Table of Contents  
ORIGINAL ARTICLE
Year : 2016  |  Volume : 9  |  Issue : 6  |  Page : 716-720  

Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India


1 Department of Nephrology, Dr. D. Y. Patil Medical College, Hospital and Research Centre; Department of Nephrology, Hemodialysis Unit, Oyster and Pearl Tulip Hospital, Pune, Maharashtra, India
2 Department of Nephrology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pune, Maharashtra, India

Date of Web Publication16-Nov-2016

Correspondence Address:
Jayraj S Korpe
Department of Nephrology, Dr. D. Y. Patil Medical College, Hospital and Research Centre, Pimpri, Pune - 411 018, Maharashtra
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.194189

Rights and Permissions
  Abstract 

Aim: Metabolic acidosis is a feature of chronic kidney disease (CKD) due to the reduced capacity of the kidney to synthesize ammonia and excrete hydrogen ions. Among the many goals of hemodialysis (HD), the role in correction of metabolic acidosis is an important one. To assess the prevalence and severity of metabolic acidosis in the Indian patients of CKD, who are on maintenance HD (MHD). Methods: This is a cross-sectional study on 35 patients conducted at two centers in Western part of India. The demographic, clinical, and laboratory assessments were done on chronic stable patients receiving MHD. The prevalence and severity of metabolic acidosis were evaluated. Results: Metabolic acidosis was found in 22 out of 35 patients (62.85%), with mean predialysis serum pH and HCO3 of 7.32 ± 0.083 and 20.37 ± 4.94 mmol/L, respectively. Conclusion: Metabolic acidosis is significantly prevalent in patients on MHD in India.

Keywords: Hemodialysis, metabolic acidosis, prevalence


How to cite this article:
Sajgure AD, Dighe TA, Korpe JS, Bale CB, Sharma AO, Shinde NS, Goel AA, Mulay AV. Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India. Med J DY Patil Univ 2016;9:716-20

How to cite this URL:
Sajgure AD, Dighe TA, Korpe JS, Bale CB, Sharma AO, Shinde NS, Goel AA, Mulay AV. Prevalence and severity of metabolic acidosis in patients on maintenance hemodialysis in India. Med J DY Patil Univ [serial online] 2016 [cited 2024 Mar 28];9:716-20. Available from: https://journals.lww.com/mjdy/pages/default.aspx/text.asp?2016/9/6/716/194189


  Introduction Top


Metabolic acidosis is a feature of chronic kidney disease (CKD) due to the reduced capacity of the kidney to synthesize ammonia and excrete hydrogen ions. [1],[2] It has two major consequences in this patient population: It can result in the consumption of bone buffers, affect bone metabolism and has a negative effect on nitrogen balance and protein metabolism independent of uremia, leading to the development of a catabolic state. [3] Among the many goals of hemodialysis (HD), the role in correction of metabolic acidosis is an important one. [4] With the advent of various clinical trials and guidelines, it has been widely accepted and agreed on that correction of metabolic acidosis should be an important goal of both the conservative management of CKD and in dialysis therapy. [5] The prevalence and severity of metabolic acidosis have not been assessed in the Indian CKD population on maintenance HD (MHD).


  Methods Top


This is a cross-sectional study conducted on 35 patients at two centers in Western part of India. The patients were diagnosed as CKD in accordance with (Kidney Disease Improving Global Outcomes [KDIGO] 2012), [6] who were receiving outpatient MHD, for more than 1 month were included whereas those with any acute illness were excluded from this study.

After procuring the consent for participation, the data on demographics, comorbid conditions, HD schedule, and medications was documented. The Fresenius machines (4008S and 4008B) with a standard bicarbonate dialysate concentration of 35 mmol/L were used for HD. Each session was of 4 h with a blood flow rate (BFR) of 300-400 ml/min and a dialysate flow rate (DFR) of 500 ml/min. Most 29 out of 35 patients (82.9%) were on twice weekly MHD schedule. The laboratory investigations including hemogram, venous blood gas, urea, creatinine renal function test (RFT) and serum electrolytes, serum total protein, and albumin was carried out in the mid-week dialysis session before dialysis. RFT was done both before and after HD (pre- and post-HD). Metabolic acidosis in these subjects was defined as a predialysis serum bicarbonate level of <22 mmol/L, in accordance with the KDIGO guidelines (2012). [6]


  Results Top


The mean age of the study population was 47.54 ± 13.71 years, age wise distribution of cases as shown in [Table 1]. Twenty-seven of 35 cases (77.1%) were male and the rest were female, with a male: female ratio of 3.3. The mean duration of MHD was 18 ± 16.68 months, 6 out of 35 (17.1%) cases were on MHD for more than 24 months, 9 of 35 (25.7%) for 18-24 months and 20 (57.2%) were on MHD for <12 months as shown in [Table 2]. Twenty-nine out of 35 (82.9%) were on twice a week dialysis schedule, 4 of 35 (11.4%) cases were on once a week dialysis and 2 of 35 (5.7%) were on thrice a week dialysis schedule. The access for HD was arteriovenous fistula in 29 of 35 (82.9%) cases and permanent cuffed tunneled catheter in 6 of 35 (17.1%) cases.
Table 1: Age - wise distribution of cases


Click here to view
Table 2: Demographic data of cases in the cohort


Click here to view


Chronic tubule-interstitial disease in 13 out of 35 (37.1%) cases followed by diabetic nephropathy in 9 of 35 (25.7%) cases was among the most common causes of CKD in this cohort as shown in Graph 1. The study population had a mean pre- and post-HD serum creatinine of 8.21 ± 2.79 and 3.90 ± 2.14 mg%, respectively. The mean pre- and post-HD blood urea was 101.94 ± 27.04 and 37.23 ± 18.50 mg%, respectively as shown below in [Table 3]. The mean calculated urea reduction ratio (URR) and estimated Kt/V was 62.85 ± 15.74 and 1.17 ± 0.40, respectively.



Metabolic acidosis was found in 22 out of 35 patients (62.85%), as shown in [Table 4]. The mean value of serum pH and HCO 3 of this cohort was 7.32 ± 0.083 and 20.37 ± 4.94 mmol/L, respectively as shown in [Table 5].
Table 3: Clinical profile and laboratory investigations of the cohort


Click here to view
Table 4: The venous blood gasses of cohort


Click here to view
Table 5: Patients having metabolic acidosis


Click here to view



  Discussion Top


The prevalence and severity of metabolic acidosis in CKD progressively rises as glomerular filtration rate (GFR) falls. Adaptations in acid excretion by the kidneys initially prevent a fall in serum bicarbonate concentration, but as GFR continues to decline below 40 ml/min/1.73 m 2 , metabolic acidosis commonly develops. Serum bicarbonate concentrations <22 mmol/L are associated with increased risk of CKD progression and increased risk of death. [6] In India, till date no such study on metabolic acidosis has been reported. This study was, therefore, undertaken to assess the prevalence and severity of metabolic acidosis in CKD patients who are on MHD.

Metabolic acidosis was found in 22 out of 35 patients (62.85%) in the present cohort, with the mean value of pre-HD serum pH and HCO 3 of 7.32 ± 0.083 and 20.37 ± 4.94 mmol/L, respectively as shown in [Table 4] and [Table 5]. This denotes that metabolic acidosis is significantly prevalent in the CKD patients who are on regular MHD.

The KDIGO CKD Work Group, in (2012) [6] published the clinical practice guidelines for the evaluation and management of CKD. Accordingly, as mentioned in the Guideline 3.4.1, "We suggest that in people with CKD and serum bicarbonate concentrations <22 mmol/L treatment with oral bicarbonate supplementation be given to maintain serum bicarbonate within the normal range, unless contraindicated." (Level 2, Grade B: To be interpreted as "Suggest" with "Moderate" quality of evidence). Although in the general summary of (KDIGO 2012), [6] it has been mentioned that the target population for the above-mentioned guideline is all people identified with CKD who are not on renal replacement therapy, certain previous studies show that uremic acidosis causes an increase in protein degradation. It has also been mentioned in the previous Kidney Disease Outcomes Quality Initiative (2002) [7] Clinical practice guidelines for CKD: Evaluation, classification, and stratification: Which states that the serum bicarbonate concentration as a measure of acid-base balance has been used to assess malnutrition in CKD.

Oettinger and Oliver, [4] noted that metabolic acidosis is common in patients with chronic renal failure because of the inability of the kidneys to excrete the nonvolatile acid load. One of the many goals of HD, the role in correction of uremic acidosis was being speculated. It was noted that despite adequate hours of HD, metabolic acidosis remains common and is reported in up to 75% of patients. The acid-base and biochemical effect of a high bicarbonate (42 mEq/L) dialysate was evaluated in 38 patients during high efficiency and high-flux dialysis over 12 weeks. The degree of acidosis present in dialysis patients can vary widely in severity depending on the length of each dialysis treatment, protein intake, frequency of dialysis treatments, and the type of buffer present in the dialysate. Persistent metabolic acidosis can have adverse consequences on bone metabolism and formation. Oettinger and Oliver [4] concluded that a high bicarbonate dialysate corrects predialysis acidosis in 75% of HD patients without causing progressive alkalemia, hypoxia, or hypercarbia with no change in the predialysis blood urea nitrogen, calcium, or phosphorus.

The prevalence and causes of metabolic acidosis in patients of CKD on MHD were studied in depth by Sepandj et al. [8] Stable patients on MHD for at least 4 months without any severe illness within the preceding 4 months were selected. All patients received HD using cellulose acetate membranes (surface area, 1.3-2.1 m 2 ), BFR of 250 and 350 ml/min, DFR of 500 ml/min, and standard bicarbonate dialysate (36 mEq/L) with 3-5 h three times weekly sessions, to achieve a goal urea reduction of at least 60%. The presence of metabolic acidosis was arbitrarily defined as mean monthly serum bicarbonate of <21 mEq/L over 4 months, drawn after the longest interdialytic period. Out of the total 70 patients, 20 patients (28%) had mean predialysis serum bicarbonate <21 mEq/L. They concluded that the prevalence of metabolic acidosis could be minimized with the adequacy of dialysis. Those patients with higher daily acid production, the rational way to correct metabolic acidosis would be to determine and rectify the underlying metabolic problem. However, when this is not possible, increasing the dialysate bicarbonate and therefore increasing the diffusive gradient would potentially be the most efficient manner when otherwise adequate dialysis is delivered.

Yang et al., [9] from China, undertook a study to assess metabolic acidosis in 28 anuric patients on MHD. All patients received HD three times weekly for 4 h with standard dialysate bicarbonate concentration (35 mmol/L) with 4 mmol/L of acetate, DFR of 500 ml/min and BFR 250 to 350 ml/min. The acid-base status and laboratory values before and 30 min after regular HD session were noted. Metabolic acidosis was defined as pre-HD pH <7.37 and HCO 3 <20 mmol/L. During the study, they noted that only 35.71% patients had pre-HD metabolic acidosis. They concluded that the higher protein intake was mainly responsible for metabolic acidosis in these patients rather than inadequate bicarbonate gain.

This study shows the significant prevalence of metabolic acidosis in Indian MHD patients as noted in 62.85% cases of this cohort versus 28% cases by Sepandj et al. [8] and 35.71% cases by Yang et al. [9] Primarily this could be due to the variation in the definition of metabolic acidosis in the previous studies. Furthermore, such a high prevalence of metabolic acidosis in this study could be attributed either to inadequate dialysis, poor nutrition, and/or inadequate oral bicarbonate supplementation. Due to the financial constraints, low socioeconomic status, lack of education and nonavailability of MHD center near the residence along with logistic problems, very few people in the Indian population receive adequate hours of HD that is 12 h/week or 4 h × 3 sessions of HD/week. Most of the patients in the present study received 4 h × 2 sessions of HD/week. Despite this, we noted that the mean calculated URR and estimated Kt/V of one session was 62.85 ± 15.74 and 1.17 ± 0.40, respectively. However, the weekly Kt/V would be definitely less indicating an overall inadequate dialysis.

The pathophysiological mechanisms of metabolic acidosis, the other factors responsible for the same are well-known to the medical science. The most important factor is the inadequate dialysis. Twice a week dialysis, poor compliance with dialysis treatments and medications and dialyzer reuse are responsible for inadequate dialysis in Indian dialysis centers. Improvement in the above-mentioned factors though very much desirable, is beyond the scope of medical practice in India. Dialysis adequacy assessment of one dialysis session every month as practiced in the Western countries is not sufficient to reflect the overall adequacy of dialysis in Indian population.

This prompts the need to carry out larger studies to assess and ascertain the true reasons for the high prevalence of metabolic acidosis in MHD patients in the developing countries like India and further to treat the modifiable factors, in this patient population.


  Conclusion Top


Metabolic acidosis is very common in patients on MHD in India. The study emphasizes the need of assessment of metabolic acidosis in patients of CKD, who are on MHD and to achieve a pre-HD serum bicarbonate level as close to the physiological range as possible. This may prove pivotal in improving the protein energy malnutrition and renal osteodystrophy commonly seen in MHD patients. Further studies in this regard will help in deriving the optimal dosing of oral bicarbonate supplementation in this patient population.

Limitation

Small sample size prohibiting the comprehensive multi-factorial analysis of the confounding factors is the limitation of this study. Further follow-up of these patients will give us insights about the appropriate oral sodium bicarbonate dose, nutritional status, quality of life, and outcomes in dialysis patients.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, et al. The Textbook of Harrisons Principles of Internal Medicine. 18 th ed., Vol. II. United States of America: The McGraw Hill; 2012. p. 2322-3.  Back to cited text no. 1
    
2.
Roderick PJ, Willis NS, Blakeley S, Jones C, Tomson C. Correction of chronic metabolic acidosis for chronic kidney disease patients. Cochrane Libr 2009;3:1-32.  Back to cited text no. 2
    
3.
Kopple JD, Kalantar-Zadeh K, Mehrotra R. Risks of chronic metabolic acidosis in patients with chronic kidney disease. Kidney Int Suppl 2005;95:S21-7.  Back to cited text no. 3
    
4.
Oettinger CW, Oliver JC. Normalization of uremic acidosis in hemodialysis patients with a high bicarbonate dialysate. J Am Soc Nephrol 1993;3:1804-7.  Back to cited text no. 4
    
5.
Chiu YW, Mehrotra R. What should define optimal correction of metabolic acidosis in chronic kidney disease? Semin Dial 2010;23:411-4.  Back to cited text no. 5
    
6.
Kidney Disease Improving Global Outcomes (KDIGO), CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 2013;3:1-150.  Back to cited text no. 6
    
7.
National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Am J Kidney Dis 2002;39 2 Suppl 1:S1-266.  Back to cited text no. 7
    
8.
Sepandj F, Jindal K, Kiberd B, Hirsch D. Metabolic acidosis in hemodialysis patients: A study of prevalence and factors affecting intradialytic bicarbonate gain. Artif Organs 1996;20:976-80.  Back to cited text no. 8
    
9.
Yang SS, Lin SH, Tsai WS, Juang JG, Lin YF. Evaluation of metabolic acidosis in chronic hemodialysis patients. J Med Sci 2002;22:165-70.  Back to cited text no. 9
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

Top
   
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
Abstract
Introduction
Methods
Results
Discussion
Conclusion
References
Article Tables

 Article Access Statistics
    Viewed3325    
    Printed87    
    Emailed0    
    PDF Downloaded235    
    Comments [Add]    

Recommend this journal