scholarly journals Effects of IV Fluids in Dogs and Cats With Kidney Failure

2021 ◽  
Vol 8 ◽  
Author(s):  
Cathy Langston ◽  
Daniel Gordon
Keyword(s):  
Kidney Disease ◽  
Kidney Injury ◽  
Hydration Status ◽  
Acid Base Balance ◽  
Acid Base ◽  
Fluid Status ◽  
Fluid Handling ◽  
Base Balance ◽  
Acid Base Status ◽  
Careful Management

Intravenous fluid therapy has long been the mainstay of treatment of kidney disease, including acute kidney injury and uremic crisis associated with chronic kidney disease. Careful management of fluid dose is critical, as animals with kidney disease may have marked derangements in their ability to regulate fluid homeostasis and acid-base status. Understanding of the physiology of renal fluid handling is necessary, along with repeated attention to parameters of fluid status, electrolytes, and acid-base balance, to achieve optimal hydration status and avoid further damage or decrease in function from dehydration or overhydration.

scholarly journals P0601SAFETY AND EFFICACY OF INTRAVENOUS ADMINISTRATION OF RINGER'S LACTATE VERSUS NORMAL SALINE 0.9% SOLUTION IN PATIENTS WITH ACUTE KIDNEY INJURY AND ESTABLISHED CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Marios Papasotiriou ◽  
Adamantia Mpratsiakou ◽  
Georgia Georgopoulou ◽  
Lamprini Balta ◽  
Paraskevi Pavlakou ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Acute Kidney Injury ◽  
Renal Function ◽  
Kidney Injury ◽  
Acid Base Balance ◽  
Acid Base ◽  
Safety And Efficacy ◽  
Ringer’S Lactate ◽  
Base Balance ◽  
The Mean

Abstract Background and Aims Crystalline solutions, such as normal saline 0.9% (N/S 0.9%) and Ringer's Lactate (L/R), are readily administered for increasing plasma volume. Despite the utility of administering N/S 0.9% to hypovolemic patients, the dose of 154 mmol of sodium (Na) contained in 1 L exceeds the recommended daily dose increasing the risk of sodium overload and hyperchloremic metabolic acidosis. In contrast, L/R solution has the advantage of lower Na content, significantly less chlorine and contains lactates which may be advantageous in patients with significant acidemia such as patients with acute kidney injury (AKI) and chronic kidney disease (CKD). The aim of the present study is to investigate the safety and efficacy of administration of L/R versus N/S 0.9% in patients with prerenal AKI and established CKD. Method The study included adult patients with known CKD stage II to V without need for dialysis, with prerenal AKI (AKIN Stage I to III Criteria). Patients with other forms of AKI as well as hypervolemia, heart congestion or hyperkalemia (serum K>5.5 meq/l) were excluded from the study. Patients were randomized in 1:1 ratio to receive intravenously either N/S 0.9% or L/R solution at a dose of 20 ml/kg body weight/day. We studied kidney function (eGFR: CKD-EPI) and response to treatment at discharge and at 30 days after discharge, duration of hospitalization, improvement in serum bicarbonate levels (HCO3), acid-base balance, serum potassium levels and the need for dialysis. Results The study included 26 patients (17 males) with a mean age of 59.1 ± 16.1 years. Thirteen patients received treatment with N/S 0.9% and the rest with L/R solution. Baseline demographic and clinical characteristics at hospital admission and historical data did not show any significant differences in both groups of patients. Renal function at the onset of AKI did not show significant differences between the two groups (16.4 ± 5.8 vs 16.9 ± 5.7 ml/min/1.73 m2, p=ns, treatment with N/S and L/R respectively). The mean volume of solutions received by the two groups (N/S 0.9% 1119 ± 374 vs L/R 1338 ± 364 ml/day, p=ns) as well as the mean total volume of liquids received per day, did not differ significantly (2888 ± 821 vs 3069 ± 728 ml/d, p=ns). Patients treated with L/R were discharged 1 day earlier than patients treated with N/S (5.2 ± 3.2 vs 6.2 ± 4.9 days of hospitalization, p=ns). Renal function improvement during hospitalization and 30 days after discharge did not differ significantly between the two groups. Patients that received L/R showed a higher increase in plasma HCO3 (ΔHCO3) concentration at discharge than those that received N/S 0.9% (4.9 ± 4.1 vs 2.46 ± 3.7 meq/l, p=ns) and pH increase (ΔpH) was slightly higher in those that received L/R solution (0.052 ± 0.066 vs 0.023 ± 0.071, p=ns). Patients treated with N/S 0.9% showed a greater decrease in serum potassium (ΔK) at discharge compared to those treated with L/R (-0.39 ± 1.03 vs -0.17 ± 0.43 meq/l, p=ns, respectively). No patient received acute dialysis treatment. Conclusion Administration of L/R solution as a hydration treatment to patients with prerenal AKI and established CKD is not inferior concerning safety and efficacy to N/S 0.9% solution. In addition, L/R administration seems to marginally improve acid-base balance in this specific group of patients.

scholarly journals Idiopathic hypercalciuria: the contribution of Dr. Jacob Lemann, Jr.

1994 ◽  
Vol 5 (5) ◽  
pp. S59
Author(s):  
F L Coe ◽  
J H Parks
Keyword(s):  
Mineral Metabolism ◽  
Idiopathic Hypercalciuria ◽  
Acid Base Balance ◽  
Acid Base ◽  
Carbohydrate Ingestion ◽  
Low Calcium Diet ◽  
Base Balance ◽  
Acid Base Status ◽  
Normal Men ◽  
Calcium Loss

The original contributions of Jacob Lemann to mineral metabolism, especially calcium metabolism and idopathic hypercalciuria, are reviewed. One group of studies concern acid base balance and calcium loss, showing that acid loads increase calcium loss in the urine. Another group of studies concern the calciuria of glucose or carbohydrate ingestion, with the observation that stone patients, who as a population are enriched with hypercalciuria, respond with more exaggerated calciuria to glucose loads than do normal people. Yet another body of work shows that normal men, when given noncalcemic loads of calcitriol, exhibit two essential features of idiopathic hypercalciuria--hyperabsorptive hypercalciuria and bone mineral loss on a low-calcium diet. The final group of studies presented worked on the problem of thiazide hypocalciuric action, and where the calcium goes that does not appear in the urine, as well as the effects of potassium bicarbonate and sodium loads on mineral balance and acid base status.

Relationship between acid-base balance and the central respiratory mechanisms

1963 ◽  
Vol 204 (5) ◽  
pp. 867-872 ◽  
Author(s):  
R. L. Katz ◽  
S. H. Ngai ◽  
G. G. Nahas ◽  
S. C. Wang
Keyword(s):  
Periodic Breathing ◽  
Acid Base Balance ◽  
Acid Base ◽  
Respiratory Effects ◽  
Inspiratory Phase ◽  
Arterial Ph ◽  
Base Balance ◽  
Acid Base Status ◽  
Definition Of ◽  
Functional Components

To study the effect of changes in acid-base balance on respiratory patterns, 2-amino-2-hydroxymethyl-1,3-propanediol (THAM, an organic buffer) and sodium bicarbonate (NaHCO3) were infused into midcollicular decerebrate, pontile, and medullary cats. NaHCO3 increased the arterial pH, HCO–3, and pCO2. THAM increased the arterial pH and HCO–3. The arterial pCO2 fell initially and then rose gradually with time. In the midcollicular decerebrate preparation with eupnea, NaHCO3 increased while THAM decreased the rate and amplitude of respiration. In the vagotomized pontile preparation with apneustic breathing, NaHCO3 accelerated and THAM decelerated the apneustic cycling; neither produced a significant change in amplitude. Larger doses of THAM abolished the apneustic cycling either by producing expiratory apnea or by prolonging the inspiratory phase. In the medullary preparation with periodic breathing, THAM decreased the rate with minimal changes in amplitude. The findings suggest that the respiratory effects of NaHCO3 and THAM were due to changes in intracellular pH and pCO2 and that all functional components of the respiratory center are influenced by changes in the acid-base status of the animals. Finally it is pointed out that elucidation of neural respiratory mechanisms requires definition of the acid-base state of the animal.

Gastric mucosal repair and release of HCO3- after damage by 2 M NaCl in cat: role of systemic acid base status

1994 ◽  
Vol 267 (4) ◽  
pp. G536-G545 ◽  
Author(s):  
K. Guttu ◽  
K. Grong ◽  
K. Svanes ◽  
J. E. Gronbech
Keyword(s):  
Mucosal Blood Flow ◽  
Mucosal Damage ◽  
Major Influence ◽  
Acid Base Balance ◽  
Acid Base ◽  
Mucosal Repair ◽  
Base Balance ◽  
Acid Base Status ◽  
Hyperemic Response

To study the influence of acid base balance on gastric mucosal repair, NH4Cl or NaHCO3 was given intravenously to anesthetized cats after mucosal damage induced by intraluminal 2 M NaCl. Saline at pH 5 or 1 was perfused via an oral tube through the stomach lumen and evacuated via a pyloric tube to a chamber with pH and PCO2 electrodes. Luminal bicarbonate (HCO3-) was markedly increased early after damage in both acidotic and alkalotic animals. In alkalotic animals mucosal blood flow increased about twofold in response to mucosal damage, whereas the early hyperemic response was either completely attenuated or blunted in acidotic animals. HCO3- release was correlated to availability of HCO3- by blood in alkalotic animals with luminal pH 5. Alkalotic animals showed improved repair compared with acidotic animals, and mucosal restitution was correlated to availability of HCO3- by blood. We conclude that luminal leakage of HCO3- or plasma after mucosal damage depends on availability by blood and consumption of HCO3- within the mucosa and that blood borne HCO3- has a major influence on gastric mucosal repair.

Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance

2002 ◽  
Vol 283 (4) ◽  
pp. F658-F662 ◽  
Author(s):  
Tong Wang
Keyword(s):  
Proximal Tubule ◽  
Knockout Mice ◽  
Proximal Tubules ◽  
Wild Type ◽  
Acid Base Balance ◽  
Acid Base ◽  
Base Balance ◽  
Acid Base Status ◽  
Inos Knockout Mice ◽  
Oxide Synthase

Our laboratory has previously shown that mice lacking neuronal nitric oxide synthase (nNOS) are defective in fluid absorption ( J v) and HCO[Formula: see text]absorption ( J HCO3) in the proximal tubule and develop metabolic acidosis. The present study examined the transport of fluid and HCO[Formula: see text] in the proximal tubule and acid-base status in mice lacking two other isoforms of NOS, inducible NOS (iNOS) and endothelial NOS (eNOS). Proximal tubules were microperfused in situ in wild-type and NOS knockout mice by methods previously described (Wang T, Yang C-L, Abbiati T, Schultheis PJ, Shull GE, Giebisch G, and Aronson PS. Am J Physiol Renal Physiol 277: F298–F302, 1999). [3H]inulin and total CO2 concentrations were measured in the perfusate and collected fluid, and net J v and J HCO3 were analyzed. These data show that J HCO3 was 35% lower (71.7 ± 6.4 vs. 109.9 ± 7.3 pmol · min−1 · mm−1, n = 13, P < 0.01) and J v was 38% lower (0.95 ± 0.15 vs. 1.54 ± 0.17 nl · min−1 · mm−1, n = 13, P < 0.05) in iNOS knockout mice compared with their wild-type controls. Addition of the iNOS-selective inhibitor l- N 6-(1-iminoethyl) lysine, reduced both J v and J HCO3 significantly in wild-type, but not in iNOS knockout, mice. In contrast, both J HCO3(93.3 ± 7.9 vs. 110.6 ± 6.18 pmol · min−1 · mm−1) and J v (1.56 ± 0.17 vs. 1.55 ± 0.16 nl · min−1 · mm−1) did not change significantly in eNOS knockout mice. These results indicated that iNOS upregulates Na+ and HCO[Formula: see text]transport, whereas eNOS does not directly modulate Na+ and HCO[Formula: see text] transport in the kidney proximal tubules.

Evaluation of bicarbonate transport in rat distal tubule: effects of acid-base status

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose
Keyword(s):  
Metabolic Acidosis ◽  
Respiratory Acidosis ◽  
Distal Tubule ◽  
Bicarbonate Transport ◽  
Acid Base Balance ◽  
Acid Base ◽  
Bicarbonate Reabsorption ◽  
Base Balance ◽  
Acid Base Status ◽  
Acute Metabolic Acidosis

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.

Glucose and lactate turnover and gluconeogenesis in chronic metabolic acidosis and alkalosis in normal and diabetic dogs

1988 ◽  
Vol 66 (1) ◽  
pp. 140-145 ◽  
Author(s):  
G. Hetenyi Jr. ◽  
H. Paradis ◽  
J. Kucharczyk
Keyword(s):  
Metabolic Acidosis ◽  
Plasma Glucose ◽  
Turnover Rate ◽  
Moderate Degree ◽  
Acid Base Balance ◽  
Acid Base ◽  
Lactate Turnover ◽  
Base Balance ◽  
Acid Base Status ◽  
Diabetic Dogs

The turnover rate of glucose, the irreversible disposal rate of lactate, and the rate of gluconeogenesis from lactate were calculated by tracer methods in four normal and four alloxan-diabetic dogs under control conditions as well as in chronic, stable metabolic acidosis and alkalosis. Acidosis was produced by feeding dogs 0.8–1 g∙kg−1∙day−1 NH4Clover 1 week, alkalosis was produced by feeding dogs a chloride-free diet and injections of furosemide. Mean plasma pH in the three states were 7.28 ± 0.013, 7.40 ± 0.024, and 7.51 ± 0.015 in normal dogs, and 7.22 ± 0.025,7.42 ± 0.009, and 7.49 ± 0.002 in the diabetic dogs. Respective mean plasma bicarbonate levels were 14.6 ± 0.88, 22.0 ± 0.80, and 32.4 ± 1.88 mequiv. in normal dogs, and 12.3 ± 1.30, 22.6 ± 0.66, and 35.0 ± 1.14 mequiv. in diabetic animals. In normal dogs shifts in acid–base balance had no effect on the level of plasma glucose or the turnover rate of glucose. In diabetic dogs plasma glucose level was significantly elevated by alkalosis. Plasma lactate was positively correlated with plasma pH(r = 0.69, p < 0.01) and was in general higher in diabetic than in normal animals. The increment in concentration was due to a decreased clearance of lactate from the plasma. The irreversible disposal rate was not changed by the acid–base status. Whereas a larger fraction of lactate removed from the plasma appeared in glucose in diabetic animals, this fraction was not changed significantly by shifts in the acid–base status. The glycemic response to i.v. injected 0.05 U/kg insulin was not appreciably altered by the shifts in acid–base status in either normal or diabetic dogs. Stable metabolic acidosis and alkalosis of moderate degree has little effect on glucose and lactate kinetics and gluconeogenesis from lactate in either normal or diabetic dogs.

Is urea formation regulated primarily by acid-base balance in vivo?

1986 ◽  
Vol 250 (4) ◽  
pp. F605-F612 ◽  
Author(s):  
M. L. Halperin ◽  
C. B. Chen ◽  
S. Cheema-Dhadli ◽  
M. L. West ◽  
R. L. Jungas
Keyword(s):  
Dietary Protein ◽  
Urea Synthesis ◽  
Acid Base Balance ◽  
Severe Metabolic Acidosis ◽  
Acid Base ◽  
Wide Range ◽  
Base Balance ◽  
Acid Load ◽  
Acid Base Status

Large quantities of ammonium and bicarbonate are produced each day from the metabolism of dietary protein. It has recently been proposed that urea synthesis is regulated by the need to remove this large load of bicarbonate. The purpose of these experiments was to test whether the primary function of ureagenesis in vivo is to remove ammonium or bicarbonate. The first series of rats were given a constant acid load as hydrochloric acid or ammonium chloride; individual rats received a constant nitrogen load at a time when their plasma acid-base status ranged from normal (pH 7.4, 28 mM HCO3) to severe metabolic acidosis (pH 6.9, 6 mM HCO3). Urea plus ammonium excretions and the blood urea, glutamine, and ammonium concentrations were monitored with time. Within the constraints of non-steady-state conditions, the rate of urea synthesis was constant and the plasma glutamine and ammonium concentrations also remained constant; thus it appears that the rate of urea synthesis was not primarily regulated by the acid-base status of the animal in vivo over a wide range of plasma ammonium concentrations. In quantitative terms, the vast bulk of the ammonium load was converted to urea over 80 min; only a small quantity of ammonium appeared as circulating glutamine or urinary ammonium. Urea synthesis was proportional to the nitrogen load. A second series of rats received sodium bicarbonate; urea synthesis was not augmented by a bicarbonate load. We conclude from these studies that the need to dispose of excess bicarbonate does not primarily determine the rate of ureagenesis in vivo. The data support the classical view that ureagenesis is controlled by the quantity of ammonium to be removed.

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