Bluthochdruck und seine Folgen werden häufig von der Öffentlichkeit, Politik und den Medien unterschätzt, seine globale Bedeutung wird nicht wahrgenommen. Dabei sind bereits heute weltweit mehr als 1 Milliarde Menschen von Bluthochdruck betroffen und es sterben pro Jahr 7,5 Millionen Menschen an zu hohem Blutdruck – das entspricht 12,8 % aller weltweiten Todesfälle. Im Jahr 2025 werden bereits 1,5 Milliarden Menschen von Bluthochdruck betroffen sein. Am meisten betroffen werden mit 2 Dritteln der Patienten die ärmsten Länder der Welt sein. Bluthochdruck ist also schon lange keine Wohlstandserkrankung mehr. Auch in der Mongolei sind Erkrankungen des Herz-Kreislauf-Systems seit 1995 häufigste Todesursache. In dem bevölkerungsarmen Land sind große Entfernungen zu medizinischen Behandlungseinrichtungen ein großes Problem in der Entdeckung und Therapie der Hypertonie. Das beschriebene Projekt schildert die Situation in der Mongolei und stellt Wege vor, Menschen in ihrem direkten Umfeld zu erreichen (Arbeitsplatz, Wohnung) und dort das Screening nach Risikofaktoren sowie die Aufklärung über Vorbeugemöglichkeiten sowie Erfolgskontrollen durchzuführen. Anders als in vielen anderen Ländern ist der politische Wille zur Etablierung von Präventionsprogrammen gegeben, was sich in der Unterzeichnung eines Gesundheitsabkommens mit der Bundesrepublik mit Schwerpunkt der Prävention von Herz-Kreislauf-Erkrankungen zeigt. Hoffentlich erfolgt eine nachhaltige Umsetzung.

: A 54-year-old man with an feverish infection of the lower respiratory tract developed severe pain in the lateral and basal part of the left thorax after a severe coughing bout. A haematoma occurred at the site and it looked as though tissue evaginated at that spot on coughing and pressing. The clinical diagnosis was pneumonia and abnormal mobility of the eighth to tenth rib on the left with crepitations. The chest radiograph demonstrated fractures of these ribs and extrathoracic sickle-shaped collection of air in the left laterobasal area. Computed tomography additionally showed prolapse of pulmonary tissue on pressing. This was thus a case of "cough fracture", complicated by herniation of lung tissue. There was no evidence of incarceration of lung tissue and, as the patient was very obese, surgery was not indicated. Symptoms and signs of infection regressed on symptomatic and antibiotic treatment. The rib fractures healed as pseudoarthroses. Lung tissue prolapse on pressing was still present 3 months later.

Two days after starting withdrawal treatment for alcohol and drug abuse a 56-year-old woman developed acute renal failure. The patient was in a poor general condition and disoriented as to time and place. She had uraemic oral fetor and leg oedema. She had previously fractured both arms 3 months before.Biochemical tests indicated renal failure: creatine 1791 mumol/l, urea 51.7 mmol/l, potassium 5.3 mmol/l, phosphate 1.86 mmol/l. Serum protein electrophoresis suggested paraproteinaemia with M gradients in the gamma-fraction. Immune fixation electrophoresis demonstrated monoclonal IgM gammopathy of kappa-type (IgM 44.1 g/l). Haemoglobin level was reduced to 66 g/l. Bone marrow biopsy showed replacement of normal haematopoiesis by highly atypical plasma cells (> 30% of cell population). Magnetic resonance imaging revealed diffuse changes in the pelvis and vertebrae suggesting plasmacytoma, confirming the diagnosis of IgM plasmacytoma of kappa-type.Focal neurological symptoms (e.g. intermittent anisocoria and visual disturbances) suggested a hyperviscosity syndrome, although the serum protein level was nearly normal. Plasma viscosity was 2.2 mPas (normal range 1.2-1.38 mPas), lowered to 1.5 mPas by plasmapheresis, after which the neuropsychiatric symptoms improved. Chemotherapy for the plasmacytoma in stage IIIB was initiated (VAD scheme) and dialysis became necessary for terminal renal failure.Due to the raised level of IgM protein level and its high molecular size a hyperviscosity syndrome with paraproteinemic coma may occur, even though total plasma protein is nearly normal.

Background: It has been shown that prolonged daily peroral magnesium (Mg) administration, as tabs of Mg(OH)(2), used as the only treatment in postmenopausal osteoporosis, causes a significant increase in BMD. Objective: In order to obtain definitive evidence of causality of magnesium deficiency in the etiology of osteoporosis, we spent 1 year examining rats given a daily Mg-deficient diet (200 ppm) and compared them with rats given a Mg-adequate diet (2000 ppm). Methods: Sixteen female Sprague-Dawley rats, mean weight 110 (S.D. 23) g, were divided into two groups and randomly assigned to a semisynthetic diet that differed only in Mg content. Urine samples were collected every 3 months and blood was collected at the end of the trial. After the animals were sacrificed, the L3-L5 vertebrae and the femoral regions were examined for bone density (BMD) using dual energy X-ray absorptiometry. The femoral bones were examined for bone fragility and the tibiae by histomorphometry, and the mineral content of the bones was estimated. Results: The mean BMD of L3-L5 vertebral bone was significantly higher in group A (adequately nourished) than in the Mg-deficient group B (p=0.035, one-tail); in addition, the BMD of the femural region was significantly higher in group A (p=0.045, one-tail). The bending stiffness of the femur was slightly higher in group A than in group B; however, after correction to diminish the influence of the difference in bone dimensions between the two groups, femur rigidity (i.e., the loss of elasticity) in group B became significantly higher than that in group A (p=0.024). The force needed to break the bone was significantly higher in group A than in group B (p=0.024) and it remained higher after correction, although no longer significantly. In group B, the diminution of the trabecular bone volume, in relation to tissue volume (BV/TV), and the increase in the degree of trabecular interconnection (TBPf) clearly showed the presence of osteoporosis. On microscopy, focal osteoporosis of the metaphyseal spongious bone was observed in the bone rendered Mg-deficient. Conclusions: Because osteoporosis is characterized by lowering of BMD, increased bone fragility, and altered bone architecture, our study showed that maintaining rats for 1 year on a Mg-deficient diet gives rise to the appearance of osteoporosis.

The role of magnesium is primarily that of a cofactor in intracellular biochemical reactions, therefore, the concentration of intracellular ionized magnesium is much more physiologically relevant. The determination of the ionized magnesium (iMg(e)) in erythrocytes by ion-selective electrode for routine clinical measurements was first time investigated. Intracellular and extracellular magnesium concentration in critically ill postoperative patients and in dialyzed patients was compared with healthy individuals. Of the investigated parameters, iMge seems to be the best magnesium parameter to observe hypo- or hypermagnesemia for both groups of patients. The correlation that was found between extracellular and intracellular magnesium concentrations can be also used to evaluate the magnesium status.

The mechanisms of tubular transport of magnesium (Mg) are still not fully understood. It was presumed by recent in vivo studies that a tubular transport maximum for Mg (TmMg) possibly exists. In addition, it is not clear whether Mg homeostasis is achieved by intrarenal mechanisms or if extrarenal factors are essential in this connection. In order to clarify the conflicting in vivo data, isolated rat kidneys were perfused with a medium containing increasing concentrations of Mg (0.25- to 2-fold of the normal Mg concentration). When Mg in the perfusate was raised linearly, the corresponding urine concentrations showed the typical behavior for a substance with a Tm. In the subnormal level, the urine concentrations run in parallel to the concentrations in perfusate; above this level, urine concentrations increased disproportionally. Other renal functional parameters such as the perfusion flow, glomerular filtration, oxygen consumption or albumin excretion remained unchanged after the addition of Mg to the perfusate. These data suggest that there is a TmMg. The renal Mg threshold concentration seems to be near the normal Mg plasma concentration.

Primary hyperoxaluria type 1 (PH1) is caused by deficiency of peroxisomal alanine-glyoxylate aminotransferase which is in humans exclusively expressed in liver cells. The disease is inherited as an autosomal recessive trait, and initial symptoms usually occur in early childhood. Up to the age of 25 years, 90% of the patients are symptomatic, and many patients develop end-stage renal failure. Pronounced medical care is necessary in PH1 patients to prevent generalized oxalosis with complications due to bone disease and peripheral gangrene. The rather short survival of patients on hemodialysis is caused by sudden arrhythmias and heart block. As no dialysis procedure is able to remove the daily produced oxalate, early transplantation is mandatory. Our 45-year-old patient is remarkable on the basis of the late manifestations of PH1. The diagnosis was delayed by unspecific symptoms of nephrolithiasis with recurrent pyelonephritis. Clinical course and diagnostic cornerstones of primary hyperoxaluria are outlined. The principles of conservative treatment and experiences with dialysis and transplantation are discussed.

In 1980, the relationship between diabetes mellitus and low serum magnesium levels was reported for the first time in this journal. Today, there is an increasing body of experimental and clinical data covering this topic. In addition, there are epidemiological data showing the negative impact of serum magnesium values in the lower range of the reference interval upon e.g. atherosclerosis and osteoporosis. And there are experimental data giving evidence to the hypothesis that magnesium supplementation may protect from diabetes late complications. The paper will review the aforementioned informations and will present original data obtained from diabetic inpatients with a bad metabolic control. Our findings confirm that there is hypomagnesemia in diabetics, but we have found magnesium deficiency, too. This may be related not only to the insufficient magnesium intake, but also to an inadaequate hypermagnesuria, which significantly was related to urinary osmolality and glucosuria. Based on the given findings, the authors recommend an oral magnesium supplementation in all diabetics with an underoptimal metabolic control, even in case of low normal serum magnesium values.

The cardiovascular risk increases with decreasing serum levels of magnesium, and this already at concentrations within the previous reference range (0.70-1.10 mmol/L). For this reason, the Society for Magnesium Research has updated its 1986 recommendations for the diagnosis of magnesium deficiency. The diagnosis is based on the patient's history, his clinical symptoms, and the results of clinical-chemical investigations of plasma/serum and urine. Further diagnostic methods used include the determination of ionized serum magnesium and the magnesium retention test. The optimal serum magnesium concentration is > 0.80 mmol/L.

Background: There is experimental and clinical evidence giving importance to the relationship between magnesium (Mg) and diabetes mellitus. The American Diabetes Society suggested that attention be given to the diagnostic significance of a Mg deficiency in diabetes mellitus. Because of regional differences in Mg supply, we studied Mg status in the surroundings of Lubeck in healthy persons as compared to diabetics. Patients and methods: 27 healthy controls (C) and 27 inpatients with an insulin-dependent diabetes mellitus (DM) and bad metabolic control were studied, Mg++ was measured by atomic absorption spectroscopy (Video 12 apparatus) in serum and erythrocytes; basic 24-hour urinary Mg excretion (b-Mg-u), fractional Mg excretion (f-Mg-u) were calculated. In addition the Mg loading test (Mg-lt) was applied. Results: In diabetics a hypomagnesemia was observed as compared to healthy subjects both in serum (0.73 +/- 0.04 vs 0.83 +/- 0.04 mmol/l, means +/- SD, p < 0.05) and in red blood cells (1.43 +/- 0.16 vs 1.84 +/- 0.10 mmol/l) (p < 0.01). The b-Mg-u was 2.75 +/- 3.62 mmol/d in DM as compared to 5.84 +/- 2.21 mmol/d in controls (p < 0.05); f-Mg-u was 5.83 +/- 2.73% in DM and 3.46 +/- 1.33% in controls. The percent retention of the given Mg load was 24.5 +/- 18 in DM and -41 +/- 12 in controls (p < 0.001). Discussion: In DM with bad metabolic control there is convincing evidence of a Mg-deficiency. Higher f-Mg-u in case of lower S-Mg in diabetics indicate an inadequate renal Mg loss which significantly correlates with the amount of glucosuria as one of the relevant pathophysiological mechanisms.

The concentration of magnesium was determined in plasma, cytosol (lymphocytes) and cell membrane (erythrocytes) of 15 control persons with normal renal function and of 12 patients with a renal insufficiency due to chronic glomerulonephritis (serum creatinine 2.5 +/- 0.8 mg%, mean +/- SD). Plasma magnesium concentrations were measured by atomic absorption spectroscopy, free magnesium of the cytosol was determined by photometry using the fluorescence indicator mag-fura-2. Membrane magnesium was measured by atomic absorption spectroscopy, too, and was referred to the membrane protein content, that was measured according to Bradford's method. Plasma magnesium concentration was 0.91 +/- 0.08 mmol/l in controls versus 0.95 +/- 0.09 mmol/l in renal insufficient patients. Free intracellular magnesium content was 2.38 +/- 0.75 mmol/l in healthy persons and 2.61 +/- 0.35 mmol/l in patients, membrane magnesium concentrations were found significantly higher in renal insufficient patients as compared to the control persons (2.85 +/- 0.62 versus 0.53 +/- 0.22 mmol/g membrane protein, mean +/- SD, p < 0.01). These results show that cell membranes are of special importance in renal insufficiency to avoid a magnesium overload of the cytosol and to keep constant the intracellular concentration of free magnesium. In addition, cell membrane magnesium content is a better tool to discover alterations in the magnesium status than measurements of serum or intracellular free magnesium concentrations.