Oxalate Nephropathy-Induced Acute Kidney Injury following Use of an Organic Hair-Treatment Product in an 8-Year-Old Child: A Case Report

Abstract

Introduction

Acute kidney injury (AKI) is defined as an increase in serum creatinine with or without a reduction in urine output, according to the Kidney Disease: Improving Global Outcomes guidelines. Oxalate nephropathy (ON) is a rare cause of AKI in children. We report a case of oliguric AKI associated with exposure to a cosmetic hair-treatment product leading to ON. To our knowledge, there are limited reports of similar pediatric cases in Saudi Arabia.

Case Presentation

An 8-year-old previously healthy girl presented with facial edema, abdominal distension, oliguria, and hypertension 2 days after a single application of an unidentified hair-treatment product. Laboratory evaluation confirmed severe AKI. Renal biopsy demonstrated acute tubular necrosis with calcium oxalate crystal deposition, confirming ON. She was managed conservatively with cautious fluid administration, intravenous furosemide, correction of electrolyte abnormalities, antihypertensive therapy, and a low-oxalate diet. Renal function normalized within 1 month, with sustained recovery and no evidence of recurrence on subsequent follow-up.

Conclusion

Exposure to certain cosmetic hair-treatment products may cause secondary hyperoxaluria and AKI in children, underscoring the need for heightened awareness and stricter regulation of unlabeled cosmetic products to prevent potential nephrotoxicity.

Introduction

Acute kidney injury (AKI) is a growing concern in the pediatric population [1]. The multinational AWARE (Assessment of Worldwide Acute Kidney Injury, Renal Angina, and Epidemiology) prospective cohort study, which included 4,683 critically ill children admitted to pediatric intensive care units (PICUs), reported that 26.9% of patients developed AKI, with 11.6% experiencing severe disease [2]. According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, it is defined as an increase in serum creatinine level, with or without a reduction in urine output [1]. Clinically, AKI results in impaired renal function, leading to a reduction in estimated glomerular filtration rate, accumulation of nitrogenous waste products such as blood urea nitrogen (BUN), and disturbances in fluid and electrolyte balance [1]. The etiology of AKI is traditionally classified into prerenal, intrinsic renal, and postrenal causes [3]. Chemical-induced nephrotoxicity is an important intrinsic mechanism and may occur through several pathways, including acute tubular necrosis (ATN), interstitial nephritis, crystal nephropathy, and glomerular injury [4]. Hair-straightening products are a recognized source of nephrotoxicity, as some formulations contain free formaldehyde, a well-known nephrotoxic agent, or glyoxylic acid derivatives [4]. Glyoxylic acid can injure renal tubules and, via metabolic pathways, generate oxalate as well as formaldehyde [4]. The resulting oxalate may precipitate as calcium oxalate (CaOx) crystals within the kidneys leading to oxalate nephropathy (ON) [4]. Here, we describe a pediatric case that most likely illustrates this mechanism following exposure to an unidentified organic hair-treatment product. Although ON associated with hair-straightening products has been reported in adults, pediatric cases – especially in Saudi Arabia – are rarely reported. This report aims to raise awareness among consumers and pediatricians regarding the potential renal risks associated with cosmetic hair products.

Case Presentation

An 8-year-old previously healthy girl, up to date with routine vaccinations, presented to our pediatric emergency room (PER) with a 2-day history of facial edema and abdominal distension, following a single application of an unidentified organic hair-care product. The facial edema was associated with a burning sensation over the scalp and postauricular regions. She also reported nausea, vomiting, oliguria, and an approximate weight gain of 3 kg. The product packaging provided no information regarding commercial status, certification, or chemical composition. She had a recent upper respiratory tract infection, but no history of exposure to nephrotoxic drugs, radiographic contrast, herbal remedies, or known food allergies. She denied dizziness, headache, or blurred vision. There were no reported changes in urine color or odor, and no history of joint or muscle pain or skin rashes. The patient was initially evaluated at another hospital for presumed allergic reaction, receiving an epinephrine injection without improvement. Elevated blood pressure and renal markers prompted referral to our PER for further management, as pediatric services were unavailable at the initial facility. On examination, she had facial edema and erythema of the scalp and postauricular areas. Her dry weight was 30 kg, slightly above the 95th percentile, and her height was appropriate for her age and sex based on World Health Organization (WHO) growth charts. Blood pressure was elevated at 136/85 mm Hg (>95th percentile) for age and sex; other vital signs were normal. A nephrology consultation was obtained in the PER, and several laboratory investigations were requested, including a renal profile, urinalysis, urine culture, serum electrolytes, urine protein-creatinine ratio, and other relevant tests. The initial renal profile revealed markedly elevated serum creatinine (574.85 µmol/L) and BUN (30.6 mmol/L). Serum phosphorus was elevated at 2.5 mmol/L, while the remaining electrolytes were within normal limits, including sodium (135 mmol/L), potassium (4.7 mmol/L), chloride (101 mmol/L), calcium (2.28 mmol/L), and magnesium (1.07 mmol/L). Urinalysis showed clear yellow urine, negative for protein, glucose, ketone bodies, nitrites, and leukocytes; pH was 5 (acidic), and specific gravity was 1.015 (normal). Microscopic examination revealed mild pyuria (10–15 WBCs/hpf) and 1–2 RBCs/hpf. Spot urine protein-to-creatinine ratio was 4 mg/mmol, within the normal range. Urine culture showed no bacterial growth. The patient was admitted to the PICU for severe oliguric AKI and significant hypertension, with an initial impression of post-streptococcal glomerulonephritis versus toxic nephropathy secondary to hair product exposure. Renal function worsened (creatinine 590 µmol/L, BUN 32.7 mmol/L), accompanied by hyperkalemia (5.4 mmol/L), hyperphosphatemia (3.3 mmol/L), hyponatremia (132 mmol/L), hypochloremia (91 mmol/L), and hypocalcemia (1.9 mmol/L). A target urine output of >3 mL/kg/h was established; measured outputs during the first 3 days were 1.7, 2.3, and 1.2 mL/kg/h, respectively. Electrolyte disturbances were managed with oral sodium polystyrene sulfonate, sevelamer, sodium chloride, and calcium carbonate. Oliguria was treated with fluid restriction and escalating doses of intravenous (IV) furosemide. Urine output gradually improved, and routine documentation was discontinued once targets were consistently achieved. Blood pressure remained persistently above the 95th percentile, prompting initiation of oral amlodipine in addition to IV labetalol. Lipid profile revealed elevated total cholesterol (228 mg/dL), which was managed conservatively with monitoring, as the dyslipidemia was mild and considered secondary to AKI. Post-infectious glomerulonephritis was excluded based on a negative antistreptolysin O titer, normal complement 3 level, and absence of hematuria on urinalysis with a negative urine sediment. Lupus nephritis was ruled out by negative antinuclear antibody and anti-double-stranded DNA tests. Hemolytic uremic syndrome was also excluded due to the absence of thrombocytopenia and microangiopathic hemolytic anemia. Ethylene glycol poisoning was considered unlikely, as there was no clinical or laboratory evidence of toxicity, including metabolic acidosis. On day five of admission, the patient was transferred from the PICU to the pediatric medical ward after clinical stabilization, improvement in renal function (Fig. 1), correction of electrolyte abnormalities, achievement of target urine output, and adequate blood pressure control. A percutaneous imaging-guided renal biopsy was performed on day 10, the earliest available appointment, after the family decided to proceed, as the etiology of AKI remained unclear. Histopathological evaluation demonstrated ATN with CaOx crystal deposition, consistent with ON, as illustrated in Figure 2. She was discharged home on oral amlodipine and scheduled for outpatient nephrology follow-up. Renal function normalized within 1 month, and antihypertensive therapy was gradually tapered and eventually discontinued as blood pressure returned to normal.

Fig. 1.

Trend of serum creatinine and BUN levels during hospitalization.

Fig. 2.

Kidney biopsy samples of ON. a Light microscopy of kidney tissue (H&E stain, ×200) showing ATN secondary to ON. The renal cortex demonstrates multiple tubules containing gray, refractile deposits consistent with CaOx crystals (white arrows), accompanied by flattening of tubular epithelial cells and loss of brush borders (black arrow). The glomeruli appear normal and the interstitial compartment is unremarkable. b Polarized light microscopy of kidney tissue (H&E stain, ×200) demonstrating CaOx crystals appearing as birefringent structures (white arrow).

Discussion

ON is a pathological syndrome in which CaOx crystals accumulate in the renal tubules, leading to renal function impairment [5]. The main cause of ON is hyperoxaluria, which can be classified as primary or secondary [6]. Primary hyperoxaluria (PH) is a group of autosomal recessive genetic disorders characterized by overproduction of endogenous hepatic oxalate due to accumulation of the glyoxylate precursor [6]. PH is also considered an inborn metabolic error caused by deficiencies in specific enzymes and is classified into three types: PH1, PH2, and PH3 [7]. Secondary hyperoxaluria is more common than PH and may result from high intake of oxalate-rich foods, fat malabsorption, or reduced intestinal oxalate breakdown due to altered gut flora (see Table 1) [8]. Recent evidence from a 2023 Israeli multicenter retrospective series reported 26 adults who developed severe AKI after hair-straightening procedures [9]. Kidney biopsy was performed in 7 patients, and the results revealed intratubular CaOx crystals consistent with ON in 6 patients and tubular microcalcifications in one [9]. Gastrointestinal symptoms and scalp rash were commonly reported, and three patients required temporary dialysis [9]. While hair-straightening products are widely used in the Saudi population, their use in children is uncommon, and pediatric cases are rarely reported in the literature [10]. Our case therefore extends the association between hair-treatment products and ON from adults to children. The product used by our patient had an unknown composition but may have contained nephrotoxic compounds similar to those implicated in hair-straightening-associated crystal nephropathy [10, 11]. Studies have reported that glycolic acid is commonly used in hair treatments as an alternative to formaldehyde, both of which may be nephrotoxic [10, 11]. After systemic absorption, glycolic acid is oxidized to glyoxylic acid by glycolate oxidase in hepatocytes, which is further metabolized to oxalic acid by lactate dehydrogenase [10, 11]. Oxalic acid then dissociates into oxalate ions that can precipitate as CaOx crystals in the renal tubules [10, 11]. Oxalate deposition in the kidney depends on several factors, including supersaturation and precipitation, crystal aggregation, and deposition within renal structures [6]. Urinary supersaturation is the driving force behind crystal formation [6]. When urinary oxalate and calcium exceed their solubility, it leads to crystal formation, tubular obstruction, and direct injury to tubular epithelial cells [6]. An in vitro study published in 2010 investigated the role of oxidative stress in CaOx-induced renal injury using renal tubular epithelial LLC-PK1 cells, with CaOx monohydrate (COM) as the representative crystal [12]. COM at concentrations ≥400 μg/mL was shown to be cytotoxic, causing reduced cell viability [12]. Crystal deposition can obstruct renal tubules and injure tubular cells, triggering oxidative stress through the generation of reactive oxygen species [12]. This oxidative stress may further promote CaOx precipitation and crystal aggregation, creating a self-perpetuating cycle of crystal deposition [12]. The study also demonstrated increased lipid peroxidation in the plasma membrane, indicating oxidative damage and highlighting the key role of oxidative stress in COM-mediated renal tubular injury [12]. ON is a histopathological diagnosis [5]. In our patient, hematoxylin and eosin staining demonstrated characteristic CaOx deposits, but specialized histochemical stains for more precise detection were unavailable at our institution [13, 14]. Von Kossa and Alizarin Red S detect calcium salts nonspecifically, whereas Pizzolato’s stain specifically highlights CaOx crystals, and the Yasue method enhances visualization by removing phosphate and carbonate [13, 14]. Other tests, such as urinary β2-microglobulin and oxalate levels, could help confirm tubular injury, quantify oxalate burden, and distinguish ON from other causes of AKI; however, these tests were not available at our institution [15]. Given the absence of a family history, gradual kidney recovery, and lack of nephrolithiasis or nephrocalcinosis on renal ultrasound, PH was considered unlikely, and genetic testing with 24-h urine oxalate measurement was not pursued [16]. Management of ON includes addressing the underlying cause and kidney injury, along with hydration, low-oxalate or low-fat diets, and calcium or sodium bicarbonate supplementation to reduce oxalate levels [8]. Our patient presented with stage 3 AKI per KDIGO guidelines and was managed with a low-oxalate, low-fat diet, IV fluids, furosemide, and correction of electrolyte disturbances [8, 17]. Dialysis was not required, as renal function improved by day five and no severe acidosis, refractory hyperkalemia, or fluid overload developed [18]. This case represents a novel instance of ON in a child following an organic hair-treatment product, highlighting that pediatric patients may also be susceptible to secondary hyperoxaluria from such exposures.

Table 1.

Examples of secondary hyperoxaluria

Food contains oxalate and its precursor

Rhubarb, Averrhoa carambola, Averrhoa bilimbi, tea, nuts, fruits rich in vitamin C

Increased intestinal oxalate absorption

Chronic pancreatitis, small bowel resection, Crohn’s disease, celiac disease, and cystic fibrosis

Decreased intestinal oxalate degradation

Antibiotics use

Conclusion

This case highlights secondary ON as a rare, but reversible, cause of severe AKI in children following exposure to cosmetic hair-treatment products. A limitation of this report is the absence of toxicological screening; therefore, the specific causative compound could not be identified. Further studies are warranted to characterize nephrotoxic chemicals in hair-treatment products and to inform regulatory measures aimed at preventing exposure. Increased awareness among caregivers and healthcare providers, along with stricter regulation of unlabeled cosmetic products, is essential to minimize the risk of nephrotoxicity in the pediatric population. The CARE Checklist has been completed by the authors for this case report and is attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000552212).

Statement of Ethics

This case report was reviewed and approved by the Research Committee of Maternity and Children Hospital in Al-Ahsa, Approval No. (0604-EP-2025). Written informed consent was obtained from the patient’s parent for publication of the details of their medical case and any accompanying images.

Conflict of Interest Statement

The authors have no conflicts of interest to declare.

Funding Sources

There is no financial support available for this case report.

Author Contributions

Arwa Aljishi, Abdulaziz AlHassan, Fatima Alkhalifah, and Yousef Almarzooq were major contributors to the writing of the manuscript. Arwa Aljishi, Amnah Qaw, Lama AlNemer, and Juwan AlNemer edited and revised the manuscript. All authors approved the final version.

Funding Statement

There is no financial support available for this case report.

Data Availability Statement

All the data that support the findings of this case report are included in this article. Further inquiries can be directed to the corresponding authors.