Lower serum sodium levels predict poor clinical outcomes in patients with insomnia.

BACKGROUND: The association between lower serum sodium levels and the clinical outcomes of insomnia patients remains unclear. We explored whether lower serum sodium is associated with poor clinical outcomes in patients with insomnia. METHODS: We retrospectively enrolled patients with a diagnosis of insomnia from January 2011 to December 2012. We divided participants into three groups according to initial serum sodium level: tertile 1 (< 138 mmol/L), tertile 2 (138.0-140.9 mmol/L), and tertile 3 (≥ 141.0 mmol/L). To calculate the relative risk of death, hazard ratios (HRs) and 95% confidence intervals (CIs) were obtained using Cox proportional hazard models. RESULTS: A total of 412 patients with insomnia were included, of whom 13.6% (n = 56) had hyponatremia. Patients with lower serum sodium concentrations were older and had lower hemoglobin, calcium, phosphorus, and albumin levels. At the median follow-up of 49.4 months, 44 patients had died and 62 experienced acute kidney injury (AKI). Kaplan-Meier analysis showed significantly higher mortality in patients in the lowest tertile for serum sodium. The lowest tertile of the serum sodium level and the AKI were associated with all-cause mortality. However, the lowest tertile of the serum sodium level was not significantly associated with AKI. CONCLUSIONS: The lowest tertile of the serum sodium level was associated with a higher mortality rate in insomnia patients. Our results suggest that the serum sodium level could serve as a prognostic factor in insomniacs; patients with lower sodium levels require particular care.

Protective Effects of Evogliptin on Steatohepatitis in High-Fat-Fed Mice.

There are few studies on the effects of dipeptidyl peptidase-4 inhibitors on steatohepatitis. We explored whether evogliptin (Evo), a dipeptidyl peptidase-4 inhibitor, protects against steatohepatitis in a high-fat diet (HFD)-fed mice and whether these effects involve modulation of mitophagy. Adult male C57BL/J mice were divided into the normal diet (ND), HFD (45% of energy from fat) with Evo (250 mg/kg) (HFD + Evo), and HFD groups at 4 weeks of age and were sacrificed at 20 weeks of age. The HFD group showed hepatic lipid accumulation; this was decreased in the Evo + HFD group. There was an increased 8-hydroxydeoxyguanosine (8-OHDG) expression in the HFD group compared to ND mice. However, 8-OHDG expression levels were significantly decreased in the HFD + Evo group. Expressions of the mitophagy markers PTEN-induced kinase 1 (PINK1), Parkin, and BNIP-3 (BCL2 Interacting Protein 3) were significantly increased in the HFD group. However, the expressions of these markers were lower in the HFD + Evo group than that in the HFD group. Phospho-Akt was upregulated and p53 was downregulated in the HFD + Evo group compared to the HFD group. Evogliptin may alleviate steatohepatitis in HFD-fed mice by ameliorating steatosis and oxidative stress and by modulating mitophagy in the liver.

Erythropoietin Ameliorates Ischemia/Reperfusion-Induced Acute Kidney Injury via Inflammasome Suppression in Mice.

Acute kidney injury (AKI) is the most common condition in hospitalized patients. As ischemia/reperfusion-induced AKI (IR-AKI) is as a major contributor to end-stage disease, an effective therapeutic intervention for IR-AKI is imperative. Erythropoietin (EPO) is a potent stimulator of erythroid progenitor cells and is significantly upregulated during hypoxia. Here, we investigated the renoprotective effects of EPO in an IR-AKI mouse model. Mice were assigned to sham, EPO only, and IR only groups, and the IR group was treated with EPO prior to injury. EPO was administered twice at 30 min prior to bilateral renal artery occlusion, and 5 min before reperfusion, with all mice sacrificed 24 h after IR-AKI. The serum was harvested for renal functional measurements. The kidneys were subjected to histological evaluation, and the biochemical changes associated with renal injury were assessed. EPO significantly attenuated the renal dysfunction associated with IR-AKI, as well as tissue injury. Apoptotic cell death and oxidative stress were significantly reduced in EPO-treated mice. Macrophage infiltration and expression of ICAM-1 and MCP-1 were also significantly reduced in EPO-treated mice. Furthermore, the expression of inflammasome-related factors (NLRP1, NLRP3, and caspase-1 cleavage), via the activation of the COX-2 and NF-B signaling pathways were significantly reduced following EPO treatment. To our knowledge, this is the first study to demonstrate that inflammasome-mediated inflammation might be a potential target of EPO as a treatment for ischemic AKI.

A case report of successfully treated nephrotic syndrome after renal angioplasty.

BACKGROUND: The standard treatment of renovascular hypertension accompanying renal artery stenosis (RAS) consists of angioplasty and administration of antihypertensive medication. Although nephrotic syndrome (NS) has been reported to be associated with RAS, the development of NS after revascularization of RAS is extremely rare. CASE PRESENTATION: A 48-year-old man presented with uncontrolled hypertension and azotemia. The right kidney was atrophic, and RAS of the left kidney was suspected based on a post-captopril DTPA scan. His blood pressure stabilized after renal angioplasty; however, he complained of edema after 1 week. NS developed and was diagnosed as focal segmental glomerulosclerosis (FSGS) based on renal biopsy. He received an angiotensin receptor blocker. Proteinuria resolved after 1 year. CONCLUSIONS: FSGS rarely develops after angioplasty of renal artery stenosis. This is the first report of successful treatment of this condition using an angiotensin receptor blocker during 1-year follow-up.

Incidence, risk factors, and clinical outcomes of acute kidney injury associated with acute pyelonephritis in patients attending a tertiary care referral center.

Acute kidney injury (AKI) associated with acute pyelonephritis (APN) rarely has been reported. The aim of this study was to evaluate the incidence and risk factors of AKI associated with APN. We retrospectively reviewed the medical records of 403 patients over 18-year old age hospitalized for APN management from October 2009 to September 2014 in tertiary care referral center. Demographic data, clinical symptoms and signs, and laboratory findings were gathered from the medical records and analyzed. The mean age of patients was 57 years and APN commonly occurred in female (87.6%). AKI occurred in 253 patients (62.8%). As per the RIFLE classification, renal injury was graded as 'Risk' (62.1%), 'Injury' (26.5%), and 'Failure' (11.4%). AKI patients were more likely a male gender and had complicated APN. The AKI group had a significantly higher tendency to present with shock. The prevalence of underlying chronic kidney disease (CKD) was significantly higher in the AKI group. There was no difference in mortality between the AKI and non-AKI groups. Multivariate analysis revealed that age over 65 (OR 1.93, 95% CI 1.18-3.13, p= .008), complicated (OR 2.13, 95% CI 1.35-3.34, p= .001) and bilateral APN (OR 1.71, 95% CI 1.01-2.88, p= .045), and initial shock (OR 2.44, 95% CI 1.05-5.71, p= .039) were independent risk factors for the occurrence of AKI in patients with APN. Physicians should attempt to prevent, detect, and manage AKI associated with APN in patients with above conditions.

The aqueous extract of aged black garlic ameliorates colistin-induced acute kidney injury in rats.

The use of colistin in the treatment of multidrug-resistant Gram-negative bacterial infections is restricted due to nephrotoxicity. We investigated the effects of aged black garlic extract (ABGE) on colistin-induced kidney injury in rats. Rats were assigned to four groups. Normal saline was intraperitoneally and intragastrically injected for control group. ABGE was intragastrically injected for garlic group. Ten mg/kg of colistin was intraperitoneally injected for 6 consecutive days for colistin group. One percent of ABGE was done 30 min prior to colistin injection for treatment group. Rats were sacrificed on the next day after last colistin injection. Colistin injection increased the serum levels of blood urea nitrogen and creatinine; however, ABGE prevented deterioration of these serum levels. ABGE also alleviated tubular damage, including vacuolation and necrosis. TUNEL-positive cells were observed less frequently for the ABGE-treated groups. CD68 positive cells were significantly decreased by pretreatment with ABGE. Levels of oxidative stress biomarkers such as 8-hydroxydeoxyguanosine and malondialdehyde were lower in the ABGE-treated groups. Levels of NF-κB, inducible NO synthase, COX-2, and TGF-ß1 were lower in rats that had been treated with ABGE injection. Renal levels of IL-1ß and TNF-α were increased by colistin administration whereas renal SOD, catalase, and GSH levels were restored by ABGE administration. These results suggest that ABGE, which has antioxidant and anti-inflammatory properties, might be a potential therapeutic agent to prevent renal toxicity of colistin.

Urinothorax after ultrasonography-guided renal biopsy: a case report.

BACKGROUND: Urinothorax is defined as the presence of urine in the pleural space and is a rather rare cause of transudate pleural effusion. The potential etiologies are urinary tract obstruction and trauma. Diagnosis requires a high index of clinical suspicion and the condition is completely reversible following relief of underlying disease. CASE PRESENTATION: We report a 27-year-old man who developed urinothorax after renal biopsy. Urine leakage was confirmed with 99mTc DTPA (diethylenetriaminepentacetate) and single-photon emission computed tomography scans and retrograde pyelography. The pleural effusion was completely resolved by removing the leakage with a Foley catheter and a double J stent. CONCLUSIONS: Urinothorax has not been reported in patients doing renal biopsy in the literature. Based on our experience, urinothorax should be suspected, diagnosed, and managed appropriately when pleural effusion occurred after renal biopsy.

The logistic organ dysfunction system score predicts the prognosis of patients with alcoholic ketoacidosis.

Alcoholic ketoacidosis (AKA) is occasionally associated with multiple complications leading to death. However, no study has yet evaluated prognostic factors in patients with AKA. It is known that the logistic organ dysfunction system (LODS) score is an objective and useful index to predict the prognosis. We used LODS score to predict prognosis of AKA. We retrospectively reviewed the medical records of 46 patients who were diagnosed as AKA in our hospital. The mean LODS score was 6.3. The probability of mortality based on the LODS score was 36.6%, and 16 patients (34.5%) did, in fact, die. The total LODS score and lactate dehydrogenase (LDH) were significantly higher in the non-survival group. Prothrombin activity, serum platelet number, and the serum albumin levels were significantly higher in the survival group. We found significant correlations between the LODS score and arterial pH, the albumin level, and the LDH concentration. Multivariate analysis showed that the serum albumin and LDH levels were independently associated with survival in AKA patients. AKA patients suffered high-level mortality and the LODS score was an accurate predictor of prognosis. Clinicians may use the LODS score to this end.

The incidence, risk factors, and clinical outcomes of acute kidney injury (staged using the RIFLE classification) associated with intravenous acyclovir administration.

Intravenous (IV) acyclovir is commonly administered medication for viral infection but is well known for its nephrotoxicity. However, there was no study for incidence, risk factors, and clinical outcomes of acute kidney injury (AKI) associated with IV acyclovir administration. We retrospectively reviewed the medical records of 287 patients who were medicated IV acyclovir from January 2008 to May 2013 in Gyeongsang National University Hospital. All had documented medical histories and underwent medical review. Demographic data, risk factors, concomitant drugs, laboratory findings and outcome were gathered from the medical records and analyzed. AKI occurred in 51 patients (17.8%). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (62.7%), renal injury (15.6%), and renal failure (21.6%). There was no significant difference in age, sex, total dose, drug duration, and presence of hydration between AKI and non-AKI group. However, systolic pressure, underlying diabetes, concomitant vancomycin and non-steroidal anti-inflammatory drugs (NSAIDs) use was positively correlated with AKI occurrence (p = .04, p < .001, 0.01, and 0.04, respectively). Two patients underwent hemodialysis and these patients died. Higher mortality was observed in AKI patients (p < .001). Multivariate analysis also presented that presence of diabetes, concomitant NSAIDs, and vancomycin use was independent risk factor of acyclovir associated with AKI (p = .001, OR 3.611 (CI: 1.708-7.633), p = .050, OR 2.630 (CI: 1.000-6.917), and p = .009, OR 4.349 (CI: 1.452-13.022), respectively). AKI is relatively common in patients administrating acyclovir injection. Physicians should attempt to prevent, detect, and manage acyclovir associated AKI in patients prescribing acyclovir due to possible association of poor prognosis.

The incidence, risk factors, and outcomes of acute kidney injury in patients with pyogenic liver abscesses.

BACKGROUND: Acute kidney injury (AKI) can occur in various infectious conditions. Liver abscess is relatively rare, but can lead to sepsis and/or other severe complications. Few studies of AKI in patients with a liver abscess have been conducted. Therefore, we analyzed the clinical and laboratory data of AKI in patients with a liver abscess. METHODS: We retrospectively reviewed the medical records of patients who were diagnosed with a liver abscess from January 2000 to March 2013. The study included 404 patients with a liver abscess confirmed by clinical presentation and computed tomography. RESULTS: AKI occurred in 137 patients (34 %). As per RIFLE classification, renal injury was graded as either at risk of renal dysfunction (35.8 %), renal injury (47.4 %), and renal failure (16.5 %). AKI occurred more frequently in males and patients with liver cirrhosis (P < 0.001 and P = 0.005). Patients with AKI had lower serum albumin and higher AST and ALT levels than did patients without AKI. Bacteria were frequently isolated in AKI patients from blood culture and liver abscess aspirates (P < 0.001 and P = 0.007). The occurrence of septic shock was positively correlated with AKI (P = 0.002) and AKI was more frequent in patients with chronic kidney disease (P = 0.04). Higher mortality was observed in CKD patients accompanied by AKI (P < 0.001). Three patients with AKI underwent hemodialysis; two patients who had initially normal renal function completely recovered whereas one CKD patient progressed to ESRD, requiring maintenance hemodialysis. CONCLUSION: AKI is relatively common in patients with liver abscess. Physicians should therefore attempt to prevent, detect, and manage AKI early in patients with liver abscess.

Macrophage depletion ameliorates glycerol-induced acute kidney injury in mice.

BACKGROUND: This study was conducted to elucidate the role of renal macrophages in the development of acute kidney injury (AKI) in a glycerol (Gly)-induced rhabdomyolysis mouse model. METHODS: The experimental model of rhabdomyolysis requires injecting 50% Gly (10 ml/kg) intramuscularly into mice. Control mice were injected into the tail vein with the liposomal vehicle. Liposome-encapsulated clodronate (LEC)-only mice were injected with LEC. Gly-only mice were injected with Gly into a hind limb. LEC+Gly-treated mice were injected intravenously with 100 µl of LEC 24 h prior to Gly injection. Mice were sacrificed 24 h after Gly injection. RESULTS: Gly injection increased the serum creatinine level, and induced tubular damage. Renal CD45(+)CD11b(+)Ly6c(+) or CD45(+)CD11b(+)Ly6c(+)F4/80(+) macrophages were decreased by pretreatment with LEC in both normal and injured kidneys. Macrophage depletion prevented Gly-induced apoptotic death of tubular epithelial cells by decreasing caspase-9, ERK and p53, while increasing Bcl-2 expression. Expression of the inflammatory mediators NF-κB, MCP-1, ICAM-1, iNOS and COX-2 were also decreased with LEC pretreatment of mice injected with Gly. CONCLUSION: These results support the hypothesis that depletion of macrophages prevents renal dysfunction by abrogating apoptosis and attenuating inflammation during AKI.

Hemolytic uremic syndrome associated with paraquat intoxication.

We report a case of a 66-year-old patient with paraquat intoxication resulting in the requirement for hemoperfusion, hemodialysis, and plasma exchange. His initial serum paraquat level was 0.24 µg/mL (0.0-0.1 µg/mL). Activated charcoal (50 g) was administered orally, and high-dose N-acetylcysteine (150 mg/kg) was administered intravenously. In addition, immediate 4 h hemoperfusion was also performed for three consecutive days after admission. Hemodialysis was started on the 4th day after admission because of uremia. On the 9th day after admission, laboratory findings demonstrated hemolytic uremic syndrome (HUS): microangiopathic hemolytic anemia (MAHA), thrombocytopenia, elevated reticulocyte count, and lactate dehydrogenase (LDH). Plasma exchange was performed three times consecutively. Anemia and thrombocytopenia were improved, and LDH was normalized after plasma exchange. Urine output increased to 2240 mL/day on the 18th day after admission, and hemodialysis was discontinued. He is currently being observed at our follow-up clinic without renal impairment or pulmonary dysfunction for 1.5 years since discharge. We should suspect paraquat-associated HUS when thrombocytopenia and anemia are maintained for a long time after paraquat intoxication.

Iodine-induced thyrotoxic hypokalemic paralysis after ingestion of Salicornia herbace.

A 56-year-old Korean man visited to emergency room due to paroxysmal flaccid paralysis in his lower extremities. There was no family or personal history of periodic paralysis. His initial potassium levels were 1.8 mmol/L. The patient had been taking Salicornia herbacea for the treatment of diabetes and hypertension. Results of a thyroid function test were as follows: T3 = 130.40 ng/dL, TSH = 0.06 mIU/L, and free T4 = 1.73 ng/dL. A thyroid scan exhibited a decreased uptake (0.6%). His symptoms clearly improved and serum potassium levels increased to 4.4 mmol/L by intravenous infusion of only 40 mmol of potassium chloride. Eight months after the discontinuation of only Salicornia herbacea, the patient's thyroid function tests were normalized. Large amounts of iodine can induce hypokalemic thyrotoxic paralysis and it may be necessary to inquire about the ingestion of iatrogenic iodine compounds, such as Salicornia herbacea.

A retrospective study of short- and long-term effects on renal function after acute renal infarction.

PURPOSE: Acute renal infarction is often missed or diagnosed late due to its rarity and non-specific clinical manifestations. This study analyzed the clinical and laboratory findings of patients diagnosed with renal infarction to determine whether it affects short- or long-term renal prognosis. METHODS: We retrospectively reviewed the medical records of 100 patients diagnosed as acute renal infarction from January 1995 to September 2012 at Gyeongsang National University Hospital, Jinju, South Korea. RESULTS: Acute kidney injury (AKI) occurred in 30 patients. Infarct size was positively correlated with the occurrence of AKI (p = 0.004). Compared with non-AKI patients, AKI occurrence was significantly correlated with degree of proteinuria (p < 0.001) and the presence of microscopic hematuria (p = 0.035). AKI patients had higher levels of aspartate transaminase (p < 0.001), alanine transaminase (p < 0.001), and lactated dehydrogenase (p = 0.027). AKI after acute renal infarction was more common in patients with chronic renal failure (CRF) (eGFR < 60 mL/min), compared with non-CRF patients, whose baseline eGFR was >60 mL/min (p = 0.003). Most patients recovered from AKI, except for seven patients (7%) who developed persistent renal impairment (chronic kidney disease progression) closely correlated with magnitude of infarct size (p = 0.015). Six AKI patients died due to combined comorbidity. CONCLUSIONS: AKI is often associated with acute renal infarction. Although most AKI recovers spontaneously, renal impairment following acute renal infarction can persist. Thus, early diagnosis and intervention are needed to preserve renal function.

Outcomes of kidney allograft in recipients with kidney disease of unknown etiology.

The etiology of renal disease is important because the primary renal pathology may affect the outcomes of kidney allograft with respect to recurrence, rejection, and survival. However, for a significant number of patients who undergo kidney transplantation, the disease etiology is unknown. Here, allograft outcomes for patients with kidney disease of unknown etiology (UEK) at three affiliated Korean hospitals were identified. The incidence of biopsy-proven acute rejection (BPAR) for UEK was 22.9%, which was similar to the rates for diabetic nephropathy (DN, 24.4%) and IgA nephropathy (IgAN, 20.0%; p = 0.345). The cumulative incidence of post-transplant glomerulonephritis (PTGN) among patients with UEK was significantly lower than that among patients with IgAN (p < 0.001). Overall graft survival of the UEK group was superior to that of the DN group (hazards ratio 0.39, 95% confidence interval 0.17-0.92, p = 0.030). Preemptive transplantation for UEK significantly reduced the incidence of BPAR (preemptive vs. non-preemptive 9.6% vs. 30.3%, p = 0.001), but graft survival and recurrence were not affected by preemptive transplantation. The outcomes of kidney transplantation for patients with UEK were not inferior to those for patients with IgAN or DN. Preemptive kidney transplantation may be encouraged for UEK patients.

Anuric acute renal failure associated with pericardial effusion without signs of cardiac tamponade.

This article describes the anuric acute renal failure (ARF) secondary to massive pericardial effusion without tamponade in an 84 year-old man. He was referred to our emergency room with progressive dyspnea and azotemia. An electrocardiogram showed sinus tachycardia. A two-dimensional echocardiogram confirmed the presence of severe pericardial effusion without prominent ventricular diastolic collapse and there were no changes in his vital signs. Laboratory findings showed that his blood urea nitrogen and serum creatinine levels were 91.8 and 3.77 mg/dL, respectively. Renal ultrasonography showed no signs of hydronephrosis. Urine output did not increase in spite of giving a saline and furosemide infusion but increased immediately after pericardiocentesis with drainage. His renal function was completely restored 3 days after the procedure. A pericardial biopsy demonstrated invasion of malignant cells. We should keep in mind that pericardial effusion is one of the causes of anuric ARF, although it is not accompanied by tamponade.

Obstructive uropathy by total uterine prolapse leading to end-stage renal disease.

A 74-year-old woman was admitted to our emergency room complaining of general weakness and anorexia that started 20 days earlier. She denied other underlying diseases that might have provoked chronic renal disease. Her serum creatinine was 12.35 mg/dL. A pelvic examination and computed tomography revealed severe bilateral hydroureteronephrosis with marked cortical thinning induced by total uterine prolapse. She was started on emergency hemodialysis due to her uremic symptoms and severe metabolic acidosis. Despite Foley catheter insertion and manual reduction of uterus for 1 month, renal function was not recovered. The department of gynecology was strongly opposed to performing a procedure to reverse the hydroureteronephrosis due to the irreversibility of her renal function. She is undergoing chronic maintenance hemodialysis. This is a case report of rare end-stage renal disease (ESRD) caused by obstructive uropathy due to pelvic organ prolapse (POP). We should consider POP as a cause of ESRD.

Incidence and risk factors for radiocontrast-induced nephropathy in patients with hepatocellular carcinoma undergoing transcatheter arterial chemoembolization.

BACKGROUND: Transcatheter arterial chemoembolization (TACE) is an effective treatment for unresectable hepatocellular carcinoma (HCC); however, large volumes of radiocontrast agents are used for TACE and may induce renal dysfunction. Most patients with HCC have coexisting liver cirrhosis (LC) at the time of diagnosis. Advanced cirrhosis is characterized by peripheral vasodilatation associated with decreased renal perfusion due to the activation of vasoconstrictor systems. We retrospectively investigated patients with HCC who had undergone TACE to determine the incidence and risk factors for radiocontrast-induced nephropathy (RCIN). METHODS: A total of 101 patients with HCC who underwent a combined 221 TACE treatment sessions were included. Follow-up serum creatinine levels within 96 h after TACE were confirmed in these patients. RCIN was defined as an increase of at least 25% in baseline serum creatinine levels between 48 and 96 h after TACE. RESULTS: RCIN developed in 20 (9%) of the 221 treatment sessions after TACE. A univariate analysis showed that the Child-Pugh score (6.0 ± 1.3 vs. 6.7 ± 1.9, P = 0.005), ascites (14.4 vs. 40%, P = 0.008), contrast medium volume (257.3 ± 66.8 vs. 275.0 ± 44.0 ml, P = 0.009), total bilirubin (1.3 ± 1.7 vs. 3.4 ± 8.0 mg/dl, P < 0.001), basal serum creatinine levels (0.9 ± 0.3 vs. 1.0 ± 0.5 mg/dl, P < 0.001) and glomerular filtration rate using the modification of diet in renal disease formula (90.5 ± 21.8 vs. 88.4 ± 29.6 ml/min, P = 0.015) were significantly associated with the development of RCIN. A multivariate analysis revealed that the Child-Pugh score was associated with RCIN [odds ratio (OR) 1.5; P = 0.015]. Overall, in-hospital mortality after TACE was 4.07% (with RCIN, 30%; without RCIN, 1.5%; P < 0.001). The multivariate analysis also showed that the Child-Pugh score and the occurrence of RCIN were associated with in-hospital mortality after TACE (OR 2.8; P = 0.001; OR 26.7, P = 0.002, respectively). CONCLUSIONS: RCIN after TACE was closely associated with the severity of LC. Effective preventive measures remain to be determined in patients with HCC and advanced LC who are undergoing TACE.

Bilateral Acute Renal Infarction Due to Paradoxical Embolism in a Patient with Eisenmenger Syndrome and a Ventricular Septal Defect.

A 52-year-old man who was diagnosed with Eisenmenger syndrome due to a muscular-type ventricular septal defect 30 years previously, visited our emergency room after experiencing six hours of severe left flank pain and vomiting. On laboratory examination, azotemia and microscopic haematuria were identified. Contrast-enhanced computed tomography also revealed pulmonary embolism (PE) and bilateral acute renal infarction. The flank pain resolved after heparin was administered for anti-coagulation and aspiration thrombectomy was performed. The patient was discharged on warfarin as anticoagulant therapy. In this case, a paradoxical embolism was considered to have been the cause of PE and bilateral acute renal infarction in a patient with Eisenmenger syndrome.

Oral cyclophosphamide-induced posterior reversible encephalopathy syndrome in a patient with ANCA-associated vasculitis: A case report.

BACKGROUND: Posterior reversible encephalopathy syndrome (PRES) manifests many neurological symptoms with typical features on neuroimaging studies and has various risk factors. Cyclophosphamide is one of the therapeutic agents for anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Cyclophosphamide as the sole cause of PRES has been reported in only a few cases. Herein, we report a unique case of early-onset oral cyclophosphamide-induced PRES in a patient with ANCA-associated vasculitis. CASE SUMMARY: A 73-year-old man was transferred to our hospital for sepsis due to acute cholangitis. He had already received hemodialysis for two weeks due to septic acute kidney injury. His azotemia was not improved after sepsis resolved and perinuclear-ANCA was positive. Kidney biopsy showed crescentic glomerulonephritis. Alveolar hemorrhage was observed on bronchoscopy. He was initially treated with intravenous methylprednisolone and plasma exchange for one week. And then, two days after adding oral cyclophosphamide, the patient developed generalized tonic-clonic seizures. We diagnosed PRES by Brain magnetic resonance imaging (MRI) and electroencephalography. Seizures were controlled with fosphenytoin 750 mg. Cyclophosphamide was suspected to be the cause of PRES and withdrawal. His mentality was recovered after seven days and brain MRI showed normal state after two weeks. CONCLUSION: The present case shows the possibility of PRES induction due to short-term use of oral cyclophosphamide therapy. Physicians should carefully monitor neurologic symptoms after oral cyclophosphamide administration in elderly patients with underlying diseases like sepsis, renal failure and ANCA-associated vasculitis.