Journal of Diabetes & Metabolism

Abstract

A rare pregnancy complication known as gestational diabetes insipidus (GDI) is thought to be caused by the increased production of vasopressinase by the placenta. The second or third trimester is typically when it occurs. In the context of newly diagnosed superimposed preeclampsia, this case of GDI is described in this report [1]. A 39-year-old Hispanic woman met the criteria for superimposed preeclampsia when she presented ten days postpartum with a persistent headache and elevated blood pressures in the context of a history of chronic hypertension (gravida 2 para 2). Rehash lab work was prominent for gentle height of liver capability compounds [2]. Her headache persisted despite a normalization of her blood pressure, and further examination revealed polyuria, which was thought to be vasopressinase-induced diabetes insipidus. When the patient's symptoms and polyuria improved, oral desmopressin was started [3].

Keywords

Gestational diabetes insipidus; Diabetes insipidus; Preeclampsia; Polyuria; Pregnancy

Introduction

Gestational diabetes insipidus (GDI) is a rare complication of pregnancy thought to be due to increased vasopressinase, an enzyme produced by the placenta that degrades arginine vasopressin (AVP). As increased urinary frequency and polyuria may be dismissed as normal symptoms in pregnancy, GDI is likely underdiagnosed [4]. Early recognition of this condition is important because if untreated, diabetes insipidus can lead to dangerous and life-threatening consequences for the mother and fetus. GDI typically occurs at the end of the second or in the third trimester, and rarely presents postpartum. This report describes a case of GDI diagnosed postpartum in the setting of newly diagnosed superimposed preeclampsia [5].

Case Summary

A pre-emptive pediatric en bloc deceased donor transplant was given to a 59-year-old woman who had a history of stage IV chronic kidney disease caused by a single kidney. In addition, the patient had hypothyroidism, biliary cirrhosis, and a seizure disorder that was treated with lacosamine and zonisamide, two anti-epileptic medications. For the past ten years, she had not had a seizure [6]. She received basiliximab induction immunosuppression, followed by tacrolimus, mycophenolate mofetil, and corticosteroids for maintenance immunosuppression because she lacked anti-HLA antibodies. The transplant was simple, requiring only two separate ureteroneocystostomies and an end-to-side anastomosis of the donor aorta and vena cava to the recipient external iliac artery and external iliac vein, respectively [s].

Her graft started working right away, and by day three after the transplant, her creatinine had dropped to 1.0 mg/dl. Deep polyuria with dilute urine (urine osmolality 100 mOsm/kg) was notable in the early postoperative course. The polyuria didn't determine suddenly, and pee yield went from 10-20 liters/day for the initial 5 post-relocate days [8]. She developed severe hypernatremia, peaking at 160 mmol/L, despite receiving hypotonic intravenous fluids to replace her urinary losses. Desmopressin (DDAVP) was started on post-operative day 5 to reduce the high urine output and correct her hypernatremia. The effects of DDAVP were immediate, with a significant decrease in serum sodium, an increase in urine osmolality, and a significant decrease in urine output. Her initial polyuria and urine concentration defect were attributed to central DI based on her response to DDAVP [9].

Due to inconsistent fluid intake and labile serum sodium levels that ranged from 125-160 mmol/L during her post-operative hospital stay, titrating the dose of DDAVP was difficult in the early post-operative period. A tonicclonic seizure in response to a rapid decrease in serum sodium complicated her condition [10]. Despite having unstable sodium levels, she did not have any subsequent seizures after her anti-epileptic dosages were adjusted. With a DDAVP dose of 50 mcg taken twice daily and 2 to 2.5 liters of fluid consumed per day, acceptable serum sodium levels were eventually achieved, stabilizing urine output at approximately 2 liters per day [11].

An MRI of her brain revealed a partially empty sella without a posterior pituitary bright spot during her evaluation for the cause of central DI. Normal levels of prolactin, luteinizing hormone, follicle stimulating hormone, and insulin growth factor were found during a hormonal evaluation [12]. Her thyroid invigorating chemical was raised at 19.7 mcIU/mL (reference range 0.4-4.3 mcIU/mL), with a Free T4 of 0.8 ng/dL (reference range 0.6-1.6 ng/ dL) and Complete T3 of 44 ng/dL. Levothyroxine, which she previously took orally, was increased to 88 mcg per day.

Discussion

We have portrayed an instance of post-relocate focal DI that was exposed after kidney transplantation prompting powerful polyuria and hypernatremia that was effectively dealt with DDAVP. Post-relocate DI is an uncommon event and presents novel difficulties in administration. Of those five reports, three of them had a diagnosis of DI prior to the transplant [13]. Of the excess two beneficiaries, one was a late show of DI after relocate and the other was a patient with expected DI optional to earlier neurosurgical mediation. There were no reports of nephrogenic DI recognized (which would require a contributor communicated condition or drug impact). This is the first case in which a patient with CKD who received a kidney transplant almost immediately revealed central DI. The management of polyuric kidney transplant recipients after surgery should take into account a number of important factors in this case [14].

First, the patient had no symptoms at all, had no polyuria before the transplant, and had no biochemical or physiologic signs that would suggest DI. Although she did not report excessive urination, it is certainly possible that her urine output was higher than usual for a patient with severely reduced renal function; however, she may not have recognized this as abnormal if she had become accustomed to a higher urine output. Despite the fact that she did not report excessive urination, prior to the transplant,she did not consider either her thirst or urinary patterns to be abnormal [15].

Conclusion

After a kidney transplant, early post-transplant polyuria is common. However, if polyuria persists and is accompanied by a lower urine osmolality, DI should be considered. To ensure adequate fluid balance and serum sodium levels, DDAVP must be diagnosed and treated promptly.

Acknowledgement

None

Conflict Of Interest

None

Author Info

Received: 27-Mar-2023, Manuscript No. jdm-23-23698; Editor assigned: 30-Mar-2023, Pre QC No. jdm-23-23698(PQ); Reviewed: 13-Apr-2023, QC No. jdm-23-23698; Revised: 20-Apr-2023, Manuscript No. jdm-23-23698(R); Published: 28-Apr-2023, DOI: 10.35248/2155-6156.1000994

Copyright: © 2023 Goldrichie A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.