SUMMARYWe measured serum immunoglobulins in 52 persons whose blood pressure was higher than 140/90 mm Hg, and 52 normotensive controls matched for age, sex and race. All were selected from a population of actively employed persons undergoing a routine health evaluation. Contrary to previous reports, the hypertensive subjects did not have higher levels of IgG or IgA than the controls. Sixteen hypertensive subjects with mean blood pressure higher than 115 mm Hg did not have elevated IgG or IgA levels when analyzed separately. Serum IgM was significantly lower in the 52 hypertensive subjects (125 ± 67 mg/dl vs 171 ± 85 mg/dl, p < 0.01).Our and Doyle studied 118 patients with severe hypertension and found IgG levels of 1568 mg/100 ml, compared to 1259 mg/100 ml in 163 normotensive blood donors.1 Olsen et al. 2 reported that 25 of 84 hypertensive patients had increased levels of either IgG, IgA, or IgM. More recently, Kristensen has described his findings in 164 patients with essential hypertension, in whom both IgG and IgA were elevated when compared to normotensive controls. 3The reason for the observed increase in serum immunoglobulin levels in hypertension is not known. Ebringer and Doyle 1 proposed that vascular damage resulting from increased arterial pressure may lead to the release of tissue components that act as antigens. Formation of antibodies against these components of the injured vessels may then be reflected in raised levels of immunoglobulins. An alternative explanation is that immunoglobulin abnormalities precede the onset of hypertension, and reflect alterations in the im- 650 mune system that might be related to the etiology of the hypertensive disease.We have studied immunoglobulin levels in a population of essentially healthy, actively employed persons from whom both hypertensive and normotensive individuals could be selected and compared. The hypertensive persons we studied did not have increased immunoglobulin levels. These findings suggest that immunoglobulin elevation is not present in all groups of people with mild to moderate hypertension, and may have implications concerning the significance of immunoglobulin elevation in this disease. MethodsThe subjects of this report are employees of a large insurance company, most of whom were engaged in sedentary or "white collar" work, who voluntarily underwent a routine annual health evaluation. This consisted of an interim history, physical examination, and laboratory studies, performed within the medical department of the company by a physician, nurse and technologist. As part of the examination two blood pressure measurements were performed by a physician, with the subject in the sitting position, and information was recorded concerning the use of antihypertensive or other medications. Each examination was performed by one of two physicians, each
The mechanisms that regulate renal survival and atrophy under pathological stress remain incompletely understood. This knowledge is essential for developing new strategies to preserve renal function in patients with various forms of renal disease. We have utilized the 5/6 nephrectomy (5/6Nx) model to study the effects of renal insufficiency in 10 week old male Sprague Dawley rats. In this model excision of 2/3 of the left kidney and the entire right kidney induced substantial hypertrophy of the remnant kidney within 7 weeks of surgery. Conversely, excision of 2/3 of the left kidney, while leaving the right kidney intact (1/3 nephrectomy; 1/3Nx), resulted in atrophy of the remnant kidney within the same period. This lead us to hypothesize that removal of the right kidney 7 weeks after 1/3 surgery could induce hypertrophic remodeling of the left remnant kidney even after atrophic remodeling has occurred. To test this, we performed sham surgeries consisting of laparotomy and renal vessel isolation, right uninephrectomy (1Nx), 1/3Nx, or 5/6Nx surgery, as described above (n= 4–11/group). After 7 weeks we performed ultrasound analysis to evaluate the transverse renal cross‐sectional area (CSA) of the left kidney in each model. Sham surgery was then performed on all animals except for a subset of the 1/3Nx group which had their right kidneys excised. The animals were allowed to recover for another 3 weeks before the left kidney remodeling was again evaluated by ultrasound, acute anesthetized blood pressure was measured, and blood and tissues were collected for analysis. Statistical analysis of ultrasound data was completed using two‐way RM ANOVA, and all other by one‐way ANOVA. Ultrasound analysis of left kidney CSA revealed significant hypertrophy in the 1Nx and 5/6Nx models by week 7, when compared to sham‐operated controls, with no further increase in size evident by week 10. We observed the anticipated reduction in CSA in the 1/3Nx group by week 7 (1.06 ± 0.02, sham vs. 0.58 ± 0.01 cm2, 1/3Nx; p <0.05). The 1/3Nx rats subjected to removal of the right kidney experienced a significant hypertrophy of the remnant kidney (1.31 ± 0.04 cm2) between weeks 7 and 10, however this hypertrophy failed to reach the level observed in the 5/6Nx model (2.06 ± 0.05 cm2). Those 1/3Nx rats that retained their right kidney had no apparent change in remnant kidney size by week 10 (0.56 ± 0.03 cm2). These changes in renal dimensions were consistent with wet weights of the remnant kidney weights. Systolic and diastolic blood pressures measured at the end of the study were not statistically different from that of sham operated controls in any surgical group, however pressures tended to be higher in the 1/3Nx rats that had their right kidneys removed at week 7. We determined that removal of the right kidney could stimulate an atrophied left kidney to hypertrophy. In conclusion, the changes observed in this study suggest that these surgical models will allow us to study the mechanisms that regulate hypertrophy and atrophy.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
Severe COVID-19 has been associated with dehydration. Recently, a genetic variant near the aquaporin 3 (AQP3) water channel was associated with severe COVID-19 (rs60840586:G, Odds Ratio: 1.07, P=2.5*10-9). We show that dehydration is associated COVID-19 mortality (OR = 2.06 [95% CI = 1.62-2.65], P = 9.13*10-9), and is modulated by interaction with rs60840586:G genotype (OR = 1.95 [95% CI = 1.22-3.28], P = 0.0075).
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