ACID‐BASE IN RENAL FAILURE: New Perspectives on Acid‐Base Balance (original) (raw)

2001, Seminars in Dialysis

https://doi.org/10.1046/J.1525-139X.2000.00061.X

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Abstract

ABSTRACTThis review will cover two main areas of acid‐base balance, both of which are attended with much misconception and misunderstanding. One is the external balance of acids and alkali; the other is the contribution of bone buffering in acute and chronic metabolic acidosis.

Opinion: What Unique Acid-Base Considerations Exist in Dialysis Patients?

Seminars in Dialysis, 2004

Because a typical modern diet results in net production of acid, and the kidney is normally the main organ responsible for generating alkali to maintain acid-base homeostasis, chronic metabolic acidosis is commonly observed in patients with chronic renal insufficiency. In this article we will deal with the clinical characteristics, pathophysiology, and therapeutic approach to this condition.

ACID-BASE IN RENAL FAILURE: Acidosis and Nutritional Status in Hemodialyzed Patients

Seminars in Dialysis, 2001

In a cross-sectional study of more than 30% of French dialysis patients (N = 7,123), we evaluated the relationships between predialysis plasma bicarbonate concentration and nutritional markers. Data including age, gender, cause of end-stage renal disease (ESRD), time on dialysis, body mass index (BMI), blood levels of midweek predialysis albumin, prealbumin, and bicarbonate were collected. Normalized protein catabolic rate (nPCR), dialysis adequacy parameters, and estimation of lean body mass (LBM) were computed from pre-and postbicarbonate-dialysis urea and creatinine levels according to the classical formulas of Garred. Average values (±1 SD) were age 61 ± 16 years, BMI 23.3 ± 4.6 kg/m 2 , dialysis time 12.4 ± 2.7 h/week, HCO 3 22.8 ± 3.5 mmol/L, albumin 38.7 ± 5.3 g/L, prealbumin 340 ± 90 mg/L, Kt/V 1.36 ± 0.36, nPCR 1.13 ± 0.32 g/kg BW/day, and LBM 0.86 ± 0.21% of ideal LBM. A highly significant negative correlation was observed between predialysis bicarbonate levels (within a range of 16-30 mmol/L, 95% of this population) and nPCR confirmed by analysis of variance using bicarbonate classes (p < 0.0001). Bicarbonate was also negatively correlated with albumin, prealbumin, BMI, and LBM. No relationship was noted between bicarbonate and Kt/V despite a positive correlation between Kt/V and nPCR. It is likely that a persistent acidosis observed despite standard bicarbonate dialysis was caused by a high dietary protein intake which results in an increased acid load, but also overcomes the usual catabolic effects of acidosis.

Managing Metabolic Acidosis in Chronic Renal Diseases

Journal of Advanced Health Informatics Research, 2023

One of the most common side effects of chronic kidney disease is metabolic acidosis (CKD). It is associated with the development of CKD and various other functional disorders. Metabolic acidosis can be a common complication associated with progressive loss of kidney function. The form can be a metabolic acidosis with a non-anion gap or metabolic acidosis with a high or mixed anion gap. Reduced kidney ability to maintain acid-base homeostasis results in acid accumulation, causing various complications such as decreased nutritional status such as wasting muscle-hypoalbuminemia, inflammation, uremic bone disease and its association with increased mortality. In addition to the side effects associated with acid retention, metabolic acidosis can also cause kidney damage, possibly through stimulation of adaptive mechanisms aimed at maintaining acid-base homeostasis in the event of decreased renal function. chronic kidney disease (CKD), and therefore offers an effective, safe and affordable reno-protective strategy. This paper will discuss the physiology and pathophysiology of acid-base homeostasis in CKD, namely the mechanism of metabolic acidosis capable of impairing kidney function, and its relation to the benefits of alkaline therapy. based on clinical trials.

Acid-base disorders and the impact on metabolic bone disease in hemodialysis patients

Journal of Research and Practice on the Musculoskeletal System

tendon rupture, and frequent occurrence of fractures 5,6. We use the term Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) to describe a wider clinical syndrome that is developed as a systemic metabolic mineral bone disturbance, as a result of the chronic kidney Abstract Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD) is a term that is used to describe a wider clinical syndrome that can be developed as a systemic metabolic mineral bone disturbance, due to the chronic kidney disease, and it manifests itself as metabolic mineral bone anomalies or extra-skeletal calcifications. Metabolic acidosis is considered to be the most widespread acid-base disorder that is found in the majority of CKD patients. Hemodialysis patients seem to be more prone to MBD due to acid base disorders. This article aims to review the available literature about the acid-base disorders and their impact on MBD in hemodialysis patients. We have conducted an electronic literature research, where titles and abstracts of relevant papers were validated by the authors for further inclusion in this work. Finally, full texts of the included articles were retrieved. The findings of our literature research have concluded that at the age of 55, the relative risk of hip fractures increases and in CKD patients is high; after 4 years of undergoing dialysis, the age-specific relative risk of suffering a hip fracture was 9.83 for males and 8.10 for females. The average relative risk of mortality associated with hip fracture was 1.99. Our review has highlighted that CKD and MBD are closely related and they consist of a phenomenon requiring further research.

Acid-Base Balance in Peritoneal Dialysis Patients: A Stewart-Fencl Analysis

Renal Failure, 2009

Background. Evaluation of acid-base disorders using the Stewart-Fencl principle is based on assessment of independent factors: strong ion difference (SID) and the total concentration of non-volatile weak acids (Atot). This approach allows for a more detailed evaluation of the cause of acid-base imbalance than the conventional bicarbonate-centered approach based on the Henderson-Hasselbalch principle, which is a necessary yet insufficient condition to describe the state of the system. The aim of our study was to assess acid-base disorders in peritoneal dialysis (PD) patients using both of these principles. Methods. A total of 17 patients with chronic renal failure (10 men), aged 60.7 (22-84) years, treated by PD for 25.7 (1-147) months were examined. A control group included 17 healthy volunteers (HV) (8 males), with a mean age of 42.7 (22-77) years and normal renal function. Patients were treated with a solution containing bicarbonate (25 mmol/L) and lactate (15 mmol/L) as buffers; eleven of them used, during the nighttime dwell, a solution with icodextrin buffered by lactate at a concentration of 40 mmol/L. The following equations were employed for calculations of acid-base parameters according to the Stewart-Fencl principle. The first is SID = where SID is the strong ion difference and [UA -] is the concentration of undetermined anions. For practical calculation of SID, the second equation, SID = [HCO 3 -] + [Alb -] + [Pi -], was used, where [Alb -] and [Pi -] are the charges carried by albumin and phosphates. The third is Atot, the total concentration of weak non-volatile acids, albumin [Alb] and phosphates [Pi]. Results. The capillary blood pH in PD group was 7.41 (7.27-7.48), [HCO 3 -] levels 23.7 (17.6-29.5) mmol/L, SID 36.3 (29.5-41.3) mmol/L, sodium-chloride difference 39.0 (31.0-44.0) mmol/L, [Pi] 1.60 (0.83-2.54) mmol/L, and [Alb] 39.7 (28.8-43.4) g/L (median, min-max). Bicarbonate in blood correlated positively with SID (Rho = 0.823; p < 0.001), with the sodium-chloride difference (Rho = 0.649; p < 0.01) and pH (Rho = 0.754; p < 0.001), and negatively with residual renal function (Rho = -0.517; p < 0.05). Moreover, the sodium-chloride difference was also found to correlate with SID (Rho = 0.653; p < 0.01). While the groups of PD and HV patients did not differ in median bicarbonate levels, significantly lower median value of SID were observed in PD patients, 36.3 vs. 39.3 mmol/L (p < 0.01); additionally, PD patients were shown to have significantly lower mean value of serum sodium levels, 138 vs. 141 mmol/L (p < 0.01), and serum chlorides levels, 100 vs. 104 mmol/L (p < 0.001). Despite the higher [UA -] levels in PD patients, 9.1 vs. 5.4 mmol/L (p < 0.001), this parameter was not found to correlate with bicarbonate levels. Conclusions. The results suggest that the decreased bicarbonate in PD patients results from a combination of decreased sodium-chloride difference and mildly increased unmeasured anions. Keywords acid-base balance, bicarbonate, icodextrin, lactate, peritoneal dialysis, Stewart principle The internal milieu of the patient with chronic renal failure is characterized by the presence of metabolic acidosis. Correction of metabolic acidosis is one of the main objectives

Acid-Base Balance in Uremic Rats with Vascular Calcification

Nephron Extra, 2014

Background/Aims: Vascular calcification (VC), a major complication in humans and animals with chronic kidney disease (CKD), is influenced by changes in acid-base balance. The purpose of this study was to describe the acid-base balance in uremic rats with VC and to correlate the parameters that define acid-base equilibrium with VC. Methods: Twenty-two rats with CKD induced by 5/6 nephrectomy (5/6 Nx) and 10 nonuremic control rats were studied. Results: The 5/6 Nx rats showed extensive VC as evidenced by a high aortic calcium (9.2 ± 1.7 mg/g of tissue) and phosphorus (20.6 ± 4.9 mg/g of tissue) content. Uremic rats had an increased pH level (7.57 ± 0.03) as a consequence of both respiratory (PaCO 2 = 28.4 ± 2.1 mm Hg) and, to a lesser degree, metabolic (base excess = 4.1 ± 1 mmol/l) derangements. A high positive correlation between both anion gap (AG) and strong ion difference (SID) with aortic calcium

Acid-base balance in chronic peritoneal dialysis patients

Kidney International, 1995

Acid-base balance in chronic peritoneal dialysis patients. Endogenous acid production has never been measured directly in dialysis patients and an empiric formula is used to estimate acid production from their protein catabolic rate. We have studied acid-base balance in 19 stable CAPD patients attending the peritoneal dialysis clinic of Mount Sinai Hospital. They obtained a 24 hour collection of peritoneal dialysis fluid and urine while consuming their usual diet and performing their usual activities. Total alkali gain was calculated from net GI alkali absorption plus urinary net acid excretion plus alkali gain from dialysate, while total acid production was measured directly from the urinary and dialysate excretions of sulfate and organic anions. Net GI alkali absorption was estimated from the difference between cations (Na + K + Ca + Mg) and anions (Cl + 1.8P) in the 24 hour dialysate and urine collections minus the daily total amount of lactate infused. All of our patients had a normal or high serum bicarbonate concentration, which was stable with time. Total alkali gain was virtually identical to total acid production (54.2 vs. 52.4 mEq/day) which suggests that these patients were in neutral acid-base balance. Net GI alkali absorption (22.7 mEq/day) was one of the same range as that of chronic renal failure patients not on dialysis and represented almost one half of the total daily alkali gain. The daily acid production of 52.4 mEq/day was numerically equal to 84% of the protein catabolic rate expressed as glday, which is similar to the predicted value of 77% of PCR reported in the literature. However, the main source of alkali loss, that is, acid production, was the loss of organic anions in dialysate and urine. Daily sulfate excretion (16 mEq/day) was lower than expected for the level of protein intake (protein catabolic rate of 62 glday). The stable serum bicarbonate concentrations on long-term dialysis suggests a steady state and neutral acid-base balance in these patients. The almost perfect agreement between acid production and total alkali gain supports the validity of our methods for measuring the various parameters of acid-base balance, including net GI absorption of alkali. The determinants of acid-base balance in chronic hemodialysis patients have been well delineated by Gotch, Sargent and Keen [1]. Using the rationale that protein metabolism is the largest contributor to acid production, these authors developed an empiric formula to calculate the endogenous acid production in dialysis patients from their protein catabolic rate (PCR). However, this formula, based on observations in normal subjects, has never been validated in dialysis patients [2]. Later, Teehan et al [3] applied similar analysis to a small group of chronic ambulatory peritoneal dialysis (CAPD) patients. Teehan's study showed a negative base balance of about 26 mEqlday. However, this study did not measure the acid production directly and ignored the

Characterization of acid-base status in maintenance hemodialysis: physicochemical approach

Journal of artificial organs : the official journal of the Japanese Society for Artificial Organs, 2008

Acidosis is a common and deleterious aspect of maintenance dialysis. Traditionally, it is considered to be an elevated anion gap acidosis caused by the inability to excrete nonvolatile anions. Stewart's approach made it possible to identify real determinants of the acid-base status and allowed quantification of the components of these disturbances, especially the unmeasured anions. We performed a cross-sectional study to identify and quantify each component of acidosis in hemodialysis maintenance patients. Sixty-four maintenance hemodialysis patients and 14 controls were enrolled in this study. Gasometrical and biochemical analysis were performed before the midweek dialysis session. Quantitative physicochemical analysis was carried out using the Stewart methodology. Hemodialysis patients were found to have mild acidemia (mean pH: 7.33 +/- 0.06 versus 7.41 +/- 0.05) secondary to metabolic acidosis (serum bicarbonate: 18.8 +/- 0.26 versus 25.2 +/- 0.48 mEq/l). The metabolic acidos...

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UK Food Standards Agency α-linolenic acid workshop report

British Journal of Nutrition, 2002

The UK Food Standards Agency convened a group of expert scientists to review current research investigating whether n-3 polyunsaturated fatty acids (PUFA) from plant oils (a-linolenic acid; ALA) were as beneficial to cardiovascular health as the n-3 PUFA from the marine oils, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). The workshop also aimed to establish priorities for future research. Dietary intake of ALA has been associated with a beneficial effect on CHD; however, the results from studies investigating the effects of ALA supplementation on CHD risk factors have proved equivocal. The studies presented as part of the present workshop suggested little, if any, benefit of ALA, relative to linoleic acid, on risk factors for cardiovascular disease; the effects observed with fish-oil supplementation were not replicated by ALA supplementation. There is a need, therefore, to first prove the efficacy of ALA supplementation on cardiovascular disease, before further investigating effects on cardiovascular risk factors. The workshop considered that a beneficial effect of ALA on the secondary prevention of CHD still needed to be established, and there was no reason to look further at existing CHD risk factors in relation to ALA supplementation. The workshop also highlighted the possibility of feeding livestock ALA-rich oils to provide a means of increasing the dietary intake in human consumers of EPA and DHA.

Effect of cation-anion balance in feed on urine pH in rabbits in comparison with other species

Journal of Animal Physiology and Animal Nutrition, 2017

In the present investigation, the impact of diet composition on urine pH in rabbits was compared with previous studies on rabbits, cats, dogs, pigs and horses. A total of 13 dwarf rabbits were fed six different diets with a cation-anion balance (CAB) between À39 and +320 mmol/kg dry matter (DM) using ammonium chloride (NH 4 Cl) as an acidifier. CAB was calculated as follows: CAB (mmol/kg DM) = 49.9*Ca + 82.3*Mg + 43.5*Na + 25.6*K À 59*P À 62.4*S À 28.2*Cl; minerals in g/kg DM. Urine, faeces and blood were collected. Urine pH ranged from 5.26 AE 0.22 at a CAB of À39 mmol/kg DM to 8.56 AE 0.24 at a CAB of +320 mmol/kg DM. A low CAB in the feed reduced blood pH and blood base excess significantly. Renal excretion of Ca, P, Na and Mg and water was significantly higher in rabbits eating acidifying diets. In comparison with other species, rabbits reacted to acidifying diets in a similar way as cats, dogs and pigs. Rabbits on a mildly alkalizing diet, however, had a trend to higher urine pH than other monogastric species on such diets (cats, dogs, pigs, horses).

Acid Balance, Dietary Acid Load, and Bone Effects—A Controversial Subject

Nutrients, 2018

Modern Western diets, with higher contents of animal compared to fruits and vegetable products, have a greater content of acid precursors vs. base precursors, which results in a net acid load to the body. To prevent inexorable accumulation of acid in the body and progressively increasing degrees of metabolic acidosis, the body has multiple systems to buffer and titrate acid, including bone which contains large quantities of alkaline salts of calcium. Both in vitro and in vivo studies in animals and humans suggest that bone base helps neutralize part of the dietary net acid load. This raises the question of whether decades of eating a high acid diet might contribute to the loss of bone mass in osteoporosis. If this idea is true, then additional alkali ingestion in the form of net base-producing foods or alkalinizing salts could potentially prevent this acid-related loss of bone. Presently, data exists that support both the proponents as well as the opponents of this hypothesis. Recent literature reviews have tended to support either one side or the other. Assuming that the data cited by both sides is correct, we suggest a way to reconcile the discordant findings. This overview will first discuss dietary acids and bases and the idea of changes in acid balance with increasing age, then review the evidence for and against the usefulness of alkali therapy as a treatment for osteoporosis, and finally suggest a way of reconciling these two opposing points of view.

Metabolic acidosis and its association with nutritional status in hemodialysis

Jornal Brasileiro de Nefrologia, 2015

Metabolic acidosis is a common problem in dialysis patients and plays an important role in the pathogenesis of protein-energy malnutrition in these patients. Objectives: To assess the prevalence of metabolic acidosis in hemodialysis and search their association with nutritional status. Methods: A cross-sectional study was performed in hemodialysis patients at a single center. Nutritional status was assessed by anthropometric, biochemical and multifrequency bioelectrical impedance analysis. Metabolic acidosis was defined as serum bicarbonate (BIC) < 22 mEq/L and patients were divided into 3 groups according to BIC (< 15.15 to 21.9 and ≥ 22). The association between BIC and continuous variables was investigated using the Kruskal Wallis test. The linear correlation between BIC and the variables of the study was also tested. Results: We studied 95 patients, 59% male, mean age 52.3 years. The prevalence of metabolic acidosis was 94.7%. BMI, interdialytic weight gain and PTH were significantly different among the 3 groups of BIC. The BIC was negatively correlated with urea, phosphorus and interdialytic weight gain. There was no significant correlation with albumin, phase angle and lean body mass index. Conclusion: The prevalence of metabolic acidosis was high in this population, and a lower BIC correlated with higher levels of urea, PTH, phosphorus, interdialytic weight gain and lower BMI. The evaluation of acid-basic status should be routinely implemented in dialysis patients by considering the negative effects of acidosis on the nutritional status, inflammation and bone disease.

Study on Acid-Base Balance Disorders and the Relationship Between Its Parameters and Creatinine Clearance in Patients with Chronic Renal Failure

Nephro-Urology Monthly, 2020

Objectives: We aimed to determine the parameters of acid-base balance in patients with chronic renal failure (CRF) and the relationship between the parameters evaluating acid-base balance and creatinine clearance. Methods: The current cross-sectional study was conducted on 300 patients with CRF (180 males and 120 females). Clinical examination and blood tests by taking an arterial blood sample for blood gas measurement as well as venous blood for biochemical tests to select study participants were performed. Results: Patients with CRF in the metabolic acidosis group accounted for 74%, other types of disorders were less common. The average pH, PCO2, HCO3, tCO2 and BE of the patient group were 7.35 ± 0.09, 34.28 ± 6.92 mmHg, 20.18 ± 6.06 mmol/L, 21.47 ± 6.48 mmHg and-4.72 ± 6.61 mmol/L respectively. These parameters are lower than normal values and decrease by progressing chronic kidney disease (CKD) stage. These parameters correlated moderately with creatinine clearance. Conclusions: In patients with CRF, metabolic acidosis is predominant, and acid-base balance parameters are positively correlated with creatinine clearance.

Role of the Kidney in Acid Base Balance

2019

Non-volatile acids including lactic acid and pyruvic acid, hydrochloric acid, sulphuric acid and phosphoric acid are produced during metabolic process.About50-150Eq of inorganic acid are flashed out through kidney in 24 hours. These acids are partially buffered with cations ,large amount of sodium in the distal tubules of the kidney some of the cations get reabsorbed and PH of the URINE falls .Kidney can buffer acids and conserve fixed bases in the production of ammonia from amino acid. It plays role to neutralize acids when they are formed in excess .In kidney disease ,tubular reabsorption of sodium in exchange for hydrogen and there occurs excessive retention of phosphates and sulphates .As acidosis takes place. It means it causes renal diseases, poisoning by an acid salt, and excessive loss of intestinal fluid and excessive losses of electrolyte.

Clinical review: Renal tubular acidosis--a physicochemical approach

Critical care (London, England), 2005

The Canadian physiologist PA Stewart advanced the theory that the proton concentration, and hence pH, in any compartment is dependent on the charges of fully ionized and partly ionized species, and on the prevailing CO2 tension, all of which he dubbed independent variables. Because the kidneys regulate the concentrations of the most important fully ionized species ([K+], [Na+], and [Cl-]) but neither CO2 nor weak acids, the implication is that it should be possible to ascertain the renal contribution to acid-base homeostasis based on the excretion of these ions. One further corollary of Stewart's theory is that, because pH is solely dependent on the named independent variables, transport of protons to and from a compartment by itself will not influence pH. This is apparently in great contrast to models of proton pumps and bicarbonate transporters currently being examined in great molecular detail. Failure of these pumps and cotransporters is at the root of disorders called renal...

Treatment of Metabolic Acidosis in Patients With CKD

American Journal of Kidney Diseases, 2014

Metabolic acidosis is a common complication of chronic kidney disease and is believed to contribute to a number of sequelae, including bone disease, altered protein metabolism, skeletal muscle wasting, and progressive glomerular filtration rate loss. Small trials in animal models and humans suggest a role for alkali therapy to lessen these complications. Recent studies support this notion, although more definitive evidence is needed on the long-term benefits of alkali therapy and the optimal serum bicarbonate level. The role of dietary modification also should be given greater consideration. In addition, potential adverse effects of alkali treatment must be taken into consideration, including sodium retention and the theoretical concern of promoting vascular calcification. This teaching case summarizes the rationale for and benefits and complications of base therapy in patients with chronic kidney disease.

Diagnosing metabolic acidosis in chronic kidney disease: importance of blood pH and serum anion gap

Kidney Research and Clinical Practice, 2022

Metabolic acidosis is one of the most common complications of chronic kidney disease (CKD). It is associated with the progression of CKD, and many other functional impairments. Until recently, only serum bicarbonate levels have been used to evaluate acid-base changes in patients with reduced kidney function. However, recent emerging evidence suggests that nephrologists should reevaluate the clinical approach for diagnosing metabolic acidosis in patients with CKD based on two perspectives; pH and anion gap. Biochemistry and physiology textbooks clearly indicate that blood pH is the most important acid-base parameter for cellular function. Therefore, it is important to determine if the prognostic impact of hypobicarbonatemia varies according to pH level. A recent cohort study of CKD patients showed that venous pH modified the association between a low bicarbonate level and the progression of CKD. Furthermore, acidosis with a high anion gap has recently been recognized as an important ...

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