Calcium, parathyroid hormone (PTH) and calcitonin (CT) in serum, and the fractional renal excretion of calcium (FE_Ca) were determined in (1) normal pregnant women, (2) patients with preeclampsia, and (3) normal nonpregnant control subjects. Serum calcium, corrected for individual variation in serum protein, was reduced and FE_Ca increased in the normal pregnant group when compared to the nonpregnant control group. In preeclampsia serum calcium did not differ significantly from the normal pregnant group, but FE_Ca was considerably lower and also reduced below the level in the nonpregnant control group. PTH was slightly lower during normal pregnancy than after delivery, but did not deviate significantly from the nonpregnant control group; in preeclampsia PTH did not deviate significantly from the levels in normal pregnancy. CT was the same in the third trimester of pregnancy in both groups. Changes in serum calcium and FE_Ca were not correlated to PTH or CT. It is concluded that both normal pregnancy and preeclampsia are accompanied by considerable alterations in calcium metabolism, that PTH and CT in both groups are mainly unchanged and at nonpregnant level, and that the increase and decrease in renal calcium excretion in normal pregnancy and preeclampsia, respectively, may be attributed to changes in kidney function.

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Renal plasma flow (RPF), glomerular filtration rate (GFR), renal proximal tubular delivery of sodium and water evaluated by lithium clearance, and hormonal parameters were measured in 12 patients with congestive heart failure NYHA class II-IV before and after captopril treatment for 4 wk and in 13 healthy control subjects. RPF and GFR were significantly decreased in heart failure, whereas the filtration fraction (FF) was increased. Treatment with captopril increased RPF and decreased FF, whereas GFR was unchanged. Total and fractional urinary excretion of sodium were reduced in the patients compared with the controls, but increased after captopril. Fractional excretion of lithium was normal in heart failure and was increased by captopril. Atrial natriuretic peptide, guanosine 3',5'-cyclic monophosphate, and aldosterone in plasma were significantly elevated in heart failure and were reduced by treatment with captopril. Plasma renin activity was increased in patients, correlated inversely with RPF, and increased further after captopril treatment. It is concluded that the reduced sodium excretion in heart failure was caused by a combination of diminished glomerular filtration and enhanced tubular reabsorption beyond the proximal tubule and that treatment with captopril increased urinary sodium excretion partly due to an attenuated sodium reabsorption in the proximal tubule. The present data in patients with congestive heart failure are consistent with an increased intrarenal angiotensin II generation and an elevated plasma level of aldosterone being involved in the pathogenesis of the glomerular hemodynamic changes and the enhanced distal tubular reabsorption, respectively.

1. In order to investigate the modulation of kidney function in insulin-dependent diabetes mellitus, intraindividual variation in glomerular filtration rate, renal plasma flow, urinary albumin excretion rate and mean arterial blood pressure was assessed in 22 normoalbuminuric patients [age 31 +/- 8 years, duration of diabetes 9 +/- 5 years, mean arterial blood pressure 90 +/- 5 mmHg (means +/- SD), urinary albumin excretion rate 5.4 x/divided by 1.6 micrograms/min]. The variation in these parameters was calculated from the results of two clearance studies (continuous infusion of [125I]-iothalamate and 131I-hippuran as markers for glomerular filtration rate and renal plasma flow, respectively) and was subsequently analysed in relation to individual variation in plasma concentrations of atrial natriuretic peptide, arginine vasopressin, angiotensin II and aldosterone and measures of glycaemic control. 2. Simple correlation analysis showed a significant association between intra-individual variation in glomerular filtration rate and atrial natriuretic peptide (sigma = 0.66, P = 0.003). Besides variation in atrial natriuretic peptide, multiple regression analysis identified variation in glycated haemoglobin (P = 0.026) and arginine vasopressin (P = 0.057) as variables having independent association with variation in glomerular filtration rate [R2 with the three variables included (adjusted for degrees of freedom) = 0.50, analysis of variance: P = 0.002]. 3. With respect to variation in renal plasma flow, differences in fasting blood glucose concentration and mean arterial blood pressure were suggested as determinants (R2 = 0.36, analysis of variance: P = 0.009). 4. Variation in urinary albumin excretion rate (after log transformation) was statistically associated with variation in glycated haemoglobin.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma concentrations of arginine vasopressin (AVP), angiotensin II (A II), aldosterone (Aldo), serum osmolality (Sosm), urine volume (V), and free water clearance (CH2O) were determined in the third trimester of pregnancy, and 5 days and 3 months after delivery in pre-eclampsia (group I), in normotensive pregnancy (group II), and in non-pregnant control subjects (group III). The AVP was the same in the third trimester of pregnancy in groups I and II and did not deviate significantly from the level in group III. However, 5 days after delivery, AVP was lower and V and CH2O higher in group I than in group II. There was no correlation between AVP and Sosm in the third trimester in either group I or II, but 5 days after delivery a significant positive correlation was found between these parameters in both groups I and II as well as in group III. The A II and Aldo changed qualitatively in the same way in groups I and II, that is, considerable elevation in the third trimester and normalization after delivery. Also, A II and Aldo were lower in group I than in II. The AVP and A II were not correlated and there was no significant relationship between systolic or diastolic blood pressure on the one hand and AVP, A II or Aldo on the other in either group I or II. Thus the osmoregulatory system appears to be altered in both pre-eclampsia and normotensive pregnancy, but becomes normal again 5 days after delivery. In pre-eclampsia a suppression of AVP seems to be responsible for the elimination of excess water in pre-eclampsia 5 days after delivery. There was no evidence for a causal relationship between blood pressure and the osmoregulatory system or the renin-angiotensin-aldosterone system in any of the pregnant groups.