Arginine vasopressin deficiency (AVP-D) is an uncommon disorder caused by deficient vasopressin production due to hypothalamic or pituitary gland dysfunction resulting in hypotonic polyuria, whose etiology oftentimes remains elusive. We present the case of a 20-year-old male patient evaluated for polyuria and polydipsia. Laboratory evaluation demonstrated hypernatremia, elevated serum osmolality, and inappropriately dilute urine with symptomatic improvement following initiation of desmopressin, consistent with AVP-D. Initial pituitary magnetic resonance imaging (MRI) showed a small enhancing lesion with pituitary stalk thickening (PST), raising concern for inflammatory or infiltrative etiologies. Extensive autoimmune and pituitary infiltrative disease work-up was unrevealing, and serial imaging remained inconclusive. Given diagnostic uncertainty, a transsphenoidal pituitary biopsy was performed, which proved consistent with a germinoma with evidence of human chorionic gonadotropin secretion. Subsequent staging studies, including spinal MRI and cerebrospinal fluid analysis, raised concern for possible disseminated disease. The patient was treated with craniospinal irradiation and continues close multidisciplinary follow-up for hypopituitarism and AVP-D. This case highlights the need for continued surveillance in patients presenting with AVP-D and nonspecific imaging findings, as early identification of etiology is critical for timely treatment and optimal outcomes.

Diabetes insipidus (DI) is a rare but significant and life-threatening complication of metastatic breast cancer, typically arising when cancer spreads to the pituitary gland. This condition results from impaired secretion or action of antidiuretic hormone (ADH) or arginine vasopressin (AVP), leading to symptoms including excessive urination and thirst. The posterior lobe of the pituitary and the infundibulum are most susceptible to metastatic involvement due to their direct arterial blood supply, making them more accessible to circulating tumor cells. This phenomenon explains why DI can be a manifestation of pituitary metastases. We report the case of a patient who presented with a five-week history of projectile vomiting, dizziness, blurred vision, headache, insatiable thirst, and nocturia. She reported urinating up to 12 times at night such that she struggled to sleep and would end up having daytime lethargy and fatigue. Biochemical evaluation demonstrated hyperosmolar serum, low urine osmolality, and low urine sodium, consistent with central DI. MRI revealed a pituitary stalk and suprasellar metastases with multiple new cerebral and cerebellar lesions. The patient underwent a desmopressin challenge leading to rapid improvement in polyuria and an increase in urine osmolality. Desmopressin confirmed an intact renal response, establishing the diagnosis of cranial DI secondary to pituitary metastases. Despite symptomatic benefit, her overall condition deteriorated due to progressive intracranial and systemic disease. She subsequently received whole-brain radiotherapy and palliative care but died three months after the diagnosis of DI. This case highlights central DI as a rare but clinically important manifestation of pituitary metastases in metastatic breast cancer. Prompt recognition and endocrine replacement, particularly with desmopressin, can provide meaningful symptomatic relief even when prognosis remains poor. Early multidisciplinary involvement, including endocrinology, oncology, radiology, and palliative care, is essential for optimizing quality of life in such complex cases.

Diabetic nephropathy is the critical microvascular complication of diabetes and a leading cause of end-stage renal disease. Its pathophysiology incriminates complex and interconnected mechanisms driven by hemodynamic and metabolic alterations, accompanied with glycation, inflammation, oxidative stress, and fibrosis. Targeting these cues through natural interventions may preserve kidney functions. The study aimed to investigate the renoprotective potential of a standardized ethyl acetate fraction of C. scarabaeoides (EAFCS), enriched with flavonoids including isoorientin, orientin, vitexin, isovitexin, and genistin, in diabetic nephropathy. In vitro mechanistic studies were performed in NRK-52E rat kidney tubular epithelial cells exposed to high glucose, while in vivo efficacy was assessed in a streptozotocin-induced diabetic rats. EAFCS markedly prevented advanced glycation end product (AGE) formation at early and intermediate stages of the glycation process and also promoted the degradation of preformed AGEs. In vitro, EAFCS attenuated glucose-induced ROS generation, inflammatory response, and pro-fibrotic gene expression. In diabetic rats, EAFCS ameliorated classical diabetic manifestations, including polyphagia, polydipsia, polyuria, and impaired glucose tolerance. Also, EAFCS reduced albuminuria and proteinuria, and improved renal function markers. Histopathological and molecular analyses demonstrated that EAFCS alleviated diabetes-induced renal structural damage and fibrosis. Mechanistically, EAFCS curbed TGF-β/Smad signaling, prevented myofibroblast activation, and reduced fibronectin and collagen accumulation in renal tissue. Additionally, EAFCS downregulated RAGE expression and inhibited NF-κB- and MAPK-mediated inflammatory signaling cascades. Collectively, the findings suggest that EAFCS attenuates multiple manifestations of renal dysfunctions and may exert renoprotective effects through mechanisms associated with reduced glycation, oxidative stress, inflammation, and fibrosis. These results support EAFCS as a potential candidate for further investigation in the management of diabetic nephropathy.

The evaluation of arginine vasopressin resistance (AVP-R) and arginine vasopressin deficiency (AVP-D), respectively, previously referred to as nephrogenic and central diabetes insipidus, often includes brain magnetic resonance imaging (MRI). Its purpose is to assess pituitary structural changes and identify the physiological T1 hyperintensity of the posterior pituitary, present in most individuals. This hyperintensity reflects vasopressin storage, which shortens the T1 relaxation time. Its absence supports a diagnosis of AVP-D over AVP-R. A 13-year-old boy was referred to endocrinology in his second year of life for polyuria and polydipsia. Brain MRI revealed normal pituitary morphology and a spontaneous T1 hyperintensity of the posterior pituitary. The AVP-R was confirmed by a hemizygous AVPR2 gene mutation. Treatment with hydrochlorothiazide, potassium supplementation, and dietary sodium restriction achieved good clinical control. During school age, progressive growth deceleration led to short stature and delayed puberty. At 13 years, repeated MRI showed a smaller pituitary gland and loss of the posterior pituitary T1 hyperintensity. Loss of posterior pituitary T1 hyperintensity is rare in AVP-R, and late disappearance has not been previously described in genetically confirmed cases. This case underscores the importance of integrating clinical, genetic, and imaging findings.

Dorsal pancreatic agenesis (DPA) is a rare congenital disorder resulting from failure of development of the dorsal pancreatic bud. Complete DPA implies absence of the pancreatic neck, body, and tail and can be associated with both diabetes mellitus and pancreatitis. The patient was an 18-year-old man admitted with a history of epigastric pain, nausea, vomiting, polyuria, polydipsia, and unintentional weight loss of 4 kg over 8 weeks. The lab investigations included elevated serum glucose (412 mg/dL), urine ketones 3+, venous pH 7.31, bicarbonate 17.2 mEq/L, anion gap 14.8 mEq/L, lipase 486 U/L, amylase 312 U/L, consistent with hyperglycemic ketosis and metabolic acidosis, treated as mild DKA. The contrast-enhanced computed tomography (CT) study was read in real time by an abdominal radiologist and demonstrated the absence of the pancreatic neck, body, and tail, increased size of the head of the pancreas, a positive dependent-stomach sign, and mild pancreatic inflammation without necrosis and fluid collections. MRCP done 8 weeks later confirmed a normal ventral pancreatic duct and absence of dorsal pancreatic duct, consistent with the diagnosis of complete DPA. Fasting C-peptide 12 weeks after presentation was found to be extremely low (0.31 ng/mL) and antibodies to GAD65, IA-2A, and ZnT8 negative. These findings decreased the likelihood of classic autoimmune type 1 diabetes, suggesting involvement of the underlying pancreatic pathology and the presence of severe insulin deficiency. However, negative antibody type 1 diabetes cannot be ruled out. DPA should be suspected in young patients with unexplained pancreatitis and insulin-deficient diabetes. Imaging is essential, and MRCP provides the most valuable ductal information. Classification of diabetes should not depend solely on age, ketosis, or insulin requirement when a major congenital abnormality of the pancreas is present.

A 7-year, 6-month-old, female neutered, Pug dog presented with lethargy, hyporexia, polydipsia, abdominal distension, and dyspnea. Point-of-care ultrasonography identified tricavitary effusions and cardiac tamponade. Pericardiocentesis yielded 83 mL of sanguineous scintillating fluid. Clinical examination, bloodwork, echocardiography, electrocardiography, thoracic and abdominal computed tomography scans, and pericardial fluid analysis including culture and sensitivity did not identify any cardiovascular, endocrine, neoplastic, or infectious causes of the pericardial effusion. Pericardial fluid analysis identified high cholesterol concentrations and numerous cholesterol crystals on cytology, supporting a diagnosis of cholesterol pericarditis. Subtotal pericardiectomy was performed 7 weeks later to address pericardial and pleural effusions. Histopathological pericardial biopsies identified pericarditis with no neoplastic tissue detected. A pleural port was placed 4 months later to manage recurrent pleural effusion. Elective euthanasia was performed 10 weeks later citing a compromised quality of life from increasingly frequent bouts of dyspnea. This is a case report of a dog with idiopathic cholesterol pericarditis presenting with cardiac tamponade.

A 10-year, 8-month-old male presented with polyuria, polydipsia, and secondary nocturnal enuresis for 4 months following a severe headache. Initial fasting studies raised concern for partial arginine vasopressin deficiency (AVP-D). Brain magnetic resonance imaging revealed a possible pituitary adenoma vs artifact. His height was >99th percentile; he was prepubertal and growth charts demonstrated growth velocity >7.5 cm/year for the past 2 years. Additional testing showed markedly elevated IGF-1 and IGF-binding protein 3. He passed a water-deprivation test, ruling out AVP-D. He underwent a GH suppression test that revealed no suppression, suggesting GH excess. Repeat magnetic resonance imaging delineated a cystic pituitary lesion, most consistent with Rathke cleft cyst or hemorrhagic adenoma. Surgery was not recommended because the hematoma obscured visualization of any underlying tumor and evacuation could result in indiscriminate removal of the native gland. Serial imaging demonstrated continued retraction of the hematoma and tumor complex over 10 months. His AVP-D resolved, growth velocity slowed, and growth factors normalized over 13 months without intervention. Tall stature with increased growth velocity in prepubertal children should raise concern for GH excess. GH excess secondary to GH-secreting pituitary adenomas may spontaneously resolve if pituitary apoplexy occurs.

A 10-year-old neutered female Maine Coon was presented with haematuria, weight loss, polyuria/polydipsia and progressive azotaemia. Diagnostic imaging revealed bilateral renal pelvic dilation, ureteral distension and ectopic ureters. Bacterial pyelonephritis was diagnosed, but the azotaemia progressed despite antibiotic therapy, and suspected ureteral obstruction prompted surgical ureteral reimplantation. The visualisation of omental nodules and thickening of the ectopic right ureterovesicular junction intraoperatively raised suspicion of malignancy, and histopathology revealed urothelial carcinoma with carcinomatosis. The cat was euthanised postoperatively due to clinical deterioration, characterised by persistent oliguria and progressive azotemia. Clinicians should consider malignancy as a differential in cats with ectopic ureters and an atypical or refractory clinical course.

Paraneoplastic endocrine syndromes are well-recognised complications of lung malignancies, specifically small-cell lung cancer. The majority of patients with panhypopituitarism associated with lung cancer result from pituitary metastasis. In those with an enlarged pituitary stalk without obvious pituitary metastasis presenting with a combination of panhypopituitarism and arginine vasopressin deficiency (AVP-D), metastatic pituitary stalk infiltration should be considered rather than a paraneoplastic immune-mediated hypophysitis. We report a case of a 67-year-old gentleman with newly diagnosed lung adenocarcinoma, found to have panhypopituitarism before starting systemic anti-cancer treatment. Further hormonal tests revealed central hypothyroidism, hypogonadotropic hypogonadism and growth hormone deficiency. MRI of the pituitary demonstrated heterogeneous contrast enhancement without an obvious focal lesion. The pituitary stalk was slightly enlarged at the level of the optic chiasm, raising the possibility of hypophysitis. The patient was initiated on hydrocortisone and levothyroxine replacement therapy. Following hormone replacement, previously occult AVP-D became clinically apparent, manifesting as worsening dehydration, polyuria and polydipsia. The overnight water deprivation test confirmed AVP-D. The patient showed subsequent clinical improvement with desmopressin. Serum prolactin was mildly elevated, likely reflecting both pituitary stalk infiltration and concomitant metoclopramide therapy. This case discusses an exceptionally rare presentation of lung adenocarcinoma with isolated pituitary stalk infiltration, panhypopituitarism, and AVP-D before exposure to immune checkpoint inhibitors. Clinicians should be aware of this unusual manifestation, as prompt hormone replacement can significantly reduce morbidity and improve patient outcomes.

Pembrolizumab, a programmed cell death protein 1 (PD-1) immune checkpoint inhibitor, is commonly used in the treatment of squamous cell carcinoma, offering improved survival and tumor response. However, it can rarely lead to immune-related adverse events (irAEs), some of which may be significant. We report a 62-year-old male with squamous cell carcinoma of the lung, a 40-pack-year smoking history, prediabetes, and coronary artery disease, who presented with polydipsia, polyuria, and weakness. He was diagnosed with sudden-onset diabetic ketoacidosis. Laboratory workup revealed negative glutamic acid decarboxylase (GAD), IA-2, and islet cell antibodies, as well as an undetectable C-peptide level, consistent with immune checkpoint inhibitor-induced type 1 diabetes. Concurrently, the patient developed hyperthyroidism with positive thyroid peroxidase (TPO) antibodies, suggesting autoimmune thyroiditis. This case underscores the importance of baseline screening and ongoing monitoring for endocrine irAEs during immunotherapy. Clinicians should maintain a high index of suspicion, even in patients without prior autoimmune disorders. Early recognition, patient education, and coordinated multidisciplinary care are critical for reducing complications and improving outcomes.

Although pregnancy-associated arginine vasopressin (AVP) disorder is rare, it is often attributed to excessive placental vasopressinase activity. However, vasopressinase-independent mechanisms, including gestational unmasking of latent AVP deficiency (AVP-D), may occur. We report a 37-year-old primigravid female who developed severe polydipsia and polyuria in the third trimester. She had hypotonic polyuria with inappropriately low plasma AVP levels and loss of the posterior pituitary bright spot on T1-weighted magnetic resonance imaging (MRI). AVP-D was suspected; desmopressin promptly relieved her symptoms. Desmopressin became unnecessary immediately following delivery; however, at 6 months postpartum, her polydipsia and polyuria recurred. Anterior pituitary dysfunction subsequently developed. Notably, at 6 months postpartum, the posterior pituitary bright spot on MRI remained absent. Herein, the transient postpartum improvement initially mimicked gestational AVP disorder; however, retrospective testing revealed anti-rabphilin-3A antibody positivity, indicating autoimmune hypophysitis involvement. Persistent MRI abnormalities, postdelivery AVP-D recurrence, and subsequent anterior pituitary dysfunction supported an underlying autoimmune etiology. This case raises the possibility that pregnancy may unmask latent autoimmune AVP-D through a vasopressinase-independent mechanism. In patients who develop AVP-D during pregnancy, anti-rabphilin-3A antibody positivity and persistent loss of the posterior pituitary bright spot on MRI may offer crucial diagnostic clues, supporting the significance of long-term endocrine follow-up.