Angiotensin II receptor blockers (ARBs) are contraindicated during pregnancy because of fetal toxicity. All previous reports on adverse fetal outcomes involved women who continued to take low-dose ARBs for hypertension and were unaware of the adverse effects. Herein, we report the case of a 23-year-old pregnant woman in her third trimester who experienced an ARB overdose after an argument with her partner. Pregnancy was complicated by transient oligohydramnios, and fetal magnetic resonance imaging suggested renal failure. Despite these concerns, the newborn had no morphological abnormalities or abnormal neurological findings. Renal impairment improved over time, and the infant grew well. A single overdose of ARBs in the third trimester can lead to fetal renal failure, similar to long-term low-dose ARB administration; however, favorable outcomes are possible. An overdose of ARBs may transiently cause renal failure, which may improve. The study findings may inform counseling for women who are unexpectedly exposed to an overdose of ARBs.

BACKGROUND Angioedema is non-pitting edema that occurs in the deep layers of the skin and subcutaneous tissue due to vascular leakage of plasma resulting from 1 of 2 major pathophysiological processes: mast cell-mediated angioedema and bradykinin-mediated angioedema. While it is a well-recognized adverse reaction of angiotensin-converting enzyme inhibitors, the association of angioedema with angiotensin receptor blockers is relatively less studied. Direct local trauma, although rarely, has been suggested to induce angioedema under certain conditions. We present a unique case of direct, local, trauma-related angioedema in a patient on an angiotensin receptor blocker. CASE REPORT The patient, an 83-year-old woman on telmisartan for hypertension, hit her neck against the edge of a chair during a fall. Shortly thereafter, she developed progressive airway compromise due to airway angioedema, as noted on direct laryngoscopy. A contrast CT scan of the neck also noted edema of the periglottic and supraglottic regions. She required intravenous corticosteroid administration and intubation in the emergency room and was successfully extubated 3 days after admission. She had no prior history of angioedema or allergy. We hypothesize that increased levels of circulatory bradykinin in the setting of telmisartan, combined with a local release of bradykinin from trauma, was the main pathophysiologic cause of the angioedema. CONCLUSIONS This case report highlights the rare and often forgotten adverse reaction of angioedema with use of angiotensin receptor blockers and confirms the finding of local trauma as a possible trigger.

Chronic lithium toxicity is a potentially serious side effect on patients taking lithium for a prolonged period with the diagnosis of mood disorders. The toxicity is even higher in patients taking drugs that interfere with the metabolism of lithium like angiotensin receptor blockers and in older patients with reduced kidney function. In this report, we present the case of a 62-year-old woman who presented to the emergency department with symptoms including loose stools, generalised body weakness, slurred speech, coarse hand tremors, and dystonia persisting for fifteen days. She had been under lithium therapy for bipolar type 1 disorder for 15 years before experiencing these symptoms, which emerged shortly after the addition of telmisartan (angiotensinogen receptor blocker) for hypertension.
UNASSIGNED: angiotensin receptor blocker; bipolar disorder; case reports; lithium; telmisartan.

BACKGROUND: Immunoglobulin A nephropathy (IgAN) is the most common type of primary glomerulonephritis, and recurrent IgAN is common after kidney transplantation (KT). Owing to the differences in various biopsy protocols and follow-ups in each study, the recurrence rate varies from 9.7% to 46%. Although the relapse rates are high, there is no definitive treatment for IgAN recurrence.
METHODS: We present a case of successful management of proteinuria in recurrent IgAN after deceased donor KT. A 60-year-old man diagnosed with IgAN 20 years prior, who progressed to end-stage renal disease, underwent deceased donor KT 5 years prior and was admitted to our hospital with progressively increasing proteinuria.
RESULTS: The pathological examination of the kidney biopsy specimen revealed recurrent IgAN. High-dose steroid treatment was initiated, and the patient was discharged while maintaining steroid treatment. However, outpatient follow-up showed that proteinuria did not decrease while steroids were maintained. Therefore, an angiotensin receptor blocker was administered after explaining its benefits to the patient. After the addition of angiotensin receptor blocker, proteinuria continued to decrease.
CONCLUSIONS: This case report highlights the importance of using renin-angiotensin system inhibitors with supportive care in cases of suspected of recurrent IgAN after KT. It also emphasizes the need to prescribe renin-angiotensin system inhibitors when steroid therapy is unsuccessful in cases of recurrent IgAN after KT.

BACKGROUND: The therapeutic efficacy of renin-angiotensin system inhibitors (RASi) in elderly patients with hypertension and at risk of fractures has been in the limelight because of accumulating evidence that localized RAS activation in bone tissue leads to osteoclastic bone resorption, resulting in osteoporosis. This study set out to investigate the association between RASi use and fracture incidence in a large cohort.
METHODS: We employed a nested case-control design to investigate the association between RASi use and newly developed fractures. A case was defined as a patient newly diagnosed with a fracture between January 2004 and December 2015. We selected 1,049 cases and controls using 1:1 propensity score matching. Conditional logistic regression analysis was conducted to estimate the association between RASi exposure and fracture incidence.
RESULTS: Overall, RASi usage was significantly associated with lower odds for fracture incidence (ever-users vs never-users: OR, 0.73; 95% CI, 0.59-0.91). We found that ARB-only users experienced fewer fractures than RASi-never users (OR, 0.65; 95% CI, 0.49-0.86), whereas ACEi-only users or ARB/ACEi-ever users did not. In subgroup analysis, RASi-ever users without cerebrovascular disease, those with a BMI exceeding 23, and statin exposure had significantly lower ORs.
CONCLUSIONS: The present study established a significant association between RASi use and reduced fracture incidence, thus highlighting the potential clinical utility of RASi use as a preventive strategy in elderly patients at risk for osteoporotic fractures.

BACKGROUND: Angiotensin II receptor blockers (ARBs) are currently considered first-line antihypertensive drugs, effectively inhibiting the renin-angiotensin-aldosterone system. However, ARBs have been associated with intraoperative hypotension during general anesthesia. Although it is recommended to discontinue ARBs for 24 hours before surgery, the optimal duration of discontinuation remains unclear. We present a severe refractory hypotension encountered during general anesthesia despite discontinuing ARBs for 48 hours before anesthesia.
METHODS: A severe refractory hypotension occurred during the induction of general anesthesia for cranioplasty in a 66-year-old male patient (170 cm/75 kg). The patient was taking azilsartan, angiotensin receptor blocker, for hypertension, which was discontinued 48 hours before anesthesia induction. Despite repeated administration of ephedrine and continuous infusion of norepinephrine, hemodynamic instability did not improve. Therefore, the surgery was postponed.
METHODS: The patient was diagnosed with angiotensin receptor blocker-induced refractory hypotension.
METHODS: Before the second surgery, the angiotensin receptor blocker was discontinued 96 hours prior to the surgery. Invasive blood pressure monitoring was performed before anesthesia induction, and vasopressin was prepared. General anesthesia was induced using remimazolam and maintained with desflurane.
RESULTS: The surgery was completed successfully without occurrence of refractory hypotension.
CONCLUSIONS: Refractory hypotension induced by Angiotensin receptor blockers can still occur even after discontinuing the medication for 48 hours before induction of general anesthesia. Despite withholding the medication, caution should be practiced regarding hypotension during general anesthesia in patient taking ARBs.

The purpose of this report is to describe the efficacy of sacubitril/valsartan in 5 hemodialysis patients with hypertension, including a patient with heart failure with reduced ejection fraction (HFrEF) and a patient with preserved ejection fraction (HFpEF) focused on the functional changes in the heart. We switched from angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) to sacubitril/valsartan and compared blood pressure post dialysis, N-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels and the findings of echocardiography for a period of 6 months. A month after the initiation of sacubitril/valsartan, there was improvement of symptoms and blood pressure post-dialysis, the NT-pro-BNP levels decreased from 23,132.2 ± 16,561.3 pg/mL to 8327 ± 3334.3 pg/mL, and the echocardiography findings showed a decrease in the left atrial dimension from 37.7 ± 5.7 mm to 33 ± 4.9 mm and an increase in the left ventricular ejection fraction from 58.2 ± 16.9% to 66.4 ± 15.0%. These results were sustained for up to 6 months. Also, blood pressure post-dialysis changed from 164 ± 11/77 mmHg to 150 ± 13/72 mmHg over the 6-month period. There were no side effects, such as hyperkalemia and lymphoedema. In conclusion, 5 patients had hypertension, including 2 patients with heart failure. Sacubitril/valsartan improved blood pressure post-dialysis, heart failure symptoms, NT-pro- BNP, the left atrial dimension, the left ventricular ejection fraction, and E/e\', E/A found via echocardiography for a 6-months period. Treatment with sacubitril/valsartan was effective in hemodialysis patients in the cardiac function.

It is necessary to complement next-generation sequencing data on the soil resistome with theoretical knowledge provided by ecological studies regarding the spread of antibiotic resistant bacteria (ARB) in the abiotic and, especially, biotic fraction of the soil ecosystem. Particularly, when ARB enter agricultural soils as a consequence of the application of animal manure as fertilizer, from a microbial ecology perspective, it is important to know their fate along the soil food web, that is, throughout that complex network of feeding interactions among members of the soil biota that has crucial effects on species richness and ecosystem productivity and stability. It is critical to study how the ARB that enter the soil through the application of manure can reach other taxonomical groups (e.g., fungi, protists, nematodes, arthropods, earthworms), paying special attention to their presence in the gut microbiomes of mesofauna-macrofauna and to the possibilities for horizontal gene transfer of antibiotic resistant genes.

The following describes a case of isolated visceral angioedema related to an angiotensin II receptor blocker (ARB) medication. Additionally, we discuss the pathophysiology of drug-induced angioedema, various presentations that can be encountered, and the leading theorized mechanisms of how renin-angiotensin-aldosterone system (RAAS) blocking medications lead to angioedema. The goal of sharing this case is to help increase awareness of the possibility of ARB-induced angioedema and to recommend keeping visceral angioedema as part of the differential diagnosis when presented with a patient who is taking an angiotensin converting enzyme inhibitor (ACEI) or ARB medication that is experiencing gastrointestinal symptoms of unclear etiology.

Angioedema is a condition characterized by swelling of the skin or mucosa resulting from loss of vascular integrity that leads to swelling of mucosal tissues and can lead to life-threatening respiratory compromise. Drug-induced angioedema is not a frequent side effect seen with angiotensin receptor blockers (ARBs), particularly when there are no other contributing risk factors like a prior episode. Few studies reported subsequent angioedema episodes after ARB use in patients who had a prior episode with angiotensin converting enzyme inhibitors; however, there are very few cases that documented non-fatal angioedema after ARB as the only therapy. We report a rare case of life-threatening anaphylaxis after losartan use. We hope that our case will bring awareness to this rare but fatal side effect in order to quickly recognize it and encourage further research.