acid, phosphorus, and magnesium were measured. Concomitant drug: okt3 (n=1).

Fractional excretion of magnesium of chronic renal failure patients in Lagos, Nigeria

The objective of this study was to explore the usefulness of the fractional excretion of magnesium (FEMg2+) in Nigerian chronic renal failure patients (mild to moderate) in determining the severity of renal insufficiency. Plasma and twenty-four hour urine samples were analysed for magnesium and creatinine in thirty-five chronic renal failure patients and twenty-five healthy controls. The mean fractional excretion of magnesium (FEMg2+) was 15.3%(13.6) in the patients and 6.1%(2.3) in the controls and this correlated negatively with the creatinine clearance in both groups (r = -0.343, p < 0.05) in patients and (r = -0.665, p < 0.001) in controls. There was a positive correlation between plasma creatinine and fractional excretion of magnesium in the patients (r = 0.463, p < 0.05) and controls (0.455, p < 0.05). FEMg2+ may therefore be a more sensitive indicator of renal insufficiency and may also be a better indicator of the progression of renal failure.