Renal response to an acute protein challenge in pregnant women with borderline hypertension.

BACKGROUND: The renal reserve (RR), assessed after an oral protein challenge or the intravenous administration of amino acids, is still present in healthy pregnant women (NP), although resting glomerular filtration rate (GFR) and renal plasma flow (RPF) increase progressively throughout normal gestation. No studies have addressed this issue in hypertensive gravidas; the aim of this trial was to evaluate renal response to an acute protein load (PL) in NP and pregnant women with borderline hypertension (HP). METHODS: Five NP, eight HP and eight healthy non-pregnant women (CG) were evaluated. After fasting overnight, all subjects received an oral water load (20 mL/kg of body weight), the urinary output was then replaced orally with equal volumes of water. After two 30 min periods, an 80 g PL was provided. Creatinine clearance (CCr) was measured every 30 min from 1 h before and for 4 h following PL. Participants remained recumbent during the study, bladder emptiness was assessed by ultrasound immediately after each micturition. Baseline CCr was taken as the average of two 30 min periods before PL and peak Ccr as the maximal CCr recorded thereafter. RESULTS: The groups were similar with regard to age, weight or gestation age. Baseline CCr (NP: 118.5+/-6.0, HP: 127.4+/-6.7 and CG: 99.8+/-2.9 mL/min, P=0.004 (CG vs NP and HP), increased after PL to NP: 223.5+/-9.8 to HP: 178.5+/-13 and to CG: 149.1+/-4.0 mL/min, P<0.0004 (CG vs HP, CG vs NP and NP vs HP)). Peak minus baseline CCr was 97.3+/-10.1; 46.3+/-12.7 and 48.3+/-4.8 for NP, HP and CG, respectively (P<0.006 HP vs CG and NP). The peak CCr was obtained significantly earlier in both pregnant groups (Period 3) compared with the healthy non-pregnant women (Period 5) (P=0.02). The fractional proximal reabsorption of sodium (FPRNa+) at peak CCr was similar in the groups (NP: 0.74+/-0.01 HP: 0.78+/-0.02 and CG: 0.74+/-0.03, P=not significant (NS)) as was the distal delivery of sodium (DDNa+) (NP: 5.8+/-0.5; HP: 4.1+/-0.5 and CG: 4.3+/-0.4 meq/min, P=NS). Fractional excretion of urea (%) increased from 91.4+/-5.5 to 105.5+/-9.8%; 80.7+/-8.0 to 97.3+/-9.8; and 44.4+/-7.8 to 86.0+/-7.1 in NP, HP and CG, respectively (P=NS). There was a trend towards a poorer maternal and fetal outcome in the HP group. CONCLUSION: Mid-term borderline HP failed to increase CCr as much as NP did after a protein challenge, suggesting altered functional response of the nephron or lessened sensitivity of renal vasculature to additional vasodilator stimuli. These results support the interest of additional prospective studies with a larger number of patients to confirm these findings and evaluate the value of RR tests as predictors of outcome of pregnancies at risk.

The faster potassium-lowering effect of high dialysate bicarbonate concentrations in chronic haemodialysis patients.

BACKGROUND: Hyperkalaemia is common in patients with advanced renal disease. In this double-blind, randomized, three-sequence, crossover study, we compared the effect of three dialysate bicarbonate concentrations ([HCO3-]) on the kinetics of serum potassium (K+) reduction during a conventional haemodialysis (HD) session in chronic HD patients. METHODS: We studied eight stable HD patients. The choice of dialysate [HCO3-] followed a previously assigned treatment protocol and the [HCO3-] used were low bicarbonate (LB; 27 mmol/l), standard bicarbonate (SB; 35 mmol/l) and high bicarbonate (HB; 39 mmol/l). Polysulphone dialysers and automated machines provided blood flow rates of 300 ml/min and dialysis flow rates of 500 ml/min for each HD session. Blood samples were drawn at 0 (baseline), 15, 30, 60 and 240 min from the arterial extracorporeal line to assess blood gases and serum electrolytes. In three of the eight patients, we measured serum K+ 1 h post-dialysis as well as K+ removal by the dialysis. The same procedures were followed until the completion of the three arms of the study, with a 1 week interval between each experimental arm. RESULTS: Serum K+ decreased from 5.4+/-0.26 (baseline) to 4.96+/-0.20, 4.90+/-0.19, 4.68+/-0.13 and 4.24+/-0.15 mmol/l at 15, 30, 60 and 240 min, respectively, with LB; from 5.38+/-0.21 to 5.01+/-0.23, 4.70+/-0.25, 4.3+/-0.15 and 3.8+/-0.19 mmol/l, respectively, with SB; and from 5.45+/-0.25 to 4.79+/-0.17, 4.48+/-0.17, 3.86+/-0.16 and 3.34+/-0.11 mmol/l, respectively, with HB (P<0.05 for high vs standard and low [HCO3-] at 60 and 240 min). The decrease in serum K+ correlated with the rise in serum [HCO3-] in all but LB (P<0.05). Potassium rebound was 3.9+/-10.2%, 5.2+/-6.6% and 8.9+/-4.9% for LB, SB and HB dialysates, respectively (P=NS), while total K+ removal (mmol/dialysis) was 116.4+/-21.6 for LB, 73.2+/-12.8 for SB and 80.9+/-15.4 for HB (P=NS). CONCLUSIONS: High dialysate [HCO3-] was associated with a faster decrease in serum K+. Our results strongly suggest that this reduction was due to the enhanced shifting of K+ from the extracellular to the intracellular fluid compartment rather than its removal by dialysis. This finding could have an impact for those patients with life-threatening pre-HD hyperkalaemia.