Xanthogranulomatous pyelonephritis in a patient with polycystic kidney disease without underlying risk factors: a case report.

Xanthogranulomatous pyelonephritis (XGP) is an extremely rare, chronic granulomatous inflammatory condition thought to arise secondary to a combination of obstruction, recurrent bacterial infection and an incomplete immune response although the etiology of XGP is more complex. We would like to report a case of XGP occurring in a patient with polycystic kidney disease (PCKD), which has not been previously documented in etiology. A 29-year-old woman presented to our hospital with right upper quadrant pain for 5 days. She had experienced a low-grade fever, generalized weakness, and myalgia throughout her body for 2 weeks. She had no history of renal stones or recurrent UTIs. Contrast-enhanced CT revealed a well-enhancing large septated cystic mass in the right kidney and numerous cysts in the liver and both kidneys. Open right radical nephrectomy was performed due to the suspicion of renal cell carcinoma, as there was no response to antibiotics over 7 days. Gross specimen demonstrated architectural distortion due to xanthomatous nodules and a dilated pelvico-calyceal system filled with pus and blood. Microscopic examination revealed infiltration of neutrophils and lipid-laden macrophages. The patient is currently being followed up in the outpatient clinic without recurrence of XGP. This is the first reported case of XGP in a patient with underlying PCKD. Physicians should consider PCKD as a potential underlying cause of XGP.

IgA nephropathy with minimal change disease associated with primary Sjögren's syndrome: A case report.

RATIONALE: Only 1 case of IgA nephropathy (IgAN) with minimal change disease (MCD) associated with primary Sjögren's syndrome (SS) has been reported. We additionally describe IgAN with MCD associated with primary SS. PATIENT CONCERNS: A 80-year-old woman visited our hospital complaining of generalized edema that had started 4 weeks prior. She reported a sense of thirst and dry eye for the last 5 years. DIAGNOSES: Her initial laboratory findings were compatible with nephrotic syndrome; both the antinuclear antibody (1:80) and anti-SS-A (Ro) antibody (200 U/mL) tests were positive. A salivary gland scan revealed markedly decreased uptake for both the parotid and submandibular glands. The Schirmer test was positive. The random urine protein/creatinine ratio was 10 mg/mg. Renal biopsy was compatible with IgAN with superimposed MCD. INTERVENTIONS: Furosemide was intravenously administered with intermittent albumin infusion for her edema control. She was started on prednisone 40mg daily for 6 weeks, which was tapered to 5 mg for another 6 months after starting prednisolone. OUTCOMES: Over the next 6 months, her edema improved and the proteinuria decreased significantly. LESSONS: Physician should suspect IgA with MCD when patient with SS clinically showed nephrotic syndrome, and perform renal biopsy for pathologically diagnosis and appropriate treatment.

24,25-Dihydroxy Vitamin D and Vitamin D Metabolite Ratio as Biomarkers of Vitamin D in Chronic Kidney Disease.

The appropriate management of vitamin D deficiency and hyperparathyroidism is essential to prevent metabolic bone disorder (MBD) and cardiovascular diseases in chronic kidney disease (CKD). Recently, the 24,25-dihydroxyvitamin D [24,25(OH)2D] and vitamin D metabolite ratio (VMR), i.e., the ratio of 24,25(OH)2D to 25-hydroxyvitamin D [25(OH)D], have emerged as biomarkers of vitamin D level. We analyzed the usefulness of vitamin D biomarkers for the evaluation of MBD in patients with CKD. We analyzed blood and urine samples from 208 outpatients with CKD stage G2-G5. 25(OH)D showed a poor correlation with the estimated glomerular filtration rate (eGFR). Conversely, the 24,25(OH)2D level and VMR were significantly correlated with eGFR and the intact parathyroid hormone level. In conclusion, 24,25(OH)2D and VMR have the potential to be vitamin D biomarkers for the detection of MBD in CKD patients.

The neutrophil-to-lymphocyte ratio may indicate when to start hemodialysis.

We evaluated whether the neutrophil-to-lymphocyte ratio (NLR) could aid dialysis decision-making in combination with the clinical presentation and biochemical findings. We retrospectively evaluated the medical records of 279 patients who commenced chronic maintenance hemodialysis. We compared the laboratory findings at 6 months before dialysis to those at dialysis initiation. NLR cutoffs and risk factors for each of six uremic symptoms were determined. Mean age was 60.7 years and mean estimated glomerular filtration rate (eGFR) was 5.7 ± 2.5 mL/min/1.73 m2 at the time of hemodialysis and 7.7 ± 3.8 mL/min/1.73 m2 6 months earlier (p < 0.001). The mean NLR increased significantly from 2.5 ± 1.0 to 4.9 ± 2.8 (p < 0.001). The NLR was positively correlated with the C-reactive protein level (r = 0.202, p = 0.009) and negatively correlated with those of albumin (r = -0.192, p = 0.001) and total CO2 (r = -0.134, p = 0.023). The NLR cutoffs for neurological and gastrointestinal symptoms as determined using receiver operator curve analysis were 2.4 (area under the curve [AUC] 0.976; 95% confidence interval [CI] 0.960-0.993; sensitivity 92.2%; specificity 94.7%) and 3.6 (AUC 0.671; 95% CI 0.588-0.755; sensitivity 68.1%; specificity 63.5%), respectively. On multiple linear regression analysis of neurological symptoms, the NLR was a significant predictor (ß = -0.218, p = 0.017), as was age (ß = 0.314, p = 0.037). In conclusion, the NLR may serve as a supplementary marker predicting uremic symptoms and a need for hemodialysis in stage 5 CKD patients.

Page kidney following spontaneous subcapsular hematoma immediately after kidney transplantation: a case report.

BACKGROUND: Page kidney (PK) is the occurrence of kidney hypoperfusion and ischemia due to pressure on the kidney by a subcapsular hematoma (SH), a mass, or fluid collection. SH after renal transplantation may result in kidney ischemia and graft loss. CASE PRESENTATION: We present a rare case of early spontaneous SH in an allograft kidney that led to a decrease in renal function. A 56-year-old male patient underwent deceased donor kidney transplantation. After declamping, appropriate renal perfusion and immediate diuresis were observed, with no evidence of SH. However, his urinary output abruptly decreased 6 h postoperatively. Abdominal ultrasonography showed 28 mm deep SH on transplant and the resistive index (RI) increased to 0.98-1 and diastolic flow reversal was observed. Surgical interventions were performed 2 days after transplantation, following a further decrease in urinary output. Serum creatinine decreased to 2.2 mg/dL, urinary output increased to an average of 200 cc per hour and the RI value was decreased to 0.7 on POD 7. CONCLUSION: In patients with abrupt decreased renal function after transplantation, SH should be suspected and the presence of PK should be determined using Doppler USG. In these cases, surgical intervention may avoid allograft dysfunction.

Clinical and histopathological analyses of kidney biopsies in a single center for 7 years.

Kidney biopsy is the most important tool for diagnosing kidney disease and can be helpful in determining treatment and prognosis. Pathological spectra vary by country, region, race, sex, and age. We are the first to investigate the pathological spectrum of biopsy-proven kidney disease in Gyeongnam province of South Korea. We retrospectively analyzed 631 patients who underwent a kidney biopsy between 2013 and 2019 at Gyeongsang National University Hospital. The mean age of the 631 patients was 51.5 ± 18.1 years, and 361 patients (57.2%) were male. The mean estimated glomerular filtration rate by serum creatinine (Chronic Kidney Disease Epidemiology Collaboration [CKD-EPI]) was 68.0 ± 45.7 mL/min/1.73 m2. The mean systolic blood pressure was higher in 2017, 2018, and 2019 than in 2013 (P = .002). Hypertension (47.4%) was the most common comorbid disease, followed by diabetes (18.2%) and dyslipidemia (10.9%). Common clinical syndromes at the time of biopsy were renal insufficiency (42.0%) and nephrotic syndrome (33.9%). The prevalence of primary and secondary glomerular disease and tubulointerstitial disease were 71.4%, 16.9%, and 5.4%, respectively. Immunoglobulin A nephropathy was the most common primary glomerular disease (34.9%). Diabetic nephropathy was the most common secondary glomerular disease, followed by lupus nephritis. Tubulointerstitial disease was underestimated, as in other reports. Our data can be a useful reference for diagnosing kidney disease and understanding the patients in our province.

Impact of phase angle and sarcopenia estimated by bioimpedance analysis on clinical prognosis in patients undergoing hemodialysis: A retrospective study.

ABSTRACT: Bioimpedance analysis (BIA) has been widely used in the evaluation of body composition in patients undergoing maintenance hemodialysis. We conducted this study to evaluate impact of phase angle (PA) and sarcopenia measured by BIA on clinical prognosis in these patients.This longitudinal retrospective study enrolled patients who underwent hemodialysis between January 2016 and March 2019. The patients were stratified into higher (> 4°) and lower (≤ 4.0°) PA groups. Sarcopenia was defined when the appendicular skeletal muscle mass was < 20 kg in men and < 15 kg in women.Of the 191 patients, 63.4% were men. The mean age was 64.2 ±â€Š12.4 years. The lower PA group was older, had a higher proportion of women, a lower body mass index, lower albumin, cholesterol, uric acid, and phosphorus levels, and a higher incidence of history of coronary artery disease than the higher PA group. Linear regression analysis revealed that PA was significantly associated with body mass index (B = 0.18, P = .005), serum albumin (B = 0.23, P = .001), and creatinine levels (B = 0.32, P < .001). During a median follow-up of 16.7 months, 14.1% (n = 27) of patients experienced major adverse cardiovascular events and 11.0% (n = 21) died. Kaplan-Meier survival analysis showed that the higher PA group had significantly better survival, regardless of sarcopenia. Multivariate Cox analyses revealed that lower PA (0.51 [0.31-0.85], P = .010), higher IDWG (1.06 [1.01-1.12], P = .028) and C-reactive protein level (1.01 [1.01-1.02], P < .001), and a history of coronary artery disease (3.02 [1.04-8.77], P = .042) were significantly related to all-cause mortality after adjusting for other covariates.PA measured by BIA was an independent factor in the prediction of mortality in maintenance hemodialysis patients, regardless of sarcopenia. Intervention studies are needed to confirm if the improvement in PA is associated with better clinical outcome.

Acute kidney injury due to direct infiltration by lymphoplasmacytic lymphoma secreting IgG paraproteins: A case report.

INTRODUCTION: Waldenström's macroglobulinemia is a lymphoplasmacytic lymphoma (LPL) associated with a monoclonal immunoglobulin M protein. Although acute kidney injury (AKI) due to immunoglobulin M paraprotein infiltration into the renal interstitium has been reported, there has been no report of AKI with invasion of the immunoglobulin G paraprotein into the renal interstitium in a patient with LPL. PATIENT CONCERNS: A 65-year-old male was admitted to our hospital with fatigue and decreased renal function. He complained of a 3-kg weight loss in the last 3 months. DIAGNOSIS: The initial blood urea nitrogen and serum creatinine levels were 55.9 and 1.83 mg/dL, respectively. Serum protein electrophoresis revealed a monoclonal component (3.5 g/dL) in the gamma region and immunofixation electrophoresis showed an immunoglobulin G kappa monoclonal protein. Renal pathology revealed that CD3-CD20+ CD138+ lymphoid cells had infiltrated the renal interstitium. A bone marrow biopsy was compatible with LPL. INTERVENTIONS: Intravenous methylprednisolone (1 mg/kg) was administered after confirming the renal pathological findings. OUTCOMES: Serum creatinine decreased to 0.8 mg/dL 14 days after treatment. CONCLUSIONS: Physicians should recognize LPL secreting various immunoglobulins as a possible cause of AKI when renal failure of unknown etiology and serum immunoglobulin paraprotein is present. A kidney biopsy should be performed for definitive diagnosis and appropriate management.

Incidence, risk factors, and prognosis of acute kidney injury in hospitalized patients with acute cholangitis.

BACKGROUND: The association between acute cholangitis (AC) and acute kidney injury (AKI) remains unclear. We investigated the incidence, and clinical course of AKI in patients with AC, and the long-term prognosis. METHODS: We performed a single-center retrospective study of patients hospitalized with AC in a tertiary care center from January 2011 to December 2017. The risk factors for AKI were evaluated, and AKI severity was analyzed using the Systemic Inflammatory Response System (SIRS), quick sequential organ failure assessment (qSOFA) score, and 2018 Tokyo Guidelines (TG) grade. To calculate the relative risk of death based on AKI, hazard ratios (HRs) and 95% confidence intervals (CIs) were obtained using Cox's proportional hazard models. RESULTS: A total of 1,438 patients with AC were included, of whom 18.2% (n = 261) developed AKI. AKI patients were older, and had a lower systolic blood pressure and more comorbidities including hypertension (HT), chronic kidney disease, and cardiovascular accidents. Disease severity (as assessed by SIRS, qSOFA, and the Tokyo Guidelines grade) was higher in the AKI group, as was the in-hospital mortality rate. Multivariate analysis revealed that age, HT, SIRS and qSOFA scores ≥ 2, and TG grade of III were significant risk factors for AKI. Kaplan-Meier analysis revealed significantly higher mortality in the AKI than non-AKI group. AKI (HR = 1.853; 95% CI: 1.115-3.079) and TG grade III (HR = 2.139; 95% CI: 1.190-3,846) were independent predictors of all-cause AC mortality, even after adjusting for all covariates. The annual rate of decline in the estimated glomerular filtration rate was faster in the AKI than non-AKI group (2.9 ± 6.7 vs. 0.5 ± 5.3 mL/min/1.73 m2/year, p < 0.001). CONCLUSIONS: AKI development increased AC severity and mortality. Our results suggest that clinicians should monitor AKI status and perform appropriate management as soon as possible.

Human Endothelial Progenitor Cells Protect the Kidney against Ischemia-Reperfusion Injury via the NLRP3 Inflammasome in Mice.

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and progression to chronic kidney disease (CKD). However, no effective therapeutic intervention has been established for ischemic AKI. Endothelial progenitor cells (EPCs) have major roles in the maintenance of vascular integrity and the repair of endothelial damage; they also serve as therapeutic agents in various kidney diseases. Thus, we examined whether EPCs have a renoprotective effect in an IRI mouse model. Mice were assigned to sham, EPC, IRI-only, and EPC-treated IRI groups. EPCs originating from human peripheral blood were cultured. The EPCs were administered 5 min before reperfusion, and all mice were killed 72 h after IRI. Blood urea nitrogen, serum creatinine, and tissue injury were significantly increased in IRI mice; EPCs significantly improved the manifestations of IRI. Apoptotic cell death and oxidative stress were significantly reduced in EPC-treated IRI mice. Administration of EPCs decreased the expression levels of NLRP3, cleaved caspase-1, p-NF-κB, and p-p38. Furthermore, the expression levels of F4/80, ICAM-1, RORγt, and IL-17RA were significantly reduced in EPC-treated IRI mice. Finally, the levels of EMT-associated factors (TGF-ß, α-SMA, Snail, and Twist) were significantly reduced in EPC-treated IRI mice. This study shows that inflammasome-mediated inflammation accompanied by immune modulation and fibrosis is a potential target of EPCs as a treatment for IRI-induced AKI and the prevention of progression to CKD.

Case Report: Acute Kidney Injury Due to Chronic Milk-Alkali Syndrome in a Patient With Colon Cancer.

BACKGROUND: Common causes of hypercalcemia include primary hyperparathyroidism and paraneoplastic syndrome of malignancy. Because of this, physicians can easily miss extrinsic causes of hypercalcemia such as milk-alkali syndrome in patients with cancer. We successfully treated a case of acute kidney injury due to severe hypercalcemia caused by milk-alkali syndrome due to long-term milk drinking in a patient with colon cancer. CASE DESCRIPTION: A 62-year-old man was referred to nephrology for hypercalcemia and azotemia that was found during preoperative evaluation for colon cancer surgery. The patient had experienced several months of dizziness and anorexia. We started hemodialysis because hypercalcemia and azotemia were not improved despite large amounts of hydration and diuretics. We suspected paraneoplastic syndrome because of concomitant colon cancer and low intact parathyroid hormone (PTH). Renal microcalcifications were observed on ultrasonography. Metastatic calcifications of the lung and stomach were present, but no malignant metastasis appeared on bone scans. There was no evidence of metastatic malignant lesions on chest or abdominal enhanced computed tomography. PTH-related peptide was not detected. Thus, other causes of hypercalcemia beyond malignancy were considered. On history-taking, the patient reported consuming 1,000 to 1,200 mL of milk daily for the prior 3 months. Hypercalcemia was due to chronic milk-alkali syndrome. We advised withdrawal of milk and nutritional pills. Hemodialysis was stopped after 2 weeks since azotemia and hypercalcemia were resolving. Acute kidney injury was improved, and mild hypercalcemia remained when he underwent hemicolectomy after 1 month. Thereafter, serum calcium and creatinine remained normal at discharge and follow-up for 1 year in the outpatient clinic. However, lung calcifications still remained on bone scan after 1 year. CONCLUSIONS: Chronic milk-alkali syndrome is a rare condition resulting from excessive calcium and alkali intake through various routes, like milk, nutritional supplements, and medicines for osteoporosis. Therefore, early management for hypercalcemia should include precise history taking including diet, previous diagnoses, and current medications.

Acute Tubular Necrosis Associated with Angiotensin Receptor-neprilysin Inhibitor.

Sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor (ARNI), significantly reduces mortality and morbidity in patients with chronic heart failure with a reduced ejection fraction (HFrEF). However, a considerable number of patients treated with sacubitril/valsartan experience hypotension, oliguria, progressive azotemia, and renal failure as adverse events. These issues have been linked to significant gaps in the usage and dosing of guideline-directed medical therapy with ARNI in patients with HFrEF. We herein report a relevant case of pathologically proven acute tubular necrosis after the first dose of sacubitril/valsartan, highlighting the importance of optimizing the medical therapy in an outpatient with HFrEF.

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.

Acute interstitial nephritis associated with ingesting a Momordica charantia extract: A case report.

RATIONALE: Momordica charantia is often used to treat type 2 diabetes mellitus in Korea. Drug-induced acute interstitial nephritis (AIN) accounts for 60% to 70% of AIN cases. However, only 1 case of AIN associated with ingesting M charantia has been reported in the English literature. We report an extremely rare case of AIN that occurred after a patient ingested a pure M charantia extract over 7 months. PATIENT CONCERNS: A 60-year-old Korean woman was admitted to our hospital for a renal biopsy. Her renal function had decreased gradually over the last 9 months without symptoms or signs. DIAGNOSIS: Her blood urea nitrogen and serum creatinine levels were 29.7 mg/dL (range: 8.0-20.0 mg/dL) and 1.45 mg/dL (range: 0.51-0.95 mg/dL) on admission. Renal histology indicated AIN; there was immune cell infiltration into the interstitium, tubulitis, and epithelial casts, although the glomeruli were largely intact. INTERVENTIONS: M charantia was discontinued and prednisolone was prescribed. OUTCOMES: The value of serum creatinine has almost been restored to the baseline level after 3 months. CONCLUSION: s: This is the first case report of AIN associated with the ingestion of a pure M charantia extract. Recognition of the possible adverse effects of these agents by physicians is very important for early diagnosis and appropriate management.

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.

Spontaneous rupture of a renal artery pseudoaneurysm in a hemodialysis patient: A case report.

RATIONALE: Renal artery pseudoaneurysm is a rare vascular lesion usually caused by trauma or percutaneous urological procedures. Spontaneous rupture of pseudoaneurysms without predisposing events, especially in hemodialysis patients, has rarely been reported. PATIENT CONCERNS: A 25-year-old man receiving maintenance hemodialysis visited the emergency room because of sudden severe right flank pain. He had no history of trauma or urological procedures except for a left renal biopsy to diagnose Alport syndrome 10 years prior. DIAGNOSIS: Contrast-enhanced computed tomography revealed a right perirenal hematoma with pseudoaneurysms. INTERVENTIONS: On renal angiography, multiple pseudoaneurysms were observed in the right renal artery branches and embolization was performed. OUTCOMES: Post-angiography showed no pseudoaneurysms. His abdominal pain improved, and he was discharged 2 weeks after embolization. LESSONS: When maintenance dialysis patients complain of severe abdominal pain, spontaneous rupture of a renal pseudoaneurysm should be considered as a differential diagnosis, even if the patient has no history of trauma or previous urological procedures.

Acute interstitial nephritis associated with ingestion of Achyranthes japonica extract: a case report.

BACKGROUND: The Japanese chaff flower, Achyranthes japonica, is used as complementary medicine to control degenerative arthritis. Although commonly used in South Korea, there has been no report of side effects. We report the first case of acute interstitial nephritis (AIN) that occurred in a woman who ingested A. japonica extract for 4 months. CASE PRESENTATION: A 56-year-old Korean woman was admitted for deterioration of renal function. She had general weakness and nausea for 1 month. Her initial blood urea nitrogen and serum creatinine levels were 26.3 mg/dL and 3.2 mg/dL, respectively. She acknowledged ingesting A. japonica extract for the past 4 months. Renal histology demonstrated AIN represented by immune cell infiltration into the interstitium, tubulitis, and tubular atrophy, but the glomeruli were intact. A. japonica was discontinued immediately and conservative management was started. Renal function was nearly restored to the baseline level without medication after 13 months. CONCLUSION: This is a rare case report of AIN associated with a pure A. japonica extract. In the case of unknown etiology of AIN, physicians should ask about the use of herbal medicines, nutraceuticals, and traditional folk medicines including A. japonica.

A case of vasculitis case with unusual renal pathological findings presenting with rapidly progressing renal failure.

Plasma cell infiltration may be an early lesion during renal invasion by ANCA-associated vasculitis (AAV), and AAV should be considered in the differential diagnosis with acute renal failure and systemic symptoms.

Paricalcitol Attenuates Contrast-Induced Acute Kidney Injury by Regulating Mitophagy and Senescence.

Contrast-induced acute kidney injury (CI-AKI) is the third most common cause of hospital-acquired renal failure, with an incidence of 11%. However, the disease mechanism remains unclear, and no effective treatment is available. Paricalcitol has been reported to be effective in animal models of kidney injury. We hypothesized that paricalcitol could play a renoprotective role against CI-AKI. Rats were divided into control, paricalcitol, contrast, and paricalcitol-plus-contrast groups. We used a previously published protocol to produce CI-AKI. Paricalcitol (0.3 µg/kg) was administered intraperitoneally before 24 h and 30 min before indomethacin. We used HK-2 cells to evaluate the effects of paricalcitol on mitophagy and senescence. Ioversol triggered renal dysfunction, increasing blood urea nitrogen and serum creatinine. Significant tubular damage, increased 8-OHdG expression, and apoptosis were apparent. Ioversol injection induced high expression levels of the mitophagy markers Pink1, Parkin, and LC3 and the senescence markers ß-galactosidase and p16INK4A. Paricalcitol pretreatment prevented renal dysfunction and reduced tissue damage by reducing both mitophagy and senescence. Cellular morphological changes were found, and expression of LC3B and HMGB1 was increased by ioversol in HK-2 cells. Paricalcitol countered these effects. This study showed that mitochondria might drive injury phenotypes in CI-AKI, and that paricalcitol protects against CI-AKI by decreasing mitochondrial damage.

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.