Influence of weather conditions, drugs and comorbidities on serum Na and Cl in 13000 hospital admissions: evidence for a subpopulation susceptible for SIADH.

OBJECTIVES: Considerable variation in serum sodium (Na) and chloride (Cl) is found in patients at hospital admission. Our goal was to quantify the respective impact of drugs, comorbidities, demographic factors and weather conditions on serum Na and Cl. DESIGN AND METHODS: For 13277 consecutive patients without terminal kidney disease admitted to the Department of Internal Medicine of the Kantonsspital St. Gallen drug history on admission, age, sex, body weight, ICD-10 diagnoses, and laboratory data were extracted from electronic medical records. Weather parameters prior to hospital admission were also integrated in a multivariate regression analysis. RESULTS: Both serum Na and Cl showed an asymmetric left-tailed distribution. Median (interquartile range) Na was 138 (136/140) and Cl 104 (101/106). The distribution of sodium in patients with one or more risk factors for SIADH was best explained by the presence of two populations: one population with a similar distribution as the unexposed patients and a smaller population (about 25%) shifted to lower sodium levels. Lower weight, lower blood pressure, kidney dysfunction, fever, and diabetes were associated with both lower Na and Cl. Higher ambient temperature and higher air humidity preceding admission were associated with both higher Na and Cl values. CONCLUSIONS: Na and Cl at hospital admission are highly influenced by ambient weather conditions, comorbidities and medication. The bimodal distribution of Na and Cl in persons exposed to risk factors for SIADH suggests that SIADH may only affect a genetically distinct vulnerable subpopulation.

Ramipril prevents extracellular matrix accumulation in cerebral microvessels.

OBJECTIVES: The stroke-prone spontaneously hypertensive rat is a genetic model of severe hypertension with secondary vascular alterations. The aim of this study was to determine the influence of chronic hypertension and ramipril treatment on the extracellular matrix in the cerebral microvasculature. METHODS: The study consisted of three groups: six normotensive Wistar rats, six untreated spontaneously hypertensive rats, and six hypertensive rats treated with an antihypertensive dose of ramipril (1 mg kg(-1)day(-1)) for 6 months. Alterations in the extracellular matrix were examined by western blot, immunohistochemistry, and immunofluorescence using an antibody against collagen type IV. RESULTS: Western blotting showed a reduction of the total amount of collagen type IV by 50% in the ramipril group compared with the untreated hypertensive group (51.0+/-9.3% reduction, p = 0.0004). Compared with the untreated hypertensive rats, ramipril treatment prevented a loss of vessel density in the cortex (23.4+/-1.0 versus 20.4+/-2.0, p < 0.0001) and revealed a reduction of the amount of collagen per vessel (0.54+/-0.04 versus 0.60+/-0.08, p = 0.037). The ratio between the vessel wall and the lumen (0.69+/-0.08 versus 1.31+/-0.13) and the relative collagen intensity was lowered in the ramipril group (18.1+/-4.7% reduction, p < 0.0001). Using these methods the ramipril group showed similar results than the normotensive group. DISCUSSION: Ramipril treatment completely prevented these hypertensive vascular changes. These results may stimulate a therapeutic approach with angiotensin converting enzyme inhibition in human hypertensive small vessel disease.