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Volume: 16 Issue: 6 December 2018

FULL TEXT

CASE REPORT
Hyperventilation Syndrome and Sustained Hyperchloremia After Kidney Transplant: Time-Sequence Swing of Acid-Base Interpretation

An interaction between regained renal function in a transplanted kidney and hyperventilation syndrome may interfere with correct diagnosis of acid-base status in patients with preoperative nongap acidosis. Here, we present a patient with glomerular nephritis and hyperchloremia who underwent kidney transplant. Progressively increasing bicarbonate reabsorption by the renal graft, which thereby changed the arterial carbon dioxide tension-to-bicarbonate ratio, resulted in a time-sequence swing of an acid-base interpretation despite persistent mixed respiratory alkalosis due to hyperventilation syndrome and nongap metabolic acidosis due to preexisting hyperchloremia. Specifically, the sequence was mixed primary metabolic acidosis and primary respiratory acidosis immediately after surgery, primary metabolic acidosis and secondary respiratory alkalosis on postoperative days 1 and 2, mixed primary hyperchloremic metabolic acidosis and primary respiratory alkalosis on postoperative day 3, and finally primary respiratory alkalosis and secondary hyperchloremic metabolic acidosis on postoperative day 7. This swing in the acid-base interpretation indicates that the acid-base imbalance described here does not fit the empirical relationship for calculating the expected bicarbonate or carbon dioxide tension value, suggesting that “correct” interpretation of acid-base status may not lead to “correct” diagnosis of acid-base status. It should be remembered that not every acid-base imbalance fits the empirical relationship.


Key words : Acid-base imbalance, Metabolic acidosis, Renal transplantation

Introduction

Hyperchloremia has been reported in 46% of patients with chronic kidney disease1 and is related to 43.2% of cases of metabolic acidosis in chronic kidney disease.2 Hyperchloremia is usually expected to return to normal soon after kidney transplant if the transplanted graft functions well and renal tubular acidosis does not occur. Here, we present a patient with hyperventilation syndrome who had sustained preexisting hyperchloremia after kidney transplant. An interaction between regained function of the renal graft and concurrent hyperventilation syndrome in this patient with hyperchloremic metabolic acidosis resulted in a time-sequence swing of acid-base interpretation by changing the arterial carbon dioxide tension-to-bicarbonate ratio, despite persistent hyperventilation and hyperchloremic acidosis. The interpretation of acid-base status did not fit the empirical relationship for calculating the expected bicarbonate or arterial carbon dioxide tension values.

Case Report

A 35-year-old man with a 6-year history of glomerular nephritis presented to us for kidney transplant. He otherwise had no remarkable medical history and had not required renal replacement therapy. Reported daily urine output was approximately 1100 to 1300 mL until kidney transplant. His laboratory findings over the previous 6 months were as follows: serum sodium of 143 to 145 mEq/L, chloride of 114 to 120 mEq/L, and potassium of 5 to 6.2 mEq/L. On the day before surgery, serum sodium was 141 mEq/L, potassium was 4.2 mEq/L, chloride was 120 mEq/L, and albumin was 3.89 g/dL. His glomerular filtration rate using the Modification of Diet in Renal Disease formula was 7.01 mL/min/1.73 m2, and his serum creatinine level was 8.79 mg/dL. Intraoperative serum electrolyte levels and acid-base status were as follows: 142 mEq/L sodium, 3.5 mEq/L potassium, 15.4 mEq/L bicarbonate, pH 7.29, and arterial carbon dioxide tension of 32 mm Hg. Anesthesia and surgery procedures were uneventful.

The function of the transplanted graft appeared to be adequate and showed decreasing serum creatinine levels (Table 1) and proper urine output (approximately 3440-5450 mL/day) postoperatively. However, chloride levels were not decreasing. During this time, 0.45% saline at 3000 to 5000 mL, 5% dextrose in water at 500 to 1300 mL, and potassium chloride were infused daily from the day of surgery until postoperative day (POD) 6 to replace the brisk urinary loss according to our institution’s protocol. Interestingly, hyperchloremia persisted even after blood pH levels had returned to normal. His arterial blood-gas analyses revealed complex changes in acid-base status. Specifically, the time sequence was as follows: mixed acid-base disorder (primary metabolic acidosis and primary respiratory acidosis) or partly compensated metabolic acidosis owing to insufficient time elapse at 1 hour after surgery (anion gap corrected for albumin 3.43 g/dL and delta gap indicated that the patient had mixed high anion gap and nongap acidosis); primary metabolic acidosis and secondary respiratory alkalosis on POD1 and POD2; mixed primary hyperchloremic metabolic acidosis and primary respiratory alkalosis on POD3; and finally primary respiratory alkalosis and secondary hyperchloremic metabolic acidosis on POD7. Urine anion gap (urine sodium 90 mEq/L, potassium 3.9 mEq/L, and chloride 93 mEq/L) and urine osmolal gap (measured osmolality of 274 mOsm/kg and calculated osmolality of 243.8 mOsm/kg, urine urea nitrogen level of 155.3 mg/dL, and urine glucose of 10 mg/dL) with urine pH 6.0 were tested and confirmed presence of impaired renal acidification, which was consistent with the inhibitory effect of hypocapnia on renal acid excretion.

To investigate the cause of hypocapnia, we reevaluated the patient. On an examination that focused on the sustained hyperventilation, history and physical findings excluded organic causes. Leukocytosis (18 100/μL immediately after surgery that decreased to approximately 9700/μL [normal level is < 8000/μL]) continued for 11 days post­operatively without fever. However, C-reactive protein values (ranging from 0.08 to 0.44 mg/dL, normal level is < 0.50 mg/dL) were in the normal range. His daily chest radiographs did not reveal any region of pneumonic consolidation or atelectasis during the postoperative course. He denied an anxiety or fear about the outcome of the kidney transplant, and his breathing was calm, without assertion of dyspnea or other discomforts related to hyperventilation. Reassurance of the patient in an attempt to alleviate distress was not effective for hyperchloremia. The patient recovered from hyperventilation spontaneously, and hyperchloremia disappeared on POD13.

Discussion

Because anxiety and fear are common peri­operatively and may mask psychologic factors, these should be suspected as causes of sustained hyperventilation after exclusion of organic causes. Anxiety disorder or other psychologic factors may induce hyperventilation syndrome. In our patient, underlying anxiety, fear, or stress regarding the outcomes of kidney transplant may have persisted throughout his perioperative period, inducing the hyperventilation syndrome. Indeed, hyperventilation syndrome is a common expression of anxiety and stress.3 We inferred that hyperventilation syndrome-induced hypocapnia interfered with recovery from hyperchloremia.

The underlying pathophysiology of the acid-base status in our case was hyperchloremia of chronic kidney disease compounded by hyperventilation syndrome after kidney transplant. Hypocapnia was relatively constant owing to hyperventilation syndrome; therefore, the respiratory alkalosis may have been primary throughout the postoperative course and the hyperchloremic metabolic acidosis may have been primary because of preexisting hyperchloremia. The renal compensation process was functioning because the graft had regained the ability to acidify urine, as the inhibitory effects of hypocapnia on renal acidification are transient.4 As a result, plasma bicarbonate levels increased progressively. This increased bicarbonate reabsorption thus changed the arterial carbon dioxide tension-to-bicarbonate ratio over a period despite hypocapnia. With this mechanism, the interpretation of acid-base status using the arterial carbon dioxide tension-to-bicarbonate ratio led to the swing in metabolic and respiratory acid-base status, in the face of persistence of both hypocapnia and hyperchloremic metabolic acidosis (ie, mixed primary respiratory alkalosis and primary metabolic acidosis) in the patient. However, both the respiratory alkalosis and the hyperchloremic metabolic acidosis could not be observed as primary until POD3 because we regarded the respiratory acid-base status as secondary respiratory alkalosis. This time-sequence swing of interpretation is rare in a patient who has no change in pathophysiology. This swing of interpretation indicates that the acid-base imbalance of our case did not fit the empirical relationship for calculating the expected bicarbonate or carbon dioxide tension values.

It is worth noting that 0.45% saline and 5% dextrose in water for replacement of urinary sodium and the fluid loss did not influence postoperative hyperchloremia. The sodium content of urine is assumed to be similar to that of 0.45% saline, and thus replacing urine volume with 0.45% saline would not attenuate hyperchloremia in postrenal transplant patients. Moreover, by inducing chloride/bicarbonate exchange in distal tubules, as in patients with distal renal tubular acidosis,5 hypocapnia, as expected, decreased bicarbonate in exchange for chloride, leading to chloride retention even though 5% dextrose in water was added. Therefore, hypotonic saline would not improve hyperchloremia in cases of hypocapnia if urine flow is adequate to exchange the electrolytes.

Serum chloride levels have been shown to be inversely correlated with blood pH.5 Blood pH would be expected to determine chloride levels. However, in our patient, chloride levels remained high despite improved blood pH. In addition, the disappearance of hyperchloremia coincided with normalization of arterial carbon dioxide tension in our case. As a result, the chloride levels appeared to be more related to arterial carbon dioxide tension levels than pH. Inhibition of renal H+-ATPase and H+-K+-ATPase by hypocapnia6 may explain our observation.

In conclusion, our case suggests that “correct” interpretation of blood-gas levels may not lead to “correct” diagnosis of acid-base imbalance. It should be remembered that not every acid-base imbalance fits the empirical relationship. The time-sequence interaction between regained function of the renal graft and concurrent hyperventilation syndrome in the presence of preexisting hyperchloremic acidosis adds a caveat in the diagnosis of an acid-base status.


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Volume : 16
Issue : 6
Pages : 754 - 756
DOI : 10.6002/ect.2018.0099


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From the Department of Anesthesiology and Pain Medicine, Yeungnam University Hospital, Daegu, Korea
Acknowledgements: The authors have no sources of funding for this study and have no conflicts of interest to declare.
Corresponding author: Daelim Jee, Department of Anesthesiology and Pain Medicine, Yeungnam University College of Medicine, 170 Hyeonchung-ro, Nam-gu, Daegu 705-717, Korea
Phone: +82 53 620 3364
E-mail: dljee@ynu.ac.kr