Renal Failure Research Articles

8089 Myxedema Coma Presenting with Reversible Cardiomyopathy and Acute Renal Failure

Abstract Disclosure: A. Mubashir: None. F. Sajid: None. M. Sattar: None. Myxedema Coma is a life-threatening complication of hypothyroidism and often presents with multi-organ failure. However, reversible cardiomyopathy and acute renal failure are rare. Here, we present a case of iatrogenic hypothyroidism leading to myxedema coma with reversible organ failure. Case Presentation: A 58-year-old male with a past medical history of iatrogenic hypothyroidism after total thyroidectomy for follicular thyroid cancer, noncompliant with levothyroxine for the past three years, was brought to the hospital due to worsening mental status, low energy, and cold extremities for three days. On admission, vital signs were within normal limits. Laboratory studies revealed Random Glucose 113 (74-200 mg/dl), Na 134 (135-149 mmol/l), TSH: 217 (0.39-4.08 MCIU/ml), Free T4 <0.25 (0.58-1.64 ng/dl), Free T3 1.01 (2.53-3.87 pg/ml), BUN 53.3 (7-21 mg/dl), Creatinine 4.9 (0.5-1.3mg/dl). Urinalysis was positive for protein of 300 mg/dl (negative). Urine studies showed hematuria, total protein/cr 3.18 (<0.10), with increased total protein of 60/24 hours (0-12 mg/dl), suggesting glomerular etiology. Additionally, Bence Jones protein and monoclonal band were negative, interpreted as mild glomerular proteinuria. FeNa >2%, Urine sodium of >40 (20-40mmol/l) suggest acute tubular necrosis. EKG showed normal sinus rhythm with low voltage. To rule out diastolic dysfunction, an echocardiogram was performed, which revealed depressed systolic function with an ejection fraction of 31-35% and a large pericardial effusion with echocardiographic features of tamponade. He also had global cardiomyopathy with akinesis, especially in the inferior segments. He was treated with IV levothyroxine. Repeat imaging in one month showed an increase in ejection fraction to 55% with moderate-sized pericardial effusion and no echocardiographic features of tamponade. Global cardiomyopathy had also resolved. However, left ventricular systolic function was borderline, with delayed diastolic expansion of the right ventricle. Repeat creatinine was 2mg/dl. The patient’s condition greatly improved, and he was discharged with follow-up with endocrinology, nephrology, and cardiology. Discussion: In the available literature, diastolic dysfunction is associated with severe hypothyroidism. However, reversible global cardiomyopathy with decreased systolic function is rare. The pathogenesis of this myopathy is not well understood. Similarly, known mechanisms of renal injury in hypothyroidism include renal hypoperfusion, rhabdomyolysis, decreased kidney-to-body weight ratio, truncated tubular mass, and altered glomerular architecture. While the need to perform a renal biopsy or the use of goal-directed therapy for dilated cardiomyopathy remains questionable in such cases, reversible complications of severe hypothyroidism should be investigated in patients with suspected myxedema. Presentation: 6/2/2024

7668 Rhabdomyolysis Associated with Severe Hypothyroidism

Abstract Disclosure: H. Soe: None. P. Mikkilineni: None. Background: Over 70% of the patients with newly diagnosed hypothyroidism can present with muscle complaints such as weakness, fatigability, cramps, myalgia. However, rhabdomyolysis, which is the rapid breakdown of skeletal muscle cells, is the rare presentation. Clinical Case: A 70-year old male patient with history of rheumatoid arthritis, hyperlipidemia, prior CVA (left hemispheric subcortical stroke) 6 months ago without residual deficit presented to the hospital with poor oral intake and generalized muscle weakness for 3 weeks. He was unable to get out of bed without assistance and also needed adult diapers. Found to have new-onset severe hypothyroidism with TSH 228 uIU/ml (Ref: 0.350-4.940) and FT4 <0.40 ng/dL (Ref: 0.70-1.50), positive TPO antibody 197 IU/ml (Ref: 0-34). No prior thyroid labs were available and no known history of thyroid disorder was recorded. He has never been on Amiodarone or Lithium before. On physical exam, he was alert and oriented. There was no goiter or palpable thyroid nodule. There was no focal neurological deficit and no peripheral edema. There were no other signs and symptoms pertinent to hypothyroidism except mild bradycardia (HR 56-60) and borderline low blood pressure. AM cortisol was 10.1 ug/dL (Ref: 3.7-19.4). EKG showed low-voltage sinus bradycardia. Echocardiogram was normal. Urinalysis was positive for large blood but only 3 RBCs were present which raised the suspicion of rhabdomyolysis. Creatinine kinase (CK) was 15,584 IU/L (Ref: 30-200). Other laboratory studies were significant for acute renal failure with mild hyperkalemia and mild hypocalcemia, also transaminitis; BUN 130 mg/dl (Ref: 8-26), Creatinine 9.51 mg/dl (Ref: 0.72-1.25), eGFR 5 ml/min/1.73 m2 (Ref: >59), AST 435 IU/L (Ref: 5-34), ALT 269 IU/L (Ref: <55), ALP 171 IU/L (Ref: 40-150). On medication review, he was started on Atorvastatin 80 mg daily during prior admission for CVA 6 months ago. He received IV fluids, s/p 1 dose of Hydrocortisone 100 mg IV, Levothyroxine IV 200 mcg, followed by Levothyroxine IV 50 mcg daily x 3 days and switched to Levothyroxine PO 100 mcg daily (weight-based dose). Atorvastatin was on hold. He became anuric during the hospital course and received 2-3 sessions of hemodialysis. 3-4 days later, CK was trending down to 3000 IU/L, FT4 improved to 0.54 ng/dl and there was also significant improvement in kidney and liver functions. The patient was diagnosed with acute renal failure secondary to rhabdomyolysis associated with severe hypothyroidism caused by Hashimoto's thyroiditis, in the setting of high dose statin use. Conclusion: Clinicians should raise the suspicion of rhabdomyolysis in a patient with severe hypothyroidism, especially in patients with recent high dose statin use as rhabdomyolysis can be a rare and fatal complication of severe hypothyroidism, in the presence of precipitating factors. Presentation: 6/2/2024

6769 Rhabdomyolysis In Diabetic Emergencies Highlighting The Necessity Of Prompt Creatine Kinase Monitoring

Abstract Disclosure: A. Tiwari: None. M. Corsten: None. W. salari: None. N. Malik: None. A. Dabaja: None. C. Saad: None. Rhabdomyolysis results from skeletal muscle necrosis, causing the release of intracellular contents into the bloodstream. While its association with life-threatening diabetic emergencies is rare, it remains a significant complication. We detail the case of a 37-year-old male admitted with acute pancreatitis who subsequently developed a hyperosmolar hyperglycemic state accompanied by significant electrolyte imbalances. Upon arrival at our emergency department, he displayed severe dehydration, stupor, a blood glucose level surpassing 2,000 mg/dl, and high anion gap metabolic acidosis. His condition worsened when his creatine kinase levels surged from 210 U/L to 39,000 U/L, leading to oliguric renal failure and the need for hemodialysis. His thyroid profile was unremarkable and was not on any medication. Comprehensive treatment included crystalloids, parenteral insulin, and rigorous ICU monitoring with mechanical ventilation. Following this, the patient showed rapid improvement and was discharged without requiring further dialysis. A thorough history and observation established a rare but strong link between rhabdomyolysis and hyperosmolar hyperglycemic states. These situations can intensify nephrotoxic events, especially in patients already facing severe dehydration and prerenal factors. This case emphasizes the critical need for consistent monitoring of creatine kinase levels in diabetic emergencies. Such monitoring ensures early detection and facilitates effective management of rhabdomyolysis-induced acute kidney injury, reducing potential complications and improving patient outcomes. Presentation: 6/3/2024

12620 Developing Hospital Protocols For Managing Patients With Hypertriglyceridemia-induced Acute Pancreatitis In Diabetic Ketoacidosis Hospitalizations

Abstract Disclosure: U. Agbedia-ejughemre: None. Methods: We queried the combined 2017-2020 nationwide inpatient sample database for all adult hospitalizations for DKA with and without HTG-AP using the ICD-10 revision codes. Baseline characteristics were compared between DKA hospitalizations with and without HTG-AP using Pearson’s χ2 tests and Student’s t-test for categorical and continuous variables. Study endpoints were the incidence, predictors, and outcomes of HTG-AP, including mortality, hospitalization duration, mean hospital costs, and acute in-hospital complications (sepsis, ARDS, and acute renal failure). Predictors of HTG-AP were assessed using stepwise multivariable logistic regression analysis. Illness severity, baseline risk of mortality, and comorbidity burden were adjusted using APR-DRG metrics and CCI. Prolonged hospitalization was defined as the length of hospital stay in the top decile of hospital stay for all hospitalizations in the study. Results: We analyzed 630,435 hospitalizations for DKA. The study cohort was 51.4% male, 57.6% white Americans and 26.1% Blacks, with a mean age of 40 (SD, 16.2) years. Incidence of HTG-AP was 2.1% (13,445). Hospitalizations with HTG-AP were older (mean age: 44 vs. 40 years; P<0.001) and had greater comorbidity (CCI score of 2: 38.7 vs. 33.8; P<0.001) compared with DKA hospitalizations without HTG-AP. While DKA hospitalizations showed an uptrend, increasing from 105,769 to 199,429 hospitalizations (Average annual percent change [AAPC]: 27.04%; P=0.029), the incidence of HTG-AP showed a downtrend from 2650 (2.5%) to 4085 (2.0%) (P=0.006). Predictors of HTG-AP included Hispanic (aOR: 2.45; 95% CI: 1.95-3.07; P<0.001) or Asian race (aOR: 2.48; 95% CI: 1.37-4.48; P=0.003), private insurance (aOR: 1.57; 95% CI: 1.10-2.25; P=0.013), self-pay (aOR: 2.2; 95% CI: 1.49-3.27; P<0.001), APR-DRG moderate risk of mortality (aOR: 1.52; 1.21-1.92; P<0.001), APR-DRG major loss of function (aOR: 1.46; 95% CI: 1.31-1.69; P<0.001), dyslipidemia (aOR: 1.87; 95% CI: 1.47-2.38; P<0.001), hypertension (aOR: 1.39; 95% CI: 1.13-1.72; P=0.002), obesity (aOR: 3.09; 95% CI: 2.42-3.96; P<0.001), obstructive sleep apnea (aOR: 2.05; 95% CI: 1.35-3.10; P=0.001), chronic liver disease (aOR: 9.44; 95% CI: 6.61-13.48; P<0.001), old MI (aOR: 2.11; 95% CI: 1.02-4.38; P=0.045), and COPD (aOR: 2.31; 95% CI: 1.47-3.64; P<0.001). DKA hospitalizations with HTG-AP were correlated with higher risk of septicemia (aOR: 1.20; 95% CI: 1.05-1.69; P=0.029), ARDS (aOR: 1.24; 95% CI; 1.04-2.07; P=0.004), and resource use, including prolonged hospitalization (26.3% vs. 11.1%; P<0.001), and higher mean hospital costs ($57,773 vs. $32,692; P<0.001). Conclusion: HTG-AP was linked to worse outcomes, excluding mortality, in hospital admissions for DKA. There is a need for enhanced diagnostic guidelines and protocols targeting this subgroup of patients could improve outcomes. Presentation: 6/2/2024

12376 Comparison Of 1 Mg Versus 2 Mg Dexamethasone Suppression In Obesity

Abstract Disclosure: H. Babu: None. A. Nawaz: None. A.J. Spiro: None. T.D. Hoang: None. M.K. Shakir: None. The overnight 1 mg dexamethasone suppression test (DST) is widely used to screen for Cushing’s Syndrome (CS), especially due to its low incidence of false negative results. Serum cortisol concentrations <1.8 µg/dL suggests adequate HPA axis suppression and usually excludes CS. Concentrations >1.8 µg/dL should be verified with a second test. However, the lack of suppression on DST has been documented previously in 1.46% to 15% of obese patients without CS. Previous studies have suggested simultaneous measurements of serum cortisol, ACTH, and dexamethasone levels after DST to ensure adequate suppression. In this retrospective analysis, we compared the plasma levels of ACTH, dexamethasone, and cortisol levels after 1 mg and 2 mg DST in healthy obese (class III) subjects. The study involved 6 subjects (2 males, 4 females, age 37.5 ± 8.79 years, BMI 43.65 ± 3.12 (kg/m2) who were referred for evaluation of abnormal weight gain. Exclusion criteria for these subjects included diabetes mellitus, pregnancy, history of CS, psychiatric disorders, chronic liver disease, chronic renal failure, malabsorption disorders and nephrotic syndrome. The exclusion of CS was done by history and physical examination showing the lack of specific clinical features of CS. Additionally, none of the subjects were taking drugs that interfered with CYP3A4 or oral contraceptives within 3 months preceding the study. None of the participants reported alcohol consumption of more than 30 g per day. Screening tests for CS involved 1 mg, 2 mg DST, LNSC and 24-hour urine cortisol levels. Results: Following 1 mg DST in 5 subjects, the mean serum cortisol levels were 1.35 ± 0.13 mcg/dL and the mean serum dexamethasone levels, and ACTH levels were 282 ± 44 ng/dL and 5.92 ± 1.56 pg/mL, respectively. However, in one subject (BMI 43.5) the post-DST cortisol level was 2.96 mcg/dL with corresponding dexamethasone level of 138 ng/dL and ACTH level of 21 pg/mL. However, following 2 mg DST in all 6 subjects the serum cortisol levels were less than 1.8 mcg/dL (1.21± 0.22 mcg/dL) with ACTH levels (3.87 ± 0.70 pg/mL) and dexamethasone levels of 482 ± 80 ng/dL. The LNSC levels were normal in 4 subjects (0.010 ± 0.005 mcg/dL), whereas in 2 subjects these were minimally elevated. 24-hour urine cortisol levels were normal in 5 subjects (29.4 ± 3.74 mcg) and in one subject this was mildly elevated (67 mcg). Long term follow-up of all subjects confirmed normal cortisol status. Previous studies have demonstrated that routine CS screening of patients affected by severe obesity is not indicated. However, other investigations have shown CS may occur in a small percentage of severe obese patients. In conclusion, 2 mg DST is a preferred test in obese patients suspected to have CS although 1 mg DST generally can be used as an initial screening test. Additionally, serum dexamethasone and ACTH measurements may still be useful in patients who are suspected to have a false-positive DST. Presentation: 6/1/2024

6695 When Pheochromocytoma Presents As Acute Renal Failure, With Complete Resolution, A Case Report

Abstract Disclosure: U.A. Siddiqui: None. D. Deyar: None. D. Bondarenko: None. M. Ahmad: None. K.K. Lessard: None. Pheochromocytomas and paragangliomas (PPGL), are rare neuroendocrine tumors (0.66/ 100,000 cases), often characterized by paroxysmal hypertension and associated symptoms. While cardiac complications have been well-documented in the literature, there is limited information regarding acute renal failure. We explore a unique case of pheochromocytoma presenting initially with hypertensive crisis, but also with an unexpected journey into acute renal failure and subsequent recovery. 62-year-old hispanic male without known past medical history presents to the emergency department with chest pain, epigastric pain, dyspnea, and emesis. He was tachypneic, febrile (101°F), hypoxic (83% on room air), and profoundly hypertensive (188/112 mmHg). CT scan showed pneumonia as well as a 7cm complex mass within the left adrenal gland. Admitting labs showed metabolic acidosis, acute kidney injury (Cr 2.52mg/dL) and elevated troponins. Echocardiogram showed a reduced ejection fraction 45-50% and coronary angiography showed mild nonocclusive coronary artery disease. MRI visualized a solid left adrenal mass measuring 6.8cm with enhanced, mixed T1/T2 signaling and drop out inconsistent with adenoma. Adrenal labs revealed ACTH 125 pg/mL (9-46 pg/mL) and cortisol 27mcg/dL free metanephrine (MN) 1,422 pg/mL (<57 pg/mL), and free normetanephrine (NMN) >20,000 pg/mL (<148 pg/mL), total free MN + NMN >40,000 pg/mL (<205 pg/mL). Preoperative MIBG scan showed increased tracer activity of the left adrenal consistent with pheochromocytoma. Alpha blockade was performed using doxazosin and carvedilol was continued. Unfortunately, he developed oliguria and rising creatinine ( 7.4mg/DL). Kidney biopsy showed findings of acute tubular necrosis and mild fibrosis. Hemodialysis was initiated, receiving 12 sessions prior to undergoing open left adrenalectomy with mass resection on day 22 of admission. Post-operative blood pressure was managed with volume re-expansion and tapering of alpha blocker. Within 72 hours, renal function fully recovered and dialysis was discontinued. Follow up metanephrines are within normal limits and genetic testing results remain pending. Cases of acute renal failure and PPGL are scarce, and this case report contributes to the topic. Mortality in p is usually due to cardiovascular complications such as stroke, cardiomyopathy, and dysrhythmia [2]. Renal complications result from hypertensive nephrosclerosis or nephrotic syndrome. To date, only one case report from 1961 exists on acute tubular necrosis and PPGL [3]. We present an interesting case of pheochromocytoma complicated by hypertensive crisis and acute renal failure requiring dialysis. Resection of the pheochromocytoma normalized renal function. This demonstrates the importance of timely resection of the tumor and meticulous blood pressure management to ensure optimal outcomes. Presentation: 6/2/2024

8165 A Case Of Rhabdomyolysis-Induced Hypocalcemia And Hypercalcemia

Abstract Disclosure: A. Desai: None. A.L. Izzi: None. B. Flores Chang: None. A. Sajan: None. Introduction: Rhabdomyolysis is a syndrome characterized by muscle breakdown and the release of intracellular muscle contents into circulation. It is associated with electrolyte abnormalities and acute renal failure that can lead to prolonged hospitalization. We report a case of persistent hypercalcemia from recovery of acute renal failure and severe rhabdomyolysis. Case Description: A 47-year-old man with past medical history of polysubstance use initially presented with opiate-induced acute encephalopathy and respiratory failure. He developed severe rhabdomyolysis during the hospital course leading to acute renal failure requiring hemodialysis with hypocalcemia. The initial labs showed corrected calcium 6.2 mg/dL [9.2-11.0], ionized calcium 3.48 mg/dL [4.65-5.28], creatinine kinase level was >72,600 U/L [38-174], BUN 110 mg/dL [8-23], creatinine 7.8 mg/dL [0.6-1.2], and GFR 7 ml/min/BSA. His renal function improved over the next several days in the hospital. The serum creatinine improved to 4 mg/dL, BUN 49 mg/dL and GFR 20 ml/min/BSA respectively after couple of intermittent dialysis sessions. Six days after the last hemodialysis session, patient developed severe hypercalcemia with corrected calcium values ranging from 13.5 to 14.7 mg/dL and ionized calcium 7.41 mg/dL. Labs showed PTH 10 pg/mL [15-65], 1,25-dihydroxyvitamin D <10.0 pg/dL [21-65] and 25-OH Vitamin D levels 15.3 ng/ mL [30-96], which is consistent non-PTH medicated hypercalcemia. The 24-hour urine calcium was 696 mg [0-300 mg/24 hrs, 2900 cc]. PTH-related peptide was not collected. He was treated with intermittent doses of calcitonin and a single dose of pamidronate when the calcium levels were >13 mg/dL. Hypercalcemia resolved in eleven days after initially noted to have hypercalcemia. The corrected calcium improved to 10.1 mg/dL on the day of discharge. Discussion:Severe rhabdomyolysis is associated with acute kidney injury. The initial hypocalcemic phase during rhabdomyolysis is due to entry of calcium into damaged myocytes and deposition of calcium salts in damaged muscle. This is seen in the oliguric phase of acute kidney injury. After the recovery of rhabdomyolysis, the polyuric phase persists during renal recovery. During this time, up to one third of patients may have rebound hypercalcemia due to massive muscle calcium release. As per case reports the hypercalcemia phase lasts from 8 days to 3.5 months. In our case, the patient initially developed hypocalcemia in the oliguric phase of acute kidney injury from rhabdomyolysis. He developed hypercalcemia in the polyuric phase of renal recovery. The hypercalcemia resolved with intravenous hydration, calcitonin and pamidronate. Rhabdomyolysis is a rare cause for both hypocalcemia and hypercalcemia. Our case highlights the biphasic calcium response associated with rhabdomyolysis in the setting of renal impairment and recovery. Presentation: 6/1/2024

7073 Treasure or Terror: Dilemmas in the Management of a Giant Parathyroid Adenoma

Abstract Disclosure: A.D. Galia: None. R. De Guzman: None. S. Suib - Salvilla: None. Background: Primary hyperparathyroidism is a common endocrine disorder with an incidence of 25 per 100,000 people in the general population. More commonly caused by parathyroid adenomas in 80-85%, giant parathyroid adenomas weighing more than 3.5 g or measuring more than 2 cm may rarely occur. There have been no reported prevalence data of parathyroid adenoma among ASEAN countries, especially in the Philippines. Clinical Case: A 43-year-old, female, Filipino, initially asymptomatic with anterior neck mass for 8 years then presented with generalized body malaise, easy fatigability, lower extremities pain and numbness. Six years ago, neck ultrasound showed left thyroid nodule; abdominal sonogram showed bilateral medullary nephrocalcinosis, with hypercalcemia, elevated intact PTH, and elevated creatinine. She was unable to undergo further workup and management until she presented a few months ago because of generalized body malaise, abdominal pain, nausea, and vomiting because of hypercalcemia and non-oliguric renal failure. Serum ionized calcium was 1.90 mmol/L (NV 1.15 - 1.30), intact PTH 2000 pg/mL, and serum creatinine 6.08 mg/dL. With unavailability of calcitonin and pamidronate, medical management of hypercalcemia included cautious hydration followed by diuresis, zoledronic acid, and cinacalcet. Sestamibi scan showed a large parathyroid adenoma. Bone densitometry showed osteoporosis (T score = below -2.5). After medical evaluation, she underwent parathyroidectomy under general anesthesia. Intact PTH level perioperatively were as follows: pre-op = 2,078.2 pg/mL; 30 mins = 477.1 pg/mL; 1 hour = 335.7 pg/mL, 1 day = 67.2 pg/mL. The resected mass was 4.2 x 2.4 x 1.6 cm and weighed 4 g; histopathology report was consistent with Parathyroid Adenoma. Post-operatively, patient did not develop hungry bone syndrome. Conclusion: Giant parathyroid adenoma is a rare condition that is usually asymptomatic but can lead to serious complications. In the Philippines, limited availability of laboratory techniques (PTH and sestamibi scan) and availability of medications for hypercalcemia may contribute to underdiagnosis and management. Early detection and treatment can help prevent further complications and improve the overall quality of life. Presentation: 6/3/2024

Estimating the prevalence of chronic kidney disease in the older population using health screening data in Japan.

In aging societies, the prevalence of chronic kidney disease (CKD) is expected to increase but may be underestimated because many asymptomatic patients remain undiagnosed. This study aimed to estimate the CKD prevalence among the general older population in Japan. This cross-sectional study used health screening data from the Japan Health Insurance Association collected between April 2014 and March 2023. Data from older people aged 65-90years who underwent renal function screening for estimated glomerular filtration rate (eGFR) and urine protein tests were analyzed. CKD was defined as eGFR < 60mL/min/1.73m2 or proteinuria ≥ 1 + . Inverse probability weighting was used to account for the selection bias. The variables used for weighting were age, sex, insurance status, and the number of previous screenings. Among 2.98 million older individuals, 588,809 (19.7%) had undergone screening (median [IQR] age, 69.9 [67.9-76.2] years, 337,862 women [57.4%]). Regarding the weighted CKD prevalence, 25.3% of the individuals aged 65-90years had CKD; 11.8% of those aged 65-75years and 34.6% of those aged 75years and over showed an increase in prevalence with age. Among the patients with CKD, over half exhibited mild renal dysfunction without proteinuria. Hypertension and diabetes were common comorbidities in older patients with CKD. This cross-sectional study revealed that the weighted prevalence of CKD in the older population aged 65-90years was high (one in four individuals), indicating that it increases with age. Further studies are required to examine the clinical significance of these findings.

12609 Navigating The Therapeutic Challenge Of Post-surgical Hypoparathyroidism And Refractory Hypocalcemia

Abstract Disclosure: D. Fawcett: None. A. Domingo: None. Introduction: Post-surgical hypoparathyroidism poses a challenge due to calcium metabolism disturbances, ranging from mild to life-threatening complications. Despite advancements, vigilant monitoring and tailored interventions are vital for optimizing outcomes. Refractory hypocalcemia, resistant to standard therapies, underscores the need for specialized care to prevent prolonged hospitalization and morbidity. Case description: A 68-year-old woman with a history of Graves' disease and parathyroid carcinoma underwent total thyroidectomy and parathyroidectomy in January 2024. She presented to the emergency department for the second time with a recurrence of bilateral hand and perioral paresthesias, along with numbness, tingling, and weakness throughout her body. Notably, she had a prior hospital admission with similar symptoms and was discharged on calcium carbonate, magnesium, calcitriol, and vitamin D3. Vital signs were not provided. Initial laboratory workup revealed a calcium level of 4.3, with corrected calcium at 5.8, and magnesium levels at 1.8, supplemented with magnesium oxide. A 24-hour urine calcium test, vitamin D, and malabsorptive workup for celiac disease were unremarkable. Immunoglobulin A was low; however, tissue transglutaminase IgA and anti-gliadin antibodies were negative. An electrocardiogram showed a normal sinus rhythm with QT prolongation to 570 ms. Despite resuming her home regimen, her calcium level remained low, prompting initiation of calcium infusion. Consultations with endocrinology and nephrology were made, necessitating close monitoring and uptitration of calcium and vitamin D supplements for achievement and maintenance of low normal calcium levels. High doses of 3g TID of calcium and calcitriol 2mcg PO TID allowed for symptom control and discharge with outpatient follow-up with endocrinology and nephrology. Conclusion: Supplemental therapy with calcium and vitamin D analogues is standard for managing post-surgical hypoparathyroidism. Early identification and adequate management prevent hypocalcemia-related complications, including tetany, seizures, and cardiovascular anomalies such as QTc prolongation, as seen in our patient, which can result in torsade de pointes. Multidisciplinary care alongside nephrology was paramount. Serum calcium should be maintained in the low normal range, and 24-hour urine calcium excretion should also be closely monitored. Daily hydrochlorothiazide can be used to prevent hypercalciuria. In recurrent cases, as in our patient, titration of calcium and vitamin D analogues is imperative. Long-term consequences, including renal dysfunction, osteoporosis, and increased cardiovascular risk, underscore the necessity for timely diagnosis and management. Presentation: 6/2/2024

A Case of Chronic Back Pain: Revealing Complete Ureteral Duplicity in an Adult Woman

Ureteral duplication is a rare congenital anomaly, often diagnosed incidentally, characterized by the presence of two distinct ureters draining a single kidney. This condition can lead to complications such as vesicoureteral reflux or upper pole obstruction, often due to ectopic ureteral insertion or ureterocele. We report the case of a 40-year-old woman presenting with left-sided chronic low-back pain. Imaging studies, including ultrasound and CT urography, revealed bilateral ureteral duplication with significant left ureterohydronephrosis due to dysplasia and ectopic insertion of the upper ureter. Radiological imaging, especially CT urography, is essential for diagnosing ureteral duplication and identifying its complications. Timely imaging and intervention are critical for preserving renal function, with treatment options depending on the extent of renal impairment. These may include partial or total ureteronephrectomy or ureteral reimplantation.

12344 Four-Month Delay In Denosumab Induced Severe Hypocalcemia And Hypophosphatemia. Case Report

Abstract Disclosure: M.M. Eid: None. S. Reutrakul: None. Introduction: Denosumab is a fully human monoclonal antibody that binds to the receptor activator of nuclear factor kappa Β ligand, blocks osteoclast function and reduces bone resorption. Case: A 91 year old male with history of osteoporosis, type 2 diabetes, chronic kidney disease (CKD) and prostate cancer. Presented with fatigue and cold intolerance. Denied confusion, muscle cramp, perioral numbness/tingling, bowel habit change. Medications included empagliflozin 12.5 mg/day, leuprorelin 45 mg every 6 months since 2021 and cholecalciferol 1000IU/day. On examination, he was alert and oriented x 3 with stable vital signs. No thyromegaly. Chvostek's sign was negative. Labs: serum calcium (Ca) 6.5 mg/dl, corrected Ca (Co Ca) 6.7mg/dl(N 8.7-10.4), ionized Ca 0.7mMol/l (N 1.13-1.32), TSH 131uIU/ml (N 0.55-4.78), free T4 0.72ng/dl (N 0.89-1.76), creatinine 1.55mg/dl, GFR 42ml/min/1.73m2, HbA1C 6.1%. EKG with corrected QT interval of 499 msec. Hypocalcemia work up : parathyroid hormone (PTH) 762 pg/ml (N 18.4-80.1), 25 OH vitamin D (Vit D) 37ng/ml (N 30-100), 1,25 OH Vit D 77pg/ml (N 18-72), phosphorus (Phos) 1mg/dl (N 2.4-5.1), magnesium (Mag) 1.7mg/dl (N 1.6-2.6),ALP 59U/L(N 45-117). Clinical impressions were a new diagnosis of primary hypothyroidism and non PTH mediated hypocalcemia with secondary hyperparathyroidism. A thorough review of medication revealed that he received the first dose of denosumab 60 mg 4 months prior to this presentation. Baseline labs 1 month prior to denosumab: Ca/Co Ca 9.1/9.2mg/dl, Phos 4.5mg/dl, PTH 199.6pg/ml, Mag 2.1mg/dl,TSH 2.72 uIU/ml. 2 months after denosumab administration, serum Ca/Co Ca 8.8/8.6mg/dl. He was admitted and received Ca gluconate 2gm IV pushes, calcitriol 0.5 mcg/day and levothyroxine 50 mcg/day and kept on cardiac monitoring. He remained asymptomatic. On the 5th day, serum Ca/Co Ca 8.4/8.6mg/dl, Phos 3mg/dl, Mag 2mg/dl. He was discharged on oral Ca Carbonate, calcitriol and levothyroxine. The second denosumab dose was cancelled. Conclusion: Denosumab is an effective anti-osteoporotic medication but can cause hypocalcemia. The risks for denosumab induced hypocalcemia include renal impairment, Vit D deficiency and lack of Ca/Vit D supplementation. Hypocalcemia usually occurs 1 - 2 weeks after denosumab, corresponding to its peak of action. Checking serum Ca and Vit D with correction of deficiencies before starting denosumab is recommended. In high risk patients with CKD, daily Ca and Vit D supplements are recommended (1). Our case has CKD and developed severe hypocalcemia and hypophosphatemia 4 months after receiving denosumab without other apparent causes for hypocalcemia. Hypothyroidism is likely an incidental diagnosis and not contributing to hypocalcemia in the absence of rhabdomyolysis. Reference: 1.Jalleh R, Basu G, Leu RL, Jesudason S: Denosumab induced severe hypocalcemia in chronic kidney disease. Case Rep Nephrol.2018 Presentation: 6/2/2024

6636 Primary Hyperaldosteronism Leading to Aldosterone Deficiency

Abstract Disclosure: N.G. Haverstick: None. J.R. Anthony: None. Primary Hyperaldosteronism is a disease process that is often missed, and under checked due to poor screening tools. The disease presents with a common problem, uncontrolled hypertension. It also presents with hypokalemia, fatigue and headaches. It can easily be masked with blood pressure medications, CKD, and pain medications. After treatment there are some rare reports of patients developing hypoaldosteronism. Some risk factors are age &amp;gt;50, duration of hypertension &amp;gt;10 years, pre-existing renal impairment and adrenal adenoma size &amp;gt;2 cm. The patient will present with the opposite: hyperkalemia and hypotension. This is due to the atrophy of the previously healthy gland. Usually this resolves within a year. However in our patient she has continued to require long standing mineralocorticoid replacement therapy. This case highlights the importance of early recognition of hyperaldosteronism. A 63 year-old-female with a medical history of hypertension and diabetes mellitus is being followed for 30+ years of uncontrolled hypertension. Patient has been on multiple agents and blood pressure remained elevated after trying triamterene/hctz, metoprolol, irbesartan, amlodipine. After changing her PCP, there was further investigation into the cause. Leading differentials were Primary Hyperaldosteronism vs Renal Artery Stenosis vs Primary Hypertension. She also had multiple labs with her Potassium below 3 mEq/l. Additional labs were obtained and her Aldosterone level 209 ng/dl and Renin &amp;lt;0.167 ng/mL/hr. The patient was referred to Endocrinology who performed a fludrocortisone suppression test, which did not suppress the levels. A CT scan of the abdomen was performed that showed a 1.3 cm right adrenal mass typical with adrenal adenoma. The patient had an adrenalectomy surgery in February 2022. The patient recovered well, however now developed hypotension off medication, and had consistent hyperkalemia with K &amp;gt; 5.5 mEq/l. The patient had now developed aldosterone deficiency. This was due to the long standing hyperaldosteronism that had caused her left adrenal gland to atrophy after 30 years. The patient was started on Fludrocortisone 0.1 mg daily and a low potassium diet. She has remained off any blood pressure medications since her right adrenalectomy. She has continued to require the mineralocorticoid replacement to date. The diagnostic work-up for primary aldosteronism involves screening, confirmatory testing, and localization studies to distinguish unilateral pathology which may be amenable to adrenalectomy from bilateral adrenal hyperplasia. Through literature review, one theory is that chronic suppression of renin may cause atrophy of the zona glomerulosa cells and hypoaldosteronism. Throughout the case report we emphasize on the importance of early diagnostic screening of secondary hypertension as well as the complications from adrenalectomy. Presentation: 6/2/2024

8071 Prevention Of Acute Kidney Injury By Reducing Mitochondrial Dysfunction In Diabetic Mice

Abstract Disclosure: M. Kim: None. C. Oh: None. A. Khang: None. J. Jeon: None. I. Lee: None. Background: Acute Kidney Injury (AKI) significantly contributes to the pathogenesis of diabetic kidney disease, often exacerbating chronic kidney disease (CKD) and accelerating the need for dialysis. Mitochondrial dysfunction, induced by an increase in reactive Oxygen Species (ROS) and inflammation, plays a crucial role in AKI. This study investigates the prevention of AKI by reducing mitochondrial dysfunction through pyruvate dehydrogenase kinase (PDK) inhibition in an ischemia-reperfusion (IR)-induced AKI model using streptozotocin (STZ)-induced diabetic mice. Methods: We utilized an IR-induced AKI model in STZ-induced diabetic C57BL6/J mice, subjecting them to IR by clamping both renal pedicles. Mitochondrial function tests, cellular apoptosis, and inflammatory markers were evaluated in NRK-52E cells and mouse primary tubular cells after hypoxia and reoxygenation using a hypoxia workstation. Results: In diabetic mice experiencing AKI following IR injury, there was a significant increase in pyruvate dehydrogenase E1α (PDHE1α) phosphorylation. This correlated with a notable increase in mitochondrial damage - TEM images of mice with IR-induced kidney injury revealed distension, loss of cristae, and fragmentation of the mitochondria. We also observed a decrease in oxygen consumption rate (OCR) accompanied by increased ROS, as well as increased production of inflammatory markers. Remarkably, the pan-PDK inhibitor, sodium dichloroacetate (DCA), mitigated apoptosis, attributable to the reduction of PDHE1α phosphorylation levels as well as normalized mitochondrial morphology and function. DCA treatment lessened oxidative stress and decreased the production of inflammatory markers following IR-induced AKI or hypoxia-reoxygenation injury. Conclusion: Restoration of mitochondrial function by DCA effectively alleviated renal injury by decreasing ROS production and inflammation, highlighting its critical role in IR-mediated damage. These results suggest another potential target for renal protection during AKI; therefore, the prevention of acute kidney injury through the inhibition of PDK could be a promising therapeutic approach for treating Diabetic Kidney Disease (DKD). Presentation: 6/1/2024

9360 Evaluating The More Accurate Indicator Of Kidney Function In Mild Autonomous Cortisol Secretion: EGFR Creatinine Versus EGFR Cystatin

Abstract Disclosure: L. Rahimi: None. J. Saini: None. E. Atkinson: None. S. Achenbach: None. A. Kattah: None. I. Bancos: None. Introduction: Patients with mild autonomous cortisol secretion (MACS) have higher prevalence of cardiovascular comorbidities including chronic kidney disease. However, considering that patients with MACS may have relative skeletal muscle atrophy, it is unclear whether the creatine-based assessment of kidney function is accurate in this population. Objective: To characterize the differences in assessing estimated glomerular filtration rate using cystatin (eGFRcys) versus creatinine (eGFRcre) in patients with MACS versus referent subjects. Methods: Cross-sectional single-center study, 2019-2022. MACS was defined as serum cortisol concentration &amp;gt;1.8 mcg/dL after the 1 mg overnight dexamethasone suppression test (DST). For each patient, eGFRcre, eGFRcys and eGFRcre/eGFRcys ratio were measured and compared between the two groups. Body composition was measured by DXA scan. The Kruskal-Wallis test was used to compare measurements between groups. Result: A total of 37 patients with MACS (median age 59 years (interquartile range, IQR 47-67), 25 (68%) women) and 45 referent subjects (median age 57 years (IQR 51-66), 30 (67%) women) were included. The distribution of BMI, total body fat mass and total body lean mass were similar between the two groups. In the MACS cohort, the median cortisol following 1-mg DST was 3.0 ug/dL (IQR, 2.2-4.0). While assessment of kidney function with eGFRcre showed no differences between patients with MACS and referent subjects (median 85.1 vs 87.0 ml/min/1.73m2, P=0.431), kidney function using eGFRcys was lower in MACS (median 78.0 vs 89.3 ml/min/1.73m2 in referents, P&amp;lt;0.014), resulting also in a higher eGFRcre/eGFRcys ratio (median 1.07 vs 0.97 in MACS vs referents, P=0.053). After adjusting for age, sex, and BMI, a higher 1 mg DST cortisol level in the MACS cohort was associated with a higher eGFRcre/eGFRcys ratio (Spearman correlation coefficient of 0.35, P = 0.042). Lower eGFRcys was associated with higher fat mass (Spearman correlation of -0.26, P = 0.023), and a higher eGFRcre/eGFRcys ratio showed a trend towards lower lean mass (Spearman correlation of -0.20, P = 0.081). Conclusion: Creatinine-based eGFR assessment in patients with MACS underestimates the degree of kidney dysfunction, likely due to underlying skeletal muscle atrophy. eGFRcys is a more accurate indicator of kidney function in patients with hypercortisolism. Presentation: 6/1/2024

8668 Total And Trunk Body Fat Are Associated With Chronic Kidney Disease Progression In Type 2 Diabetes Patients: A Prospective Study

Abstract Disclosure: T. Zelmanovitz: None. D. Weber: None. C. Pavinatto: None. G. Bello: None. M.R. de Souza: None. R.B. Junior: None. M. Azevedo: None. B.L. Dama: None. S. Silveiro: None. Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease and obesity is considered an independent risk factor for the development and progression of this complication. However, BMI alone, the most commonly used measure to assess adiposity, may not be enough to identification of high risk patients. The ideal markers of adiposity in these patients still need to be better determined. The aim of this study was to evaluate the association between the progression of DKD in type 2 diabetes patients and the following body adiposity markers: BMI, waist circumference (WC) and estimated total and trunk body fat. Research design and methods: In this prospective cohort study, at baseline, type 2 diabetes outpatients were submitted to percentage body fat (PBF) evaluation estimated by bioelectrical impedance (BIA; InBody 230, Biospace, Korea) as well as Dual Energy X-Ray Absorptiometry (DXA; Lunar - iDXA), as a reference standard. Clinical evaluation consisted of glycemic and lipid profile, blood pressure control and the search for diabetic chronic complications. Urinary albumin was measured twice and estimated glomerular filtration rate (eGFR) was estimated by using the CKD-EPI equation. The progression of DKD was defined by the presence of at least one of the following: worsening of albuminuria, a decline of eGFR ≥ 5 ml/min/1.73m2 per year, a decline in eGFR of ≥ 40% from baseline or kidney failure defined by sustained eGFR &amp;lt; 15 ml/min/1.73m2. Results: A total of 201 patients with type 2 diabetes (aged 63 ± 9 years; 42% male), were followed during 6 years. In a multivariate Cox regression analysis, the PBF was associated with progression of DKD (HR=1.04, 95% CI: 1.008 - 1.08; P= 0.015), adjusted for age, gender, using ACE inhibitors or angiotensin receptor blockers, and systolic blood pressure values. In a different model, percentage of trunk fat was also associated with progression of DKD (HR=1.05, 95% CI: 1.02 - 1.09; P= 0.003), adjusted for the same covariates. No association was observed with BMI and WC. Conclusion: In patients with type 2 diabetes, percentage total and trunk body fat, as markers of body adiposity, seem to be associated with progression of DKD. Confirming these findings with further studies, it could provide one more tool in the evaluation and management of a modifiable risk factor of this complication. Presentation: 6/1/2024

12431 14-year-old Presenting With Thrombocytopenia-Associated Multi-Organ Failure In The Setting Of Diabetic Ketoacidosis/Hyperosmolar Hyperglycemic Syndrome

Abstract Disclosure: N.C. Gunaratne-Breaux: None. D. Deplewski: None. Title: 14-Year-Old Presenting with Thrombocytopenia Associated Multi-Organ Failure in the setting of Diabetic Ketoacidosis/Hyperosmolar Hyperglycemic Syndrome Background: Coagulation complications are rare in hyperglycemia emergencies in children and adolescents. In patients presenting with severe and atypical hyperglycemia emergencies, special considerations need to be made to rule out life-threatening coagulopathy. Clinical Case: A 14-year-old male with history of Type 1 Diabetes presented in severe Diabetic Ketoacidosis/Hyperosmolar Hyperglycemic Syndrome overlap. Initially had severe hypotension and altered mental status concerning for cerebral edema. Initial venous blood gas showed pH of 6.82, pCO2 17.1, and HCO3 2.8, serum glucose was 1375 mg/dL, serum ketones &amp;gt;7.00 mmol/L, and serum osmolality was 384 mOsm/kg. Once insulin drip was started, glucose, ketones, and serum osmolality improved, but patient continued to be encephalopathic and had worsening tachypnea and desaturations. Patient was eventually intubated. After intubation, patient’s acidosis improved, but patient developed kidney failure (prompting initiation of dialysis), liver injury, decreased cardiac function, and high inflammatory state. A comprehensive multi-specialty team including pediatric intensive care, infectious diseases, rheumatology, neurology, and cardiology were involved in the care. On day three of admission, patient had multiple areas of ischemia on fingertips and ear and clotting of multiple IV and dialysis catheters, prompting a coagulopathy evaluation. Labs showed microcytic anemia (hemoglobin 10.0 g/dL; mean corpuscular volume 75fL), thrombocytopenia (platelet count 17 10e3/uL), coagulopathy (prothrombin time 16.8 sec, INR 1.3, prolonged thrombin time 48.8 sec), and elevated ferritin (507 ng/mL). Given labs and multi-organ involvement, determined by hematology to be Thrombocytopenia Associated Multi-Organ Failure (TAMOF). Patient was started on plasmapheresis and had dramatic improvement – was eventually extubated and returned to neurologic baseline without any notable deficits. Multi-specialty team ruled out all other possible causes of TAMOF; determination that the TAMOF developed secondary to DKA/HHS. Conclusion: Hyperglycemia emergencies can lead to a hyperinflammatory state that can lead to disruption of the coagulation cascade, including disseminated intravascular coagulopathy or thrombotic thrombocytopenia purpura. There have been rare reports of thrombocytopenia associated multi-organ failure provoked by DKA, thought secondary to critical illness mediated low ADAMST13 levels. This is a novel case of TAMOF caused by DKA/HHS overlap syndrome. It is important to screen for coagulopathy in cases of patients with DKA or DKA/HHS who do not show clinical improvement with resolution of ketosis and hyperosmolarity. Presentation: 6/2/2024

7331 A Rare Case Of Familial Hypoparathyroidism

Abstract Disclosure: N. Sekhon: None. K.Z. Win: None. Background: Autosomal dominant hypoparathyroidism disorders are very rare and mostly asymptomatic. We present an interesting case of autosomal hypoparathyroidism with a new variant of gene defect on genetic analysis. Case: A 66-year-old female was referred to the endocrinology clinic for familial hypoparathyroidism and calcium oxalate nephrolithiasis. She had onset of seizures at age 16. She was diagnosed with hypocalcemia and hypoparathyroidism at age 30 when she had her first episode of nephrolithiasis. She had recurrent nephrolithiasis and lithotripsies, ultimately developing chronic kidney impairment that was at stage 3b at the time of evaluation. Renal Ultrasound revealed bilateral nephrolithiasis, and nephrocalcinosis. There was a history of hypoparathyroidism in her father, paternal uncle, and son. Her medications included calcium carbonate-vitamin D3 600-400 mg-unit oral 2 tablets daily and calcitriol 0.5 mcg daily. The pertinent physical examination finding was a short stature with height 4’11” and calluses in fingers. Her recent serum chemistry showed calcium 8.8 mg/dL (reference range 8.3 - 10.6 mg/dL), PTH &amp;lt; 6.3 pg/mL (reference range 18.4 - 80.1 pg/ mL), and phosphorus 3.3 mg/dL (reference range 2.4 - 5.5 mg/dL). 24 hr urine calcium was 96 mg (reference range 50-300 mg/24h). She was treated with hydrochlorothiazide for nephrolithiasis but was discontinued due to hypokalemia. We performed genetic testing that resulted positive for CASR NM_001178065.1 with heterozygosity and damaging missense predictions inherited as autosomal dominant or recessive. Discussion: The calcium-sensing receptor (CaSR) has an important role in calcium homeostasis by regulating parathyroid hormone (PTH) secretion and urinary calcium excretion. Familial hypoparathyroidism disorders are divided into Autosomal dominant hypocalcemia (ADH) type 1 and Autosomal dominant hypocalcemia (ADH) type 2. ADH1 is caused by an activating mutation of calcium-sensing receptor (CASR). The estimated prevalence of ADH1 ranges from 1 per 70,000 to 3.9 per 100,000. It is characterized by mild to moderate hypocalcemia, hyperphosphatemia, hypercalciuria, and inappropriately low but detectable PTH levels. It can be associated with Bartter syndrome Type 5. ADH2 is due to mutations in the alpha subunit of the G protein G11 (Gα11). Our patient had classic symptoms of hypocalcemia including short stature, seizures, kidney stones and its sequelae. Her 24-hour urine analysis showed inappropriately normal urine calcium with low normal serum calcium, undetectable serum PTH, and normal phosphorus. Our patient’s genetic analysis revealed a heterozygous defect in gene CASR with DNA variants c.2564G&amp;gt;A with damaging missense predictions. There is no such variant reported or listed in the ClinVar database. To our knowledge, this is the first such case of an autosomal dominant hypoparathyroidism with this gene defect. Presentation: 6/1/2024

Urinary cyclophilin A as an early marker of chronic kidney disease with underlying type 2 diabetes

Cyclophilin A (CypA) is a novel renal inflammation biomarker, with levels altered in various diseases, particularly in patients with diabetes mellitus (DM) and kidney damage. This study aimed to investigate the correlation between urinary cyclophilin A (uCypA) and chronic kidney disease (CKD) conditions with and without type 2 diabetes mellitus (T2DM) using an in-house enzyme-linked immunoassay (ELISA) method. A uCypA strip-test prototype was also developed. An indirect ELISA was performed to determine the uCypA levels. A 0.48 µg/mL uCypA cutoff differentiated healthy patients from those with early-stage CKD (stages I and II). The uCypA levels were significantly increased in patients with progression of renal deterioration, especially in the T2DM with late-stage CKD group, compared to the control group. Fasting blood sugar (FBS), estimated glomerular filtration rate (eGFR), albumin/creatinine ratio, and metformin use were associated with uCypA levels. Multinomial logistic regression analysis revealed an association between uCypA levels and T2DM diagnosed for over five years and early-stage CKD. This finding shows that uCypA could be used as a biomarker for distinguishing early-stage CKD as well as T2DM complications, which is beneficial for patients to be aware of their health status and change their behavior to slow kidney deterioration.

Causes of death in Japanese patients with diabetes based on the results of a survey of 68,555 cases during 2011-2020: Committee report on causes of death in diabetes mellitus, Japan Diabetes Society (English version).

The principal causes of death among 68,555 patients with diabetes and 164,621 patients without diabetes who died in 208 hospitals throughout Japan between 2011 and 2020 were determined based on a survey of hospital records. The most frequent cause of death in patients with diabetes was malignant neoplasms (38.9%) (lung 7.8%, pancreas 6.5%, liver 4.1%), followed, in order of descending frequency, by infectious diseases (17.0%) and then vascular diseases (10.9%) (cerebrovascular diseases 5.2%, ischemic heart diseases 3.5%, renal failure 2.3%). The proportion of deaths from malignant neoplasms and vascular diseases has trended upward and downward, respectively. Almost all deaths from ischemic heart diseases were due to myocardial infarction, and the proportion of deaths from heart diseases other than ischemic heart diseases was relatively high (9.0%), with most cases due to heart failure. Diabetic coma associated with hyperglycemia accounted for only 0.3% of deaths. The proportion of deaths from malignant neoplasms, infectious diseases, renal failure, ischemic heart diseases, and heart failure was significantly higher in patients with diabetes than in those without diabetes, and the proportion of deaths from cerebrovascular diseases was significantly lower in patients with diabetes. With regard to the relationship between the age and cause of death in patients with diabetes, malignant neoplasms were the most frequent cause of death in all age groups, and the incidence was around 50% for those in their 50s and 60s. The incidence of death due to infectious diseases was highest in patients older than their 70s. The incidence of death due to vascular diseases for patients in their 40s and 50s was higher than that due to infectious diseases. The highest incidence of death due to ischemic heart diseases was observed for patients in their 40s, and that due to renal failure and heart failure in patients older than their 70s. Compared with patients without diabetes, patients with diabetes demonstrated a higher incidence of death due to pancreatic cancer, infectious diseases, renal failure, ischemic heart diseases, and heart failure, and a lower incidence of death due to cerebrovascular diseases in all age groups. The average age at death of patients with diabetes was 74.4 years old in men and 77.4 years old in women, which were lower than the average lifespan of the Japanese general population in 2020 by 7.2 and 10.3 years, respectively. However, these differences were smaller than in previous surveys. The average age at death due to all causes, especially due to ischemic heart diseases, cerebrovascular diseases, heart failure, infectious diseases, and diabetic coma, was lower in patients with 'poorer' glycemic control than in those with 'better' glycemic control. In the total survey population, the average age at death of patients with diabetes was significantly higher than that of patients without diabetes. The average age at death due to malignant neoplasms and cerebrovascular diseases was higher in patients with diabetes than in those without diabetes and that due to renal failure, ischemic heart diseases, and infectious diseases was lower in patients with diabetes than in those without diabetes.