H Metin, E Sevinc

Abstract

Background: Acute kidney injury (AKI) which is potentially life-threatening condition. In this case, we present a case of AKI triggered by sparkling water consumption. Case: An 11-year-old male patient was admitted to the emergency department with complaints of loss of appetite, oliguria and altered level of consciousness. In his history, he had undergone tonsillectomy a week ago. It was noted that after tonsillectomy, he drank only sparkling water and energy drinks. His vital signs were tachypnea of 45 breaths/min, and increased heart rate of 140 beats/min. Initially, fluid resuscitation was performed and hypernatraemia was to be corrected within 72 hours. Renal function of the patient improved within two weeks. Conclusions: We conclude consuming sparkling water is a rare cause of AKI. Despite its rarity, paediatricians should be careful to ask about sparkling water and energy drink consumption during history taking.

Introduction

Acute kidney injury (AKI) which is potentially life-threatening condition is defined as a 50% increase in basal creatinine value or a 25% decrease in glomerular filtration rate or urine output below 0.5 ml/kg/h for at least 6 hours.¹ Considering the causes of AKI, there are sepsis, renal ischaemia and nephrotoxic drugs in developed countries. On the other hand diarrhoea, dehydration and infectious diseases are more common in underdevelop countries.² Regardless of the aetiologic agent, both the occurrence of hyperchloraemia and the presence of metabolic acidosis aggravate renal damage by causing renal vascular smooth muscle constriction.³

Once renal failure has developed, management of complications of AKI needs careful attention to electrolyte status, fluid balance, acid-base balance and nutrition.⁴ Children with AKI followed in intensive care unit can require renal replacement therapy to remove uremic toxins and maintain fluid, electrolyte and acid-base balance until renal function improves. In this case, we present a case of AKI triggered by sparkling water consumption. To our knowledge, this is the first report revealing that sparkling water consumption is a rare cause of AKI in children.

Case

An 11-year-old male patient was admitted to the emergency department with complaints of loss of appetite, oliguria and altered level of consciousness. In his history, he had undergone tonsillectomy a week ago. It was noted that after tonsillectomy, he drank only sparkling water and energy drinks. In 1000 ml of mineral water taken by the patient, there was a Na load of 138.18 mg. He drank 2000 ml of mineral water daily. There was 210 mg Na in 100 ml of the energy drunk he drinks with it. He consumed 1000 ml of energy drink daily. The total daily Na intake of the patient was 2376.36 mg.

On physical examination, the patient was lethargic, pupils were bilaterally miotic, and auscultation of heart with lung were normal without organomegaly. Glascow Coma Score, Pediatric Mortality Risk Score (PRISM II) and Pediatric Logistic Organ Dysfunction Score (PELOD) were 13, 3 and 10, respectively, while the predicted mortality score was, 1% according to both PRISM II and PELOD. The patient's vital signs were for oxygen saturation of 98% tachypnoea of 45 breaths/min, BP of the patient 90/60 mmHg and increased heart rate of 140 beats/min. There were signs of sinus tachycardia on the electrocardiogram. His body temperature was 36.7°C. Consolidation and cardiomegaly were not observed on chest X-ray. The patient's blood test results were as follows: Hgb; 14.4 g/dL; Neu: 20.4 10³/uL; PLT: 314 10³/uL; WBC: 23.6 10³/uL; Urea: 247 mg/dL; Creatine: 2.9 mg/dL; Albumin: 5.5 g/dL; LDH: 259 U/L; Sodium: 165 mEq/L; Cl: 134 mEq/L; CRP: 18.1 mg/L and Procalcitonin: 0.72 μg/L. Blood analyses showed metabolic acidsis with Ph; 7.21, pCO₂; 39.5 mmHg, HCO₃; 15.8 mmol/L, lactate; 1.7 mmol/L and Base Deficit of :-12.

Initially fluid resuscitation was performed in the emergency department and the theraphy was continued in the paediatric intensive care unit. A urinary catheter was inserted and hourly urine output was monitored. As the patient hypernatraemia was planned to be corrected within 72 hours, fluid therapy was started with saline and then hypotonic fluids were administered. Spontaneous urine output was 1.5 cc/kg/h in the first 12 hours of hospitalisation and decreased in the follow-up. During intensive care units (ICU) follow-up macroscopic haematuria and proteinuria developed. The protein/creatine ratio in spot urine was calculated as 0.971. Protein creatine ratio in spot urine was significantly higher. It was found his abdominal ultrasound (USG) and renal doppler USG were unremarkable. To provide adequate urine output, it was administered intermittent furosemide (3 mg/kg/d) and aminophylline infusion (0.25 mg/kg/h). Regarding on his medical history and excluding other aetiologic causes, he was diagnosed as AKI owing to consumpting excessive sparkling water and energy drink.

Blood, urine cultures, Covid polymerase chain reaction (PCR) and respiratory viral panel were taken. We ampirically administered intravenous ceftazidime and flucanozole because of the appearance compatible with oral candidiasis, In the follow-up, acute phase reactant regressed and thrombocytopenia tended to improve. No pathogenic agent was identified in cultures. In addition Covid PCR and respiratory viral panel were negative. The kidney functions of the patient was recovered within two weeks in the ICU. Then his therapy was gone on to in the pediatric ward. On day 21 of his hospitalisation, the patient was discharged with no complaints.

Written informed consent was obtained from the family.

Discussion

Although the exact incidence of AKI is not known in children, Sethi et al reported that the incidence of AKI in pediatric intensive care units (PICU) is between 10% and 35%.⁵ Identifying the underlying cause of AKI will affect both the course of treatment and the patient's prognosis. Kidney Disease Improving Global Outcomes, a recognised organisation that develops and implements clinical practice guidelines in kidney disease, is the widely used grading system for diagnosing kidney injury in children.

Although herbal and dietary supplements including sparkling water have long been known to be potential hepatotoxins, the potential toxic effects of these products on the kidneys have not been adequately investigated. Excessive use of soft drinks exacerbates dehydration and as a result worsening of kidney damage due to dehydration. Recurrent episodes of dehydration are known to cause chronic kidney damage.⁶ Our patient was oligouric with elevated serum creatinine and hypernatraemia on admission but not required renal replacement theraphy. We think that sparkling water exacerbates acute kidney injury by causing hypernatraemia due to its high sodium content.

In a study by Rahman et al, they emphasized that a detailed medical history and physical examination can help determine the aetiology and management strategies in AKI. In the present study, aggressive fluid resuscitation was performed in our patient with a history of excessive sparkling water consumption. Both the present study and the previous research suggest that early diagnosis and aggressive treatment in AKI might be a remarkable factor in the course of the disease.⁷

A limited number of cases of AKI after drinking soft drinks have been reported. In three cases reported by Choo et al, severe hypernatraemia was observed in children with Type 2 Diabetes Mellitus with Diabetic Ketoacidosis and Hyperglycaemic hyperosmolar state after drinking soft osmotic diuresis, leading to severe intravascular dehydration and consequent renal failure.⁸ In a study on rats, Garcia-Arroyo et al revealed that repeated exposure to dehydration with fructose drinks. They also suggested that excessive carbohydrate rich soft drink consumption may cause-containing soft drinks caused kidney damage in rats by stimulation of the vasopressin and polyolfructokinase pathways.⁴ The results of both studies reveal that excessive consumption of carbohydrate rich beverages can produce adverse effects on the renal system with complex mechanisms.

As with other organ injuries, determining the cause and severity of kidney damage is crucial for the treatment plan. The main objective of treatment is to cure the primary disease and to prevent complications related to renal failure by providing adequate protein and caloric support. Recently, a study carried out by Vega et al, they recommended mainly oral nutrition to provide adequate calories in paediatric patients with AKI. Despite fact that the previous researcher advised primarily oral caloric support. When our patient was admitted to the PICU, he was unconscious and was fed by nasogastric route.

In the case series reported by da Silva et al; paediatric patients with volume overload refractory to furosemide, aminophylline infusion was associated with an increase in urine output and a decrease in serum creatinine levels.⁹ Similar to the hypotesis of Mai et al; combination of two drugs played an important role in determining the outcome prognosis of AKI in our patient.¹⁰ After the furosemide stress test, adequate urinary output was achieved in our patient. then, aminophylline infusion and intermittent intravenous furosemide were added to the patient's management. And eventually, the oliguric phase ended on the 7th day. After 7 days of treatment, the patient's urine output was adequate without these two medications. The findings of both the present study and previous studies indicate that combined drug use is beneficial in the management of diuresis.

Conclusions

We conclude consuming sparkling water is a rare cause of AKI. Despite its rarity, paediatricians should be careful to ask about sparkling water and energy drink consumption during history taking.

Conflict of Interest Statement

The authors report no conflict of interest.

Acknowledgements

None

Funding

This study received no funding.

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