scholarly journals A randomized comparison of 1-h sodium bicarbonate hydration versus standard peri-procedural saline hydration in patients with chronic kidney disease undergoing intravenous contrast-enhanced computerized tomography

2014 ◽  
Vol 29 (5) ◽  
pp. 1029-1036 ◽  
Author(s):  
Judith Kooiman ◽  
Yvo W.J. Sijpkens ◽  
Jean-Paul P.M. de Vries ◽  
Harald F.H. Brulez ◽  
Jaap F. Hamming ◽  
...  
Author(s):  
Dominique M. Bovée ◽  
Lodi C. W. Roksnoer ◽  
Cornelis van Kooten ◽  
Joris I. Rotmans ◽  
Liffert Vogt ◽  
...  

Abstract Background Acidosis-induced kidney injury is mediated by the intrarenal renin-angiotensin system, for which urinary renin is a potential marker. Therefore, we hypothesized that sodium bicarbonate supplementation reduces urinary renin excretion in patients with chronic kidney disease (CKD) and metabolic acidosis. Methods Patients with CKD stage G4 and plasma bicarbonate 15–24 mmol/l were randomized to receive sodium bicarbonate (3 × 1000 mg/day, ~ 0.5 mEq/kg), sodium chloride (2 × 1,00 mg/day), or no treatment for 4 weeks (n = 15/arm). The effects on urinary renin excretion (primary outcome), other plasma and urine parameters of the renin-angiotensin system, endothelin-1, and proteinuria were analyzed. Results Forty-five patients were included (62 ± 15 years, eGFR 21 ± 5 ml/min/1.73m2, plasma bicarbonate 21.7 ± 3.3 mmol/l). Sodium bicarbonate supplementation increased plasma bicarbonate (20.8 to 23.8 mmol/l) and reduced urinary ammonium excretion (15 to 8 mmol/day, both P < 0.05). Furthermore, a trend towards lower plasma aldosterone (291 to 204 ng/L, P = 0.07) and potassium (5.1 to 4.8 mmol/l, P = 0.06) was observed in patients receiving sodium bicarbonate. Sodium bicarbonate did not significantly change the urinary excretion of renin, angiotensinogen, aldosterone, endothelin-1, albumin, or α1-microglobulin. Sodium chloride supplementation reduced plasma renin (166 to 122 ng/L), and increased the urinary excretions of angiotensinogen, albumin, and α1-microglobulin (all P < 0.05). Conclusions Despite correction of acidosis and reduction in urinary ammonium excretion, sodium bicarbonate supplementation did not improve urinary markers of the renin-angiotensin system, endothelin-1, or proteinuria. Possible explanations include bicarbonate dose, short treatment time, or the inability of urinary renin to reflect intrarenal renin-angiotensin system activity. Graphic abstract


2006 ◽  
Vol 17 (5) ◽  
pp. 1472-1480 ◽  
Author(s):  
William L. Henrich ◽  
Richard L. Clark ◽  
Judith P. Kelly ◽  
Vardaman M. Buckalew ◽  
Andrew Fenves ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
María M. Adeva-Andany ◽  
Carlos Fernández-Fernández ◽  
David Mouriño-Bayolo ◽  
Elvira Castro-Quintela ◽  
Alberto Domínguez-Montero

Metabolic acidosis occurs when a relative accumulation of plasma anions in excess of cations reduces plasma pH. Replacement of sodium bicarbonate to patients with sodium bicarbonate loss due to diarrhea or renal proximal tubular acidosis is useful, but there is no definite evidence that sodium bicarbonate administration to patients with acute metabolic acidosis, including diabetic ketoacidosis, lactic acidosis, septic shock, intraoperative metabolic acidosis, or cardiac arrest, is beneficial regarding clinical outcomes or mortality rate. Patients with advanced chronic kidney disease usually show metabolic acidosis due to increased unmeasured anions and hyperchloremia. It has been suggested that metabolic acidosis might have a negative impact on progression of kidney dysfunction and that sodium bicarbonate administration might attenuate this effect, but further evaluation is required to validate such a renoprotective strategy. Sodium bicarbonate is the predominant buffer used in dialysis fluids and patients on maintenance dialysis are subjected to a load of sodium bicarbonate during the sessions, suffering a transient metabolic alkalosis of variable severity. Side effects associated with sodium bicarbonate therapy include hypercapnia, hypokalemia, ionized hypocalcemia, and QTc interval prolongation. The potential impact of regular sodium bicarbonate therapy on worsening vascular calcifications in patients with chronic kidney disease has been insufficiently investigated.


2016 ◽  
Vol 17 (1) ◽  
Author(s):  
Wei Chen ◽  
Michal L. Melamed ◽  
Thomas H. Hostetter ◽  
Carolyn Bauer ◽  
Amanda C. Raff ◽  
...  

2018 ◽  
Vol 44 (1) ◽  
pp. 8
Author(s):  
Diana Vergnano ◽  
Emanuela Valle ◽  
Natascia Bruni ◽  
Rita Rizzi ◽  
Mauro Bigliati ◽  
...  

Background: Chronic kidney disease (CKD) is a very common pathology in cats, especially in the geriatric age. A proper renal diet is considered the current standard of care to enhance patients’ long-term survival and quality of life. However, when diet alone is not sufficient, it is necessary to supplement it with specific substances: these are phosphate binders and alkalinizing agents. The aim of this study was to evaluate the effectiveness of a feed supplement containing calcium carbonate, calcium lactate gluconate, chitosan and sodium bicarbonate in controlling hyperphosphatemia and metabolic acidosis in cats with severe CKD (IRIS, International Renal Interest Society, stage 3 and 4).Materials, Methods & Results: 10 cats (median BW 4.00 (3.20; 5.70) Kg, BCS 3/5 (2.25; 3.75), 11 (8.25;12.00) years) fed with a balanced renal diet were included in the study. To be enrolled in the study cats had to be affected by CKD in stages 3 or 4 and show hyperphosphatemia. Treatment consisted in oral administration of the product (Renal, Candioli Pharma) at 0.2 g/kg/day mixed with the food for 60 days. The animals were evaluated at the beginning of the study and at 15, 30, 60 days (T0, T15, T30, T60) for: clinical condition, BW, BCS, blood pressure and for routinely hematochemical, biochemical and urinary parameters. Owners were asked to assess appetite of the cat, palatability of the supplement, presence of vomit and/or diarrhoea, general health and vitality. All statistical analyses were performed using SAS software. After checking normality data were analyzed using Kruskal-Wallis and Wilcoxon tests. Results are expressed as median (interquartile range). For the parameters P (P < 0.0001), iCa (P = 0.0008) and HCO3 (P = 0.0002) there were statistically significant differences among times of supplementation (T0, T15, T30, T60). Statistically significant reduction of serum phosphorus concentration was obtained through the study (reduction of 59% at T60 vs T0). Also a statistically significant increase of bicarbonate was seen (7% from T0 to T60). At T60 was also recorded an increase of ionized calcium level, which however was in normal range. For the other laboratory parameters, no statistical difference was recorded. All the owners reported a good palatability of the product. The decrease of vomit and diarrhea episodes and the increase of the appetite reported were statistically significant (P < 0.05).Discussion: The restriction of available dietary phosphorus is now recognised as one of the major contributors in slowing the disease progression and improving survival rates. Phosphate binders are able to absorb phosphate (P) in the intestine, forming insoluble products that are eliminated with the faeces, thus decreasing serum phosphate levels. The phosphate binders contained in the product tested in the present trial were chitosan, calcium lactate gluconate and calcium carbonate. During the study P decreased significantly from T0 to T60, reaching the target post-treatment plasma P concentration for IRIS stage 3 after 30 days. Another important recommendation for CKD treatment is to use alkalinisation therapy if metabolic acidosis is present. The feed supplement tested in this study also contained sodium bicarbonate. In our study, 90% of the patients at the inclusion examination had metabolic acidosis. At the end of the study, the median blood bicarbonate concentration was in the normal range, thus reaching the IRIS treatment target. The feed supplement tested was therefore effective in reducing blood phosphate levels and in increasing blood bicarbonate levels, thus improving the cats’ clinical conditions for the duration of the study without any adverse effect.


2016 ◽  
Vol 46 (9) ◽  
pp. 1332-1340 ◽  
Author(s):  
Aarti Luhar ◽  
Sarah Khan ◽  
J. Paul Finn ◽  
Shahnaz Ghahremani ◽  
Rachel Griggs ◽  
...  

2021 ◽  
Author(s):  
Carmen Sebastia ◽  
Alfredo Páez-Carpio ◽  
Elena Guillen ◽  
Blanca Paño ◽  
JoanAlbert Arnaiz ◽  
...  

Abstract Background The objective of this study is to evaluate oral hydration compared to intravenous (i.v.) hydration in the prevention of post-contrast acute kidney injury (PC-AKI) in the oncologic subgroup of patients with stage IIIb chronic kidney disease (CKD) included in the NICIR study referred for elective contrast-enhanced computed tomography (CE-CT). Material and Methods We performed a retrospective subanalysis of the oncological subgroup (174/228 patients, 74%) from a continuous prospective database of patients included in the recently published non-inferiority NICIR study. Patients received prophylaxis against PC-AKI with either oral hydration (500 mL of water two hours before and 2000 mL during the 24 hours after CE-CT) or i.v. hydration (sodium bicarbonate (166 mmol/L)3 mL/kg/h starting one hour before and 1 mL/kg/h during the first hour after CE-CT). The primary outcome was to compare the proportion of PC-AKI in the first 48 to 72 hours after CE-CT in the two hydration groups. Secondary outcomes were to compare persistent PC-AKI, the need for hemodialysis, and the occurrence of adverse events related to prophylaxis in each group. Results Of 174 patients included in the subanalysis, 82 received oral hydration and 92 received i.v. hydration. There were no significant differences in clinical characteristics or risk factors between the two study arms. Overall the PC-AKI rate was 4.6% (8/174 patients), being 3.7% in the oral hydration arm (3/82 patients) and 5.4% (5/92 patients) in the i.v. hydration arm. The persistent PC-AKI rate was 1.8% (1/82 patients) in the oral hydration arm and 3.3% (3/92 patients) in the i.v. hydration arm. No patient required dialysis during the first month after CE-CT or had adverse effects related to the hydration regime. Conclusion In oncological patients with stage IIIb CKD referred for elective CE-CT, the rate of PC-AKI in those receiving oral hydration did not significantly differ from that of patients receiving i.v. hydration.


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