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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2012  |  Volume : 23  |  Issue : 1  |  Page : 58-62
Acid-base and electrolyte disorders in patients with diabetes mellitus


Renal Department, General Hospital of Komotini, Sismanoglou 45, Komotini, Greece

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Date of Web Publication3-Jan-2012
 

   Abstract 

Diabetes mellitus is the most common metabolic disorder in the community. The diabetics may suffer from acid-base and electrolyte disorders due to complications of diabetes mellitus and the medication they receive. In this study, acid-base and electrolyte disorders were evaluated among outpatient diabetics in our hospital. The study consisted of patients with diabetes mellitus who visited the hospital as outpatients between the period January 1, 2004 to December 31, 2006. The patients' medical history, age and type of diabetes were noted, including whether they were taking diuretics and calcium channel blockers or not. Serum creatinine, proteins, sodium, potassium and chloride and blood gases were measured in all patients. Proteinuria was measured by 24-h urine collection. Two hundred and ten patients were divided in three groups based on the serum creatinine. Group A consisted of 114 patients that had serum creatinine <1.2 mg/dL, group B consisted of 69 patients that had serum creatinine ranging from 1.3 to 3 mg/dL and group C consisted of 27 patients with serum creatinine >3.1 mg/dL. Of the 210 patients, 176 had an acid-base disorder. The most common disorder noted in group A was metabolic alkalosis. In groups B and C, the common disorders were metabolic acidosis and alkalosis, and metabolic acidosis, respectively. The most common electrolyte disorders were hypernatremia (especially in groups A and B), hyponatremia (group C) and hyperkalemia (especially in groups B and C). It is concluded that: (a) in diabetic outpatients, acid-base and electrolyte disorders occurred often even if the renal function is normal, (b) the most common disorders are metabolic alkalosis and metabolic acidosis (the frequency increases with the deterioration of the renal function) and (c) the common electrolyte disorders are hypernatremia and hypokalemia.

How to cite this article:
Sotirakopoulos N, Kalogiannidou I, Tersi M, Armentzioiou K, Sivridis D, Mavromatidis K. Acid-base and electrolyte disorders in patients with diabetes mellitus. Saudi J Kidney Dis Transpl 2012;23:58-62

How to cite this URL:
Sotirakopoulos N, Kalogiannidou I, Tersi M, Armentzioiou K, Sivridis D, Mavromatidis K. Acid-base and electrolyte disorders in patients with diabetes mellitus. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2019 Jul 22];23:58-62. Available from: http://www.sjkdt.org/text.asp?2012/23/1/58/91302

   Introduction Top


The incidence of diabetes mellitus in the community is 5-10%. [1],[2],[3],[4] Diabetes mellitus damages every organ in the body, mainly the kidneys, leading to end-stage renal disease (ESRD). [5],[6],[7],[8] The patients suffering from diabetes mellitus have disturbances in the electrolytes and in the acid-base balance. These disturbances are caused by the diabetes (glucose balance), renal diseases and medications (diuretics and calcium channel blockers). [9],[10] In this study, we investigated the disturbances of electrolytes and acid-base balance in diabetic outpatients.


   Patients and Methods Top


In this prospective study, patients with diabetes mellitus who visited our hospital for hypertension and renal diseases for three years (from January 1, 2004 to December 31, 2006) as outpatients were included. We recorded the medical history, age of the patients and type of diabetes (type 1 or 2) and whether they were taking diuretics and calcium channel blockers. The serum creatinine, proteins, albumin, potassium, sodium, chloride, the protein in 24-h urine collection and the blood gases were determined.

The presence of more than 250 mg of protein per 24-h urine collection was characterized as proteinuria and the presence of total serum protein less than 6.0 mg/dL or serum albumin less than 2.5 mg/dL was considered as hypoproteinemia.

The blood gases were evaluated by the same investigator (KM) combined with the medical history, clinical signs and serum electrolytes and lactates. The serum electrolytes were determined by an ion selective electrode analyzer serum creatinine and serum proteins by an auto-analyzer and the blood gases and lactate by the analyzer, GEM Primer 2000.

A t-test for non-paired observations and x 2 -test was used for the statistical analysis. Differences of more than 0.05 were considered statistically significant.


   Results Top


A total of 210 patients were included in this study (118 F, 92 M), with an age range from 31 to 89 years, and suffering from diabetes mellitus for 3-55 years. They were divided in three groups depending on the serum creatinine. The first group consisted of 114 patients (70 F, 44 M), with the age ranging from 31 to 86 years (median value 66 years), who had serum creatinine below 1.2 mg/dL (normal) (group A). The second group consisted of 69 patients (33 F, 36 M), with the age ranging from 45 to 89 years (median value 79 years), with serum creatinine from 1.3 to 3 mg/dL (group B). The third group consisted of 27 patients (15 F, 12 M), with the age ranging from 38 to 77 years (median value 68 years), who had serum creatinine more than 3.1 mg/dL (group C) [Table 1].
Table 1: Characteristics of patients of each group (age, duration of diabetes, type of diabetes, patients with hypoproteinemia or proteinuria, patients who take diuretics or calcium channel blockers).

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Eight patients from group A, six patients from group B and nine patients from group C had diabetes mellitus type 1. In group C, the relationship of number of patients with type 2 diabetes were statistically significant, compared with the number of patients in group A (p = 0.0001) and in group B (p = 0.011) [Table 1]. Hypoproteinemia was found in one patient from group A, ten in group B and five in group C, the differences of which were statistically significant between groups A and B (P = 0.0001) and between groups A and C (P = 0.0001). Forty patients from group A, 45 from group B and 14 from group C had proteinuria as defined, of which eight, 12 and 10 patients, respectively, in groups A, B and C had proteinuria in the nephrotic range. Statistically significant difference was found only between group A and B (P = 0.0001). The anion gap was high in two patients with lactic acidosis, four with ketoacidosis and five with severe chronic kidney disease (CKD). The serum lactate levels were high only in two patients with low cardiac output.

In group A, 35 patients received diuretics, 25 calcium channel blockers and seven both. In group B, 34 patients received diuretics, 28 calcium channel blockers and 12 patients received both. In group C, 12 patients received diuretics, 11 calcium channel blockers and three patients received both. In patients taking diuretics, a statistically significant difference was found only between groups A and B (P = 0.043) [Table 1].

In [Table 2], the acid-base and electrolyte disorders for every group are presented. Specifically, seven patients from group A had metabolic acidosis (simple or mixed), nine patients from group B and 17 from group C. Seventy-four patients from group A, 34 from group B and eight from group C had metabolic alkalosis (simple or mixed), respectively [Table 3]. [Table 3] shows the mean values of the acid-base parameters of each group. It was noted that as the GFR deteriorates, the pH, PaCO2 , HCO3- were reduced, but this was not to a clinically significant level.
Table 2: Acid-base and electrolyte disorders of the patients of each group.

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Table 3: Mean ± SD of pH, PaCO2 and HCO3- of the patients of each group.

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   Discussion Top


Acid-base disorders are quite common. To diagnose and adequately treat patients with acid-base disorders, we must:

  1. use the Henderson-Hasselbalch equation,
  2. take the patient's full medical history and make a thorough physical examination,
  3. estimate the anion gap,
  4. identify the primary acid-base disorder and estimate whether it is simple or mixed and
  5. estimate the urine pH and urine anion gap.
The most serious disorder of diabetes mellitus is metabolic acidosis (ketoacidosis, lactic acidosis, hyperchloremic acidosis or renal tubular acidosis). The metabolic acidosis with a high anion gap is due to an increased production and presence of b-hydroxybutyric acid, acetate or lactate, as we found in nine of our patients. Many diabetics develop CKD that is related with:

  1. a medium acidosis due to a reduction in the production of ammonium and
  2. acidosis with an increased anion gap due to withholding of non-countable anions. [11]
Nevertheless, diabetic patients could have hyperchloremic metabolic acidosis. [12] In our study, the frequency of metabolic acidosis is higher with the progression of the renal failure. Clearly, the mean pH in all the patients was not very low because of the coexisting metabolic alkalosis in 65% of the cases (74/114).

The existence of diabetic ketoacidosis combined with alkalaemia is well known. A case was reported concerning a patient with diabetic ketoacidosis combined with alkalemia. In these cases, intense vomiting caused the loss of electrolytes (K + , Na + ) and water, which lead to hypovolemia and caused the withholding of HCO3- and alkalaemia. [13] Metabolic alkalosis may occur in diabetics because of the use of diuretics and other medications that reduce the total sodium of the body and lead to hypovolemia, as we found in many of our patients, obviously because most of them were taking diuretics. Nevertheless, severe respiratory alkalosis may occur. [14] It is evident that the metabolic alkalosis improves the pH of diabetics who are expected to have metabolic acidosis because of the CKD. Nearly half the patients in every group had metabolic alkalosis (especially group C), which contributes to the restoration of the pH to normal levels as severe CKD causes metabolic acidosis and acidemia.

Elisaf et al studied 40 insulin-dependent patients with diabetic ketoacidosis and found that 21 had simple metabolic acidosis with an increased anion gap, seven had ketoacidosis with hypochloremic metabolic acidosis, nine had diabetic ketoacidosis with metabolic alkalosis and three had diabetic ketoacidosis with respiratory alkalosis. They evaluated the degree of hydration from the ratio of urea/creatinine, and calculated that hydration plays a critical role in the occurrence of mixed acid-base disorders. [15] We also reached the same conclusions because many of our patients had metabolic alkalosis due to hypovolemia from the use of diuretics.

What are the consequences of the acid-base disorders in diabetic patients? The academia suggests that pH <7.1-7.2 reduces myocardial contractility, predisposes patients to cardiac arrhythmias, causes vascular constriction and may reduce peripheral vascular resistance, blood pressure, hepatic blood flow and tissue oxygen release. These changes contribute to increased mortality and morbidity. [16] Our patients usually had mixed acid-base disorders, where one of them neutralizes the other, which is very important to protect the patient from intense pH changes, particularly in those cases with severe CKD.

The total potassium of the body in insulin-dependent patients and in non-insulin-dependent patients and in non-insulin-dependent patients is reduced during periods of poor control of diabetes mellitus and increases when the blood glucose levels are normal. [17] The levels of potassium were reduced because of diuretics [9] as well as due to diabetic ketoacidosis (increased loss in urine). This explains the existence of hypovolemia in these patients. We verified the presence of hyperkalemia because of the reason mentioned above, and because the metabolic acidosis can occur frequently.

Diabetics usually take medication that influences the electrolyte balance. Thus, loop diuretics and thiazides may cause hyponatremia, hypokalemia and deficiency of magnesium, disturbances in calcium handling (increased renal loss with loop diuretics and reabsorption by thiazides) and hyperglycemia. Potassium-sparing diuretics may cause hyperkalemia and calcium channel blockers may disturb the metabolism of carbohydrates in diabetics. [9] In our patients, electrolyte disorders were mainly due to diuretic consumption, acid-base disorders and uncontrolled diabetes mellitus.

It is concluded that:

  1. disturbances of the acid-base balance are common in diabetics,
  2. more common are metabolic disorders (mainly simple metabolic alkalosis),
  3. metabolic alkalosis contributes to the restoration of pH to normal levels and, finally,
  4. the most common electrolyte disorders are hyperkalemia and hypernatremia.


 
   References Top

1.Garancini MP, Calori G, Ruotolo G, et al. Prevalence of NIDDM and impaired glucose tolerance in Italy: an OGTT-based population study. Diabetologia 1995;38(3):306-13.  Back to cited text no. 1
    
2.Harris MI, Flegal KM, Cowie CC, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes care 1998;21(4):518-24.  Back to cited text no. 2
    
3.Onkamo P, Väänänen S, Karvonen M, Tuomilehto J. Worldwide increase in incidence of type I diabetes-the analysis of the data on published incidence trends. Diabetologia 1999;42(12):1395-403.  Back to cited text no. 3
    
4.Fagot-Campagna A, Pettitt DJ, Engelgau MM, et al. Type 2 diabetes among North American children and adolescents: an epidemiologic review and a public health perspective. J Pediatr 2000;136(5):664-72.  Back to cited text no. 4
    
5.Bojestig M, Arnqvist HJ, Hermansson G, Karlberg BE, Ludvigsson J. Declining incidence of nephropathy in insulin-dependent diabetes mellitus. N Engl J Med 1994;330(1):15-8.  Back to cited text no. 5
    
6.Frei U, Schober-Halstenberg HJ. Annual Report of the German Renal Registry 1998. QuaSi-Niere Task Group for Quality Assurance in Renal Replacement Therapy. Nephrol Dial Transplant 1999;14(5):1085-90.  Back to cited text no. 6
    
7.Amenábar JJ, Garcva-Lapez F, Robles NR, et al. 1997 Spanish nephrology association (Sociedad Espaòola de nefrologia) report on dialysis and transplantation. Nephrol Dial Transplant 1999; 14(12):2841-5.  Back to cited text no. 7
    
8.American Diabetes Association: Position statement: Diabetic nephropathy. Diabetes Care 1999; 22(Suppl 1):S66-9.  Back to cited text no. 8
    
9.Zawada ET Jr. Metabolic considerations in the approach to diabetic hypertensive patients. Am J Med 1989;87(6A):S34-8.  Back to cited text no. 9
    
10.Patel KP, Zhang PL, Zeigler DW, Kauker ML. Renal response to volume expansion in streptozotocin-induced diabetic rats: influence of calcium channel blockade. Diabetes Res Clin Pract 1997;35(2-3):69-74.  Back to cited text no. 10
    
11.Ishihara K, Szerlip HM. Anion gap acidosis. Semin Nephrol 1998;18:83-97.  Back to cited text no. 11
    
12.Yoshimi T. Acid-base balance disorder in various diseases-diabetes mellitus. Nippon Rinsho 1992; 50(9):2206-12.  Back to cited text no. 12
    
13.Sanders G, Boyle G, Hunter S, Poffenbarger PL. Mixed acid-base abnormalities in diabetes. Diabetes Care 1978;1(6):362-4.  Back to cited text no. 13
    
14.Goldman JM, Chiriboga M. Diabetic ketoacidosis with alkalemia. J Emerg Med 1989;7 (4):369-72.  Back to cited text no. 14
    
15.Elisaf MS, Tsatsoulis AA, Katopodis KP, Siamopoulos KC. Acid-base and electrolyte disturbances in patients with diabetic ketoacidosis. Diabetes Res Clin Pract 1996;34(1):23-7.  Back to cited text no. 15
    
16.Kraut JA, Kurtz I. Use of base in the treatment of severe acidemic states. Am J Kidney Dis 2001;38(4):703-27.  Back to cited text no. 16
    
17.Walsh CH, Soler NG, James H, et al. Studies in whole body potassium and whole body nitrogen in newly diagnosed diabetics. Q J Med 1976;45 (178):295-301.  Back to cited text no. 17
    

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Correspondence Address:
Konstantinos Mavromatidis
Nephrologist, Director of Renal Department, General Hospital of Komotini, Ant. Rossidi 11, N. Mosinoupoli - 69100, Komotini
Greece
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PMID: 22237220

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