Objective To determine whether use of an automated urinalysis device will improve the accuracy of detecting proteinuria, and whether spot urine protein to creatinine ratio will provide accurate quantitation of proteinuria in hypertensive pregnant women.Design Prospective studies assessing the accuracy of both detection and quantitation of proteinuria.Setting Antenatal ward and pregnancy day assessment unit of St George Hospital, a teaching hospital in Sydney, Australia.Population Hypertensive pregnant women admitted to hospital or day assessment unit for management of their hypertensive disorders.Methods I. Routine dipstick urinalysis and 2. Urinalysis by an automated device (Clinitek 100 Ames) on a midstream urine sample were compared with measurement of protein concentration on that sample (n = 103). In a third study, the pr0tein:creatinine ratio on a midstream (spot) urine sample was compared with protein excretion over the subsequent 24 hours (n = 100). Main outcome measuresRelations between urine protein concentrations and 1. dipstick urinalysis and 2. automated urinalysis; 3. Positive and negative predictive values of spot protein : creatinine ratio for true proteinuria (2 300 mglday).Results Automated urinalysis improved the percentage of true positive urinalyses from 48% with visual urinalysis to 74% (P = 0.02). True negatives were 98% to 100% for both methods. Spot urine protein: creatinine ratio correlated well with subsequent 24-hour urine proteinuria (r = 0.93, P < 0.001). A pr0tein:creatinine ratio > 30 mg proteidmmol creatinine was the optimum discriminant value for true proteinuria, with sensitivity 93%, specificity 92%, positive predictive value 95% and negative predictive value 90%.Use of an automated urinalysis device improved accurate detection of proteinuria, particularly reducing false positive tests. A random urine protein: creatinine ratio provides an accurate and rapid quantitation of proteinuria in hypertensive pregnant women. This should improve clinical care, especially when managing hypertensive pregnant women as outpatients. Conclusions

Hypocalciuria has been associated with preeclampsia (gestational hypertension with proteinuria or other maternal organ dysfunction) but not usually with pure gestational hypertension or normal pregnancy. We hypothesized that hypocalciuria would be a marker of emerging preeclampsia in women presenting with gestational hypertension who later developed preeclampsia. Eighty-one women with de novo hypertension in the second half of pregnancy (n = 81) were enrolled prospectively. At first assessment, calcium/creatinine ratio was determined in a spot urine. Patients were followed until delivery and were classified subsequently according to the occurrence of preeclampsia. Gestational hypertensive patients who became preeclamptic (n = 31) had lower urinary calcium/creatinine ratios at presentation (ratio = 0.07, interquartile range [IQR] = 0.04-0.11) than women who remained as gestational hypertensives (n = 50; ratio = 0.17, IQR = 0.08-0.21; P = .002). Intact plasma parathyroid hormone (PTH) concentrations were similar between groups. Using a receiver operator curve, the best threshold value for the development of preeclampsia was a calcium/creatinine ratio of 0.10, which yielded a sensitivity of only 68% and a specificity of 70%. A low calcium/creatinine ratio preceded the emergence of preeclampsia by 12 (7-24) (median [IQR]) days among a group of women with gestational hypertension. Though this implies primary or secondary disturbances of renal calcium handling even before preeclampsia is clinically apparent, this measurement does not have sufficient sensitivity to recommend its use as a screening test for the emergence of preeclampsia.

Somatostatin secretion was investigated from rodent antral mucosal biopsies maintained in organ culture. Under control conditions, the somatostatin secretory output was fairly constant, with each biopsy releasing a mean value of 29.1 +/- 7.5 pg of hormone over a 15-min period. Incubation of the mucosa in medium containing 5% peptone directly induced a 20-fold increase in medium somatostatin levels to 622.5 +/- 15.5 pg/ml. In contrast, a peptone dialysate was a weaker stimulant of hormone release, inducing a three- to fourfold increase in medium somatostatin concentration. Additionally, it was determined that a peptic hydrolysate of bovine serum albumin was a significantly more potent in vitro stimulant of somatostatin secretion than the intact undigested molecule. These results suggest that the amino acid and peptide constituents of these proteinaceous substances are the major stimulants of somatostatin release in vitro. It is presently uncertain whether this direct peptone-induced release of somatostatin from antral mucosal explants can account for the previously reported [Am. J. Physiol. 235 (Endocrinol. Metab. Gastrointest. Physiol. 4): E410-E415, 1978] gastrin secretory "off response" to the same agent, because addition of exogenous somatostatin to the medium failed to block this peptone-induced gastrin secretory response.