scholarly journals Nephrogenic Diabetes Insipidus with New-Onset Diabetic Ketoacidosis in a Child- Challenges in Fluid and Electrolyte Management

2021 ◽  
Author(s):  
Yu-Shan Tseng ◽  
Nicole Swaney ◽  
Katherine Cashen ◽  
Amrish Jain ◽  
Nina Ma ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Diabetic Ketoacidosis ◽  
Mental Status ◽  
Nephrogenic Diabetes Insipidus ◽  
Hypovolemic Shock ◽  
Free Water ◽  
Serum Osmolality ◽  
Rapid Decline ◽  
Fluid Deficit ◽  
New Onset

Abstract BackgroundIntensive care management of diabetic ketoacidosis (DKA) is targeted to reverse ketoacidosis, replace the fluid deficit, and correct electrolyte imbalances. Adequate restoration of circulation and treatment of shock is key. Pediatric treatment guidelines of DKA have become standard but complexities arise in children with co-morbidities. Congenital nephrogenic diabetes insipidus (NDI) is a rare hereditary disorder characterized by impaired renal concentrating ability and treatment is challenging. NDI and DKA together have only been previously reported in one patient.Case Diagnosis/TreatmentWe present the case of a 12-year-old male with NDI and new onset DKA with hyperosmolality. He presented in hypovolemic shock with altered mental status. Rehydration was challenging and isotonic fluid resuscitation resulted in increased urine output and worsening hyperosmolar state. Use of hypotonic fluid and insulin infusion led to lowering of serum osmolality faster than desired and increased the risk for cerebral edema. Despite the rapid decline in serum osmolality his mental status improved so we allowed him to drink free water mixed with potassium phosphorous every hour to match his urinary output (1:1 replacement) and continued 0.45% sodium chloride based on his fluid deficit and replacement rate with improvement in his clinical status.ConclusionsThis case illustrates the challenges of managing hypovolemic shock, hyperosmolality, and extreme electrolyte derangements driven by NDI and DKA.

scholarly journals MON-LB65 Lithium: The Culprit of Multiple Endocrinopathies

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Alice Yau ◽  
Gul Bahtiyar ◽  
Giovanna Rodriguez ◽  
Jose R Martinez Escudero
Keyword(s):  
Bipolar Disorder ◽  
Diabetes Insipidus ◽  
Mental Status ◽  
Nephrogenic Diabetes Insipidus ◽  
Kidney Injury ◽  
Urine Osmolality ◽  
Altered Mental Status ◽  
Clinical Findings ◽  
Volume Depletion ◽  
Collecting Tubules

Abstract Background: Lithium, commonly used to treat various psychiatric disorders such as bipolar disorder, can cause acute toxicity that presents with nausea, vomiting and diarrhea. Lithium can also cause life-threatening endocrine abnormalities, including hypercalcemia, hypernatremia, and both hypo- and hyperthyroidism. Clinical Case: A 61-year old female with hypothyroidism, bipolar disorder, hyperparathyroidism with two-gland parathyroidectomy on lithium for over 30 years presented with altered mental status. Initial labs revealed elevated creatinine 1.92 mg/dL (0.8-2.00mg/dL) compared to baseline 0.82 mg/dL, sodium 154 mg/dL (135-147 mg/dL), Corrected calcium 11.7 mg/dL (8.5-10.5 mg/dL), PTH 96 pg/mL (15-65 pg/mL), and high lithium levels 1.45 mmol/L (0.60-1.20 mmol/L). Further studies showed hypotonic polyuria with no increase in urine osmolality after desmopressin, consistent with nephrogenic diabetes insipidus. Lithium was held and she was treated with aggressive intravenous hydration with dextrose 5% water. Hypercalcemia is thought to result from increased secretion of PTH due to an increased set point at which calcium suppresses PTH release; this often resolves once lithium is stopped. Lithium can also unmask previously unrecognized mild hyperparathyroidism, and/or raise serum PTH concentrations independent of calcium levels.1 The drug interferes with the kidneys’ ability to concentrate urine in the collecting tubules by desensitizing response to antidiuretic hormone, causing diabetes insipidus. The resulting volume depletion from excessive urinary water loss in turn lead to acute kidney injury and hypernatremia.2 Hypothyroidism results from lithium-inhibited synthesis and release of thyroid hormones and decreases iodine trapping. Conclusion: Although these are infrequent complications of lithium use, they remain pertinent clinical findings to consider due to their morbidity. In this case, our patient may have avoided multiple chronic electrolyte abnormalities leading to altered mental status if lithium toxicity had been recognized earlier. References:1. García-Maldonado, Gerardo, and Rubén de Jesús Castro-García. “Endocrinological Disorders Related To The Medical Use Of Lithium. A Narrative Review”. Revista Colombiana De Psiquiatría (English Ed.), vol 48, no. 1, 2019, pp. 35-43. Elsevier BV, doi:10.1016/j.rcpeng.2018.12.005. 2. Tasci, E. “Lithium-Induced Nephrogenic Diabetes Insipidus Responsive To Desmopressin”. Acta Endocrinologica (Bucharest), vol 15, no. 2, 2019, pp. 270-271. ACTA Endocrinologica Foundation, doi:10.4183/aeb.2019.270.

Mechanism of Action of Indomethacin in Tubular Defects

PEDIATRICS ◽  
1985 ◽  
Vol 75 (3) ◽  
pp. 501-507
Author(s):  
Mario Usberti ◽  
Carmine Pecoraro ◽  
Stefano Federico ◽  
Bruno Cianciaruso ◽  
Bruna Guida ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Diabetes Insipidus ◽  
Mechanism Of Action ◽  
Nephrogenic Diabetes Insipidus ◽  
Fanconi Syndrome ◽  
Free Water ◽  
Synthesis Inhibitor ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Load

Indomethacin, a potent prostaglandin synthesis inhibitor, has been proven to be effective in a number of tubular defects characterized by enhanced prostaglandin (namely, prostaglandin E2 (PGE2) production, but its mechanism of action is poorly understood. To elucidate further the mechanism(s) by which indomethacin reverses the abnormal tubular functions, five children with different tubular defects (nephrogenic diabetes insipidus, three cases; Fanconi syndrome, one case; and pseudohypoaldosteronism, one case) were treated with indomethacin. Indomethacin, 1 mg/kg every eight hours, was given for 1 week to all children and then was given chronically to four of the children who responded to the drug. Its use was suspended in a 10 year-old-boy with nephrogenic diabetes insipidus because it proved ineffective. To assess the site along the nephron where indomethacin affects the solute and water excretion, an acute water load study was performed in three responsive children before and during the treatment. Indomethacin did not significantly alter the glomerular filtration rate but was effective in reducing diuresis and levels of urinary sodium and potassium excretion. In the child with Fanconi syndrome, indomethacin was also effective in controlling the urinary loss of phosphate, urate, glucose, and bicarbonate. Results of the water load studies show that indomethacin decreases the delivery of solute from the proximal tubule, reduces the fractional free water clearance, and increases the urine-plasma osmolar ratio. The rate of urinary excretion of prostaglandin E2 was high in all five children; it decreased below normal values in four of them after 1 week of treatment. In the child with nephrogenic diabetes insipidus who did not respond to indomethacin therapy, prostaglandin E2 excretion decreased but the rate remained higher than normal. These results suggest that indomethacin induces retention of solute and water mainly through an enhanced proximal tubular reabsorption.

THE USE AND MODE OF ACTION OF ETHACRYNIC ACID IN NEPHROGENIC DIABETES INSIPIDUS

PEDIATRICS ◽  
1966 ◽  
Vol 37 (3) ◽  
pp. 447-455
Author(s):  
David M. Brown ◽  
John W. Reynolds ◽  
Alfred F. Michael ◽  
Robert A. Ulstrom
Keyword(s):  
Renal Function ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Acid Metabolism ◽  
Ethacrynic Acid ◽  
Sodium Intake ◽  
Urine Volume ◽  
Free Water ◽  
Chloride Excretion ◽  
Diuretic Agents

The use of diuretic agents in the treatment of nephrogenic diabetes insipidus had been reported to result in decreased urine volume and decreased clearance of free water. A study of the use of ethacrynic acid, a potent saluretic agent, was instituted in patients with nephrogenic diabetes insipidus in an attempt to achieve a significant antidiuretic response while allowing a liberal sodium diet. Intravenous ethacrynic acid resulted in decreased urine volume, decreased clearance of free water and decreased RPF and GFR. Prolonged oral administration of ethacrynic acid promoted a significant antidiuretic response when the daily sodium intake was limited to 60 mEq. The effect of ethacrynic acid on renal function, potassium and chloride. excretion, and uric acid metabolism are discussed.

scholarly journals A Case Series of Hyperglycemic Hyperosmolar State During the Global COVID-19 Pandemic

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A334-A335
Author(s):  
Benjamin Donald Hoag ◽  
Michelle Knoll ◽  
Emily Paprocki
Keyword(s):  
Blood Glucose ◽  
Diabetic Ketoacidosis ◽  
Care Center ◽  
Tertiary Care ◽  
Case Series ◽  
Serum Osmolality ◽  
Laboratory Evaluation ◽  
Antibody Testing ◽  
Hyperglycemic Hyperosmolar State ◽  
New Onset

Abstract Hyperglycemic hyperosmolar state (HHS) is rare in pediatrics, particularly in patients with antibody positive diabetes mellitus (DM). Recent literature has implicated COVID-19 in the reported increase in new-onset DM cases, as well as mixed diabetic ketoacidosis (DKA) and HHS cases, however a rise in HHS cases alone has not been well reported [1,2]. We noted an anecdotal increase in the frequency of HHS cases in our pediatric tertiary care center following the onset of the global COVID-19 pandemic. To investigate further, a retrospective chart review evaluating all patients with DM admitted in the first 6 months of 2019 and the first 6 months of 2020 was conducted. A diagnosis of HHS was defined as a blood glucose over 600 mg/dL with a serum osmolality (calculated or measured) greater than 320 mOsm/kg on initial laboratory evaluation. Patients with DKA, defined as a serum bicarbonate level less than 16 mmol/L with evidence of significant ketosis (serum ketones greater than 3 mmol/L), were excluded from the study. During the first 6 months of 2019, 1 patient met inclusion criteria. However, the diagnosis of HHS was complicated by a concurrent diagnosis of diabetes insipidus, which may have contributed to the hyperosmolar state, and a nonketotic lactic acidosis. Five HHS cases were noted in the first 6 months of 2020, 4 of which occurred in May and June. For the 2020 HHS cohort, the average patient age ± SD was 12 ± 3.34 years. The mean ± SD laboratory values included bicarbonate 18.2 ± 1.64 mmol/L, serum blood glucose 776.8 ± 30.75 mg/dL, calculated serum osmolality 328 ± 4.18 mOsm/kg, and HgA1C 12.72 ± 1.16%. All 5 patients in the 2020 cohort had new-onset DM, with 4 of the 5 patients having at least 1 positive DM antibody (GAD antibodies were positive in 3, ICA/IA-2 antibodies in 2, and Zinc Transporter 8 antibodies in 1). No patients displayed COVID-19 symptoms, and only 1 patient was tested for COVID-19 by PCR, which returned negative. However, SARS-CoV2 antibody testing was not available, and it is unknown if these patients had prior COVID-19 illness. In conclusion, we noted an increased incidence of HHS at our hospital, particularly among new-onset, antibody positive DM patients during the initial months of the COVID-19 pandemic. Further study and investigation are needed to determine the cause of this increased local incidence, and if infectious, social, or economic influences related to the COVID-19 pandemic contributed. References: [1] Chan, K.H., et al., Clinical characteristics and outcome in patients with combined diabetic ketoacidosis and hyperosmolar hyperglycemic state associated with COVID-19: A retrospective, hospital-based observational case series. Diabetes Res Clin Pract, 2020. 166: p. 108279. [2] Unsworth, R., et al., New-Onset Type 1 Diabetes in Children During COVID-19: Multicenter Regional Findings in the U.K. Diabetes Care, 2020.

Cooperative mechanisms of acute antidiuretic response to bendroflumethiazide in rats with lithium-induced nephrogenic diabetes insipidus

2010 ◽  
Vol 88 (12) ◽  
pp. 1191-1201 ◽  
Author(s):  
S. Mostafa Shid Moosavi ◽  
Masoud Haghani
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Urine Volume ◽  
Free Water ◽  
Urine Flow ◽  
Water Reabsorption ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Antidiuretic Effect ◽  
Water Clearance

The exact mechanism underlying thiazides-induced paradoxical antidiuresis in diabetes insipidus is still elusive, but it has been hypothesized that it is exerted either via Na+-depletion activating volume-homeostatic reflexes to decrease distal delivery, or direct stimulation of distal water reabsorption. This study examined how these two proposed mechanisms actually cooperate to induce an acute bendroflumethiazide (BFTZ)-antidiuretic effect in nephrogenic diabetes insipidus (NDI). Anaesthetized rats with lithium (Li)-induced NDI were prepared in order to measure their renal functional parameters, and in some of them, bilateral renal denervation (DNX) was induced. After a 30 min control clearance period, we infused either BFTZ into 2 groups, NDI+BFTZ and NDI/DNX+BFTZ, or its vehicle into a NDI+V group, and six 30 min experimental clearance periods were taken. During BFTZ infusion in the NDI+BFTZ group, transiently elevated Na+ excretion was associated with rapidly increased urinary osmolality and decreased free water clearance, but Li clearance and urine flow declined in the later periods. However, in the NDI/DNX+BFTZ group, there was persistently elevated Na+ excretion with unchanged Li clearance and urine flow during the experimental period, while alterations in free water clearance and urinary osmolality resembled those in the NDI+BFTZ group. In conclusion, BFTZ initially exerted two direct effects of natriuresis–diuresis and stimulating free water reabsorption at the distal nephron in NDI, which together elevated Na+ excretion and urinary osmolality but kept the urine volume unchanged in the first hour. Thereafter, the resultant sodium depletion led to the activation of neural reflexes that reduced distal fluid delivery to compensate for BFTZ-induced natriuresis–diuresis which, in cooperation with the direct distal BFTZ-antidiuretic effect, resulted in excretion of urine with a low volume, high osmolality, and normal sodium.

Comparative therapeutic benefit of indomethacin, hydrochlorothiazide, and acetyl-salicylic acid in a patient with nephrogenic diabetes insipidus

1984 ◽  
Vol 106 (3) ◽  
pp. 311-316 ◽  
Author(s):  
H. Vierhapper ◽  
J. Jörg ◽  
L. Favre ◽  
M. B. Vallotton ◽  
W. Waldhäusl
Keyword(s):  
Salicylic Acid ◽  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Free Water ◽  
Therapeutic Benefit ◽  
Prostaglandin Synthesis ◽  
Acetyl Salicylic Acid ◽  
Free Water Clearance ◽  
Endogenous Prostaglandin ◽  
Excretion Rates

Abstract. To define the importance of renal prostaglandins in nephrogenic diabetes insipidus (NDI), diuresis and the urinary excretion of PGE2 and PGF2α were studied in a patient with NDI before and during inhibition of endogenous prostaglandin synthesis with either indomethacin (IND) or acetyl-salicylic acid (ASA). The excretion rates of PGE2 and PGF2α were in the low normal range for the patient's age group, remained unchanged during 6 h of fluid deprivation and were suppressed by IND (150 mg/day), ASA (3 g/day), and by the combination of IND and hydrochlorothiazide (HCT, 50 mg/day). However, whereas IND, HCT, and the combination of IND and HCT reduced diuresis ASA did not. Free water clearance as determined during fluid deprivation remained positive during each phase of therapy. These data fail to demonstrate a direct effect of endogenous ADH on renal prostaglandin synthesis in NDI. The ineffectiveness of ASA to reduce diuresis indicates that indomethacin affects diuresis in NDI by a mechanism other than inhibition of cyclooxygenase.

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