Ginekologia i Poloznictwo
ISSN 1896-3315 e-ISSN 1898-0759

The Clinical Impact of L-Carnitine Deficiency on Secondary Hyperparathyroidism and Phosphocalcium Levels in Hemodialysis Women

Received: 21-Apr-2025, Manuscript No. gpmp-25-163405; Editor assigned: 23-Apr-2025, Pre QC No. P-163405; Reviewed: 05-May-2025, QC No. Q-163405; Revised: 23-Jun-2025, Manuscript No. R-163405; Published: 30-Jun-2025

Author info »

Introduction

Secondary Hyperparathyroidism (sHPT) is a common complication in patients with chronic kidney disease (CKD) [1], resulting from dysregulated mineral metabolism, particularly involving calcium (Ca²⁺) and phosphate (PO₄^-³) due to impair renal function. The kidneys play a crucial role in maintaining mineral homeostasis and activating 1,25-dihydroxyvitamin D (calcitriol) [2,3], which is essential for calcium absorption. As kidney function declines the production of active vitamin D decreases, leading to hypocalcemia. In response, the parathyroid glands increase the secretion of Parathyroid Hormone (PTH) in an attempt to restore calcium balance, which can result in parathyroid hyperplasia and excessive PTH secretion, a hallmark of sHPT [4].

Furthermore, hyperphosphatemia, a direct consequence of reduced renal phosphate excretion, serves as an additional stimulus for excessive PTH secretion [5]. This dysregulated phosphate-calcium balance contributes to Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD), increasing the risk of bone demineralization, vascular calcification, and cardiovascular complications in affected patients [6].

On the other hand, L-Carnitine, a vital compound involved in fatty acid metabolism and mitochondrial bioenergetics, plays a key role in energy production by facilitating the transport of long-chain fatty acids into the mitochondria for β-oxidation [7]. Several studies have shown that L-Carnitine deficiency is prevalent among CKD patients, particularly those undergoing Maintenance Hemodialysis (MHD). This deficiency is thought to exacerbate oxidative stress, chronic inflammation, and metabolic dysregulation, potentially influencing parathyroid function and disrupting calcium-phosphate homeostasis [8,9].

Emerging evidence suggests a correlation between L-Carnitine deficiency and altered parathyroid hormone regulation, along with imbalances in calcium and phosphate levels in CKD patients. For instance, research has indicated that patients with CKD experience endocrine disturbances [10], including abnormalities in both thyroid and parathyroid function, with concomitant hypocalcemia and hyperphosphatemia, which may further drive the progression of sHPT. Based on these findings, L-Carnitine deficiency may contribute to the pathophysiology of secondary hyperparathyroidism by exacerbating calcium and phosphate dysregulation [11]_.

Aims of the Study

L-Carnitine levels in hemodialysis patients and determine their correlation with the severity of secondary hyperparathyroidism (sHPT).

Materials and Methods

The Imam Al-Sadiq Teaching Hospital in the Babli Governorate, Division of the Industrial College (dialysis), was the site of a case-control study. The period of data collection was August 2024–March 2025. The study population consisted of 40 female patients with chronic kidney disease who were receiving renal dialysis for three to four months to a year. The patients were at the age of 21 to 62 and were spread over different periods of time. Most women had diabetes, high blood pressure and kidney stones. Handling and finishing stages, which took place three months after the end of the therapy, were two studies. The daily dose of 1600 mg was taken oral as a capsule as part of the treatment. Each dialysis patient received a medical examination and a quick questionnaire, which asked about his height, weight, age, gender, length of the disease, the number of weekly dialysis treatment and the presence of further diseases. Data on the existence of chronic or hereditary diseases, using SPSS software, were also collected and stored in computerized systems.

Statistical analysis

Statistical analysis was carried out using SPSS version 27. Categorical variables were presented as frequencies and percentages. Continuous variables were presented as (Means ± SD). Paired t-test was used to compare means for two paired readings. McNemar test was used to compare paired categorical variables. A p-value of ≤ 0.05 was considered as significant.

Results

According to the findings of our study, the distribution of patients who are undergoing hemodialysis is presented in accordance with their socio-demographic characteristics, which include their current age and gender. The mean age of the patients was found to be 36.93 ± 10.99, with the oldest patient being 21 years old and the youngest being 62 years old. The majority of patients (N=25, 62.5%) were male (Tab. 1.).

Tab. 1. Distribution of patients according to the gender.

After three months of therapy with L-carnitine, a statistically significant decrease in the mean levels of phosphorus (mg/dl) and parathyroid hormone (pg/ml) was found in patients who were receiving hemodialysis. On the other hand, our findings revealed that individuals receiving hemodialysis had a considerable mean rise of calcium (measured in millimoles per liter) (Fig. 1. and Tab. 2.).

Fig. 1. The mean differences of parathyroid hormone before and after treatment.

Tab. 2. The mean differences of parathyroid hormone before and after treatment.

Discussion

Our study found that after three months of therapy with L-carnitine, a statistically significant decrease in the mean levels of phosphorus (mg/dl) and parathyroid hormone (pg/ml) was reported in patients who were receiving hemodialysis. On the other hand, our findings demonstrated that people having hemodialysis experienced a large mean elevation of calcium

Patients with chronic renal failure suffer from an increase in hospitalization and need dialysis due to the loss of kidney function [12]. They are more likely to suffer from low levels of carnitine which is one of the factors responsible for the various disorders that chronic kidney disease patients suffer from, such as anemia, muscle weakness, low pressure during dialysis, and cardiomyopathy, Maintaining the level of carnitine in the serum or tissues can reduce these disorders [13,14].

Secondary hyperparathyroidism and enlarged parathyroid glands are common complications in patients with renal failure due to the inability of the affected kidney to produce 1-alpha hydroxylase and the inability of the patient to convert vitamin D to its active form [15]. Decreased calcitriol in the blood, moderate decrease in ionized calcium, inability of the kidneys to excrete phosphate, and its rise in the blood contribute to the Increase in the synthesis and secretion of PTH hormone with the progression of the disease [16]. The increase in the level of PTH is associated with the occurrence of hyperparathyroidism in hemodialysis patients which is a physiological disease caused mainly by hyperphosphatemia and hypocalcemia [17].

L-Carnitine supplementation was used to investigate its effect on secondary hyperparathyroidism in hemodialysis patients and found that L-Carnitine had little effect and non-significant expression in patients with secondary PTH hyperactivity and this is inconsistent with the results of the current study [11,18].

Pre-treatment, patients with elevated PTH levels had hyperparathyroidism and elevated serum phosphorus levels [18], which is believed to be caused by an increase in the secretion of bone cells and not due to a decrease in kidney filtering [19]. Also, most of the dialysis patients were suffering from calcium deficiency due to irregular metabolism, as hyperparathyroidism stimulates the bone to release bone from the calcium in the blood [20].

Conclusion

This study suggests that L-Carnitine deficiency may contribute to calcium and phosphate imbalances, leading to the progression of sHPT in patients with kidney failure. Correcting L-Carnitine deficiency through supplementation could be a potential strategy for improving mineral and bone disorder management in these patients. Further research is needed to determine the clinical benefits of L-Carnitine therapy in kidney failure women.

References

1. Kellum JA, Romagnani P, Ashuntantang G, et al. Acute kidney injury. Nat Rev Dis Primers. 2021;7(1):52.

Google Scholar

2. Fairbrother A. Clinical biochemistry. In: Nondestructive Biomarkers in Vertebrates. CRC Press; 2020. p. 63-89.
3. Mammen JS, McGready J, Oxman R, et al. Thyroid hormone therapy and risk of thyrotoxicosis in community-resident older adults: Findings from the baltimore longitudinal study of aging. Thyroid. 2015;25(9):979-986.

Google Scholar, Cross Ref, Indexed at

4. Freethi R, Raj AV, Ponniraivan K, et al. Study of serum levels of calcium, phosphorus and alkaline phosphatase in chronic kidney disease. Int J Med Res Health Sci. 2016;5(3):49-56.

Google Scholar

5. Carneiro-Pla D. Contemporary and practical uses of intraoperative parathyroid hormone monitoring. Endocr Pract. 2011;17:44-53.

Google Scholar, Cross Ref, Indexed at

6. Demir AD. A review of parathyroid mass and patients with nonspecific complaints. J Int Med Res. 2020;48(1):0300060519827169.

Google Scholar, Cross Ref, Indexed at

7. Almannai M, Alfadhel M, El-Hattab AW. Carnitine inborn errors of metabolism. Molecules. 2019;24(18):3251.

Google Scholar, Cross Ref, Indexed at

8. Nazari L, Salehpour S, Hosseini S, et al. Effect of antioxidant supplementation containing L-carnitine on semen parameters: A prospective interventional study. JBRA Assist Reprod. 2021;25(1):76-82.

Google Scholar, Cross Ref, Indexed at

9. Calvani M, Benatti P, Mancinelli A, et al. Carnitine replacement in end-stage renal disease and hemodialysis. Ann N Y Acad Sci. 2004;1033(1):52-66.

Google Scholar, Cross Ref, Indexed at

10. Osadnik K, Osadnik T, Delijewski M, et al. Calcium and phosphate levels are among other factors associated with metabolic syndrome in patients with normal weight. Diabetes Metab Syndr Obes. 2020;13:1281-1288.

Google Scholar, Indexed at

11. Cibulka R, Racek J, Pikner R, et al. Effect of L-carnitine supplementation on secondary hyperparathyroidism and bone metabolism in hemodialyzed patients. Calcif Tissue Int. 2007;81:99-106.

Google Scholar, Cross Ref, Indexed at

12. Asim M, El Esnawi M. Renal dysfunction manifesting in subclinical hypothyroidism—a possible role for Thyroxine. NDT Plus. 2010;3(3):282-284.

Google Scholar, Cross Ref, Indexed at

13. Bartel LL, Hussey JL, Shrago E. Perturbation of serum carnitine levels in human adults by chronic renal disease and dialysis therapy. Am J Clin Nutr. 1981;34(7):1314-1320.

Google Scholar, Cross Ref, Indexed at

14. Dębska-Ślizień A, Kawecka A, Wojnarowski K, et al. Carnitine content in different muscles of patients receiving maintenance hemodialysis. J Ren Nutr. 2007;17(4):275-281.

Google Scholar, Cross Ref, Indexed at

15. Slatopolsky E, Brown A, Dusso A. Role of phosphorus in the pathogenesis of secondary hyperparathyroidism. Am J Kidney Dis. 2001;37(1):S54-S57.

Google Scholar, Cross Ref, Indexed at

16. Jacquillet G, Unwin RJ. Physiological regulation of phosphate by vitamin D, Parathyroid Hormone (PTH) and phosphate (Pi). Pflugers Arch. 2019;471:83-98.

Google Scholar, Cross Ref, Indexed at

17. Singh PA, Bobby Z, Selvaraj N, et al. An evaluation of thyroid hormone status and oxidative stress in undialyzed chronic renal failure patients. Indian J Physiol Pharmacol. 2006;50(3):279-284.

Google Scholar, Indexed at

18. Mercadal L, Tezenas du Montcel S, Chonchol MB, et al. Effects of L-carnitine on mineral metabolism in the multicentre, randomized, double blind, placebo-controlled CARNIDIAL trial. Am J Nephrol. 2018;48(5):349-356.

Google Scholar, Cross Ref, Indexed at

19. Schwarz C, Leichtle AB, Arampatzis S, et al. Thyroid function and serum electrolytes: Does an association really exist? Swiss Med Wkly. 2012;142:w13669.

Google Scholar, Cross Ref, Indexed at

20. Wolf M. Forging forward with 10 burning questions on FGF23 in kidney disease. J Am Soc Nephrol. 2010;21(9):1427-1435.

Google Scholar, Cross Ref, Indexed at