Diabetes and chronic kidney disease (CKD) which are risk facters of cardiovascular disease, are increasing global public health problems. Microalbuminuria is an early sign of progressive cardiovascular and renal disease in individuals with or without diabetes. Screening for microalbuminuria and early treatment are recommended for patients with increased cardiovascular and renal risk factors. However, the procedure used to measure urinary albumin is expensive. Alternatively, the measurement of total urinary protein is simple and inexpensive. Thus, we aimed to establish a method that could predict the presence of microalbuminuria by measuring the total protein-to-creatinine ratio. Spot urine samples were obtained from 150 patients with diabetes mellitus, and the total protein-to-creatinine ratio and the albumin-to-creatinine ratio (ACR) were measured. There was a significant positive correlation between the protein-to-creatinine ratio and the ACR (r = 0.95). The presence of albuminuria (both micro-and macroalbuminuria) could be predicted from the value of the protein-to-creatinine ratio in more than 90% of patients. A receiveroperating characteristic curve analysis revealed that the protein-to-creatinine ratio had a sensitivity and a specificity of 90.8% and 91.9%, respectively, for the detection of albuminuria and a cutoff value of 0.091 g/g creatinine. These results suggest that screening for microalbuminuria can be replaced by the detection of the protein-to-creatinine ratio, which may be cost-effective for patients with cardiovascular risks as well as for the general population.
We studied the role of the sodium-potassium pump in erythrocytes of 12 patients with sickle cell anemia (SS). Ouabain-binding sites per cell and pump-mediated Rb/K uptake were significantly higher in SS patients than in white or black controls. Ouabainresistant Rb/K influx was also greater than in normal controls or patients with sickle cell trait.Deoxygenation of SS erythrocytes increased ouabain-sensitive Rb/K influx without altering ouabain binding, presumably as the consequence ofan increase in the passive influx of sodium. Deoxygenation increased mean corpuscular hemoglobin concentration (MCHC) by 5.5%, and studies of the density distribution of SS cells indicated an increase in highly dense fractions known to contain sickled erythrocytes. Ouabain prevented the rise in MCHC and reduced the percentage of dense cells.These findings indicate a magnified role for the sodium-potassium pump in the pathophysiology of SS erythrocytes and suggest that its inhibition might prove useful in therapy.
The number of erythrocyte Na,K-ATPase pump units has been found to be reduced in some populations of obese humans, but the effect of dietary factors upon the status of the erythrocyte pump has not been delineated. We have measured the number of Na,K-ATPase pump units by [3H]ouabain binding and the activity of the pump by ouabain-inhibitable 86rubidium uptake in response to nutritional maneuvers in several patient groups. There was no consistent change in the number or activity of Na,K-ATPase units in response to 1) an acute 600-cal meal, 2) a 3-day fast or refeeding after a fast in normal weight or obese subjects, 3) 2 weeks of hypocaloric (600 cal) feeding in obese subjects. Individuals with anorexia nervosa were also not significantly different from age- and sex-matched control subjects with respect to the erythrocyte Na,K pump. It is concluded that the circulating erythrocyte does not regulate the number or activity of Na,K pump units in response to short or medium term nutritional maneuvers. Differences between obese and thin populations with respect to the Na,K pump are not likely to be secondary to nutritional differences between the two groups.
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