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Abstract Background Bromadiolone is a wide-use long-acting anticoagulant rodenticide known to cause severe coagulation dysfunction. At present, there have been no detailed reports of acute kidney injury (AKI) resulting from bromadiolone poisoning. Case presentation A 27-year-old woman was admitted to the hospital due to severe coagulopathy and severe AKI. Coagulation test revealed a prothrombin time exceeding 120 s and an international normalized ratio (INR) greater than 10. Further examination for coagulation factors showed significantly reduced level of factors II, VII, IX and X, indicating a vitamin K deficiency. The AKI was non-oliguric and characterized by gross dysmorphic hematuria. Following the onset of the disease, the patient’s serum creatinine rose from 0.86 to 6.96 mg/dL. Suspecting anticoagulant rodenticide poisoning, plasma bromadiolone was identified at a concentration of 117 ng/mL via gas chromatography/mass spectrometry. All other potential causes of AKI were excluded, except for the presence of a horseshoe kidney. The patient’s kidney function fully recovered after the coagulopathy was corrected with high doses of vitamin K and plasma transfusion. At a follow-up 160 days post-discharge, the coagulation function had normalized, and the serum creatinine had returned to 0.51 mg/dL. Conclusion Bromadiolone can induce AKI through a severe and prolonged coagulation disorder. Kidney function can be restored within days following treatment with high-dose vitamin K1.

Abstract Background Urinary ascites represents a scarcely observed pseudo-acute kidney injury in clinical settings. Protracted or missed diagnosis may hold grave ramifications for patient outcomes. Case presentation We reported a case involving an elderly female patient experiencing pseudo-acute kidney injury accompanied by ascites, wherein her renal dysfunction persisted despite medical intervention and hemodialysis. Urinary ascites was identified via a methylene blue test and by contrasting creatinine levels in serum and ascites. This patient’s kidney function was multiple typified by a marked elevation in serum creatinine/Cystatin C ratio (> 2 L/dL), potentially serving as a clue for the clinical diagnosis of pseudo-acute kidney injury engendered by urinary ascites. Conclusions This case suggested the potential diagnostic value of an asynchronous increase in serum creatinine and serum CysC (or an increased ratio of blood creatinine to blood CysC) in patients with pseudo-acute kidney injury.

Abstract Background Renal replacement therapy (RRT) with regional citrate anticoagulation (RCA) is an important therapeutic approach for refractory hypercalcemia complicated with renal failure. However, RCA has the potential to induce arrhythmia caused by rapid calcium loss. We report a case of arrhythmia associated with rapid calcium loss during RCA-RRT. Case presentation A 51-year-old man with hypercalcemia, primary hyperparathyroidism, and acute kidney injury was treated by predilutional-RCA-hemofiltration at a rate of 4.3 L/h. The effect of lowering serum calcium was unsatisfactory despite reducing calcium substitution gradually from 5.3 to 2.2 mmol/h in the first 8-h session of RCA-hemofiltration. New-onset sinus tachycardia with a prolonged QT interval occurred when calcium substitution was infused at rate of 1.1 mmol/h after 15 min of starting the second RCA-hemofiltration session (estimated net calcium loss was 7.54 mmol/h). When the calcium substitution was increased to usual rate of 5.6 mmol/h, the arrhythmia disappeared after 2 min. Arrhythmia did not recur when the calcium substitution rate was 2.2 mmol/h during the third session (estimated net calcium loss was 6.44 mmol/L). After the third RCA-hemofiltration session, the patient underwent parathyroidectomy and serum calcium returned to normal. Conclusions This case indicated that rapid calcium loss may cause arrhythmia in RCA-hemofiltration, and the rate of net calcium loss should be limited below a threshold value to prevent similar adverse effect during RCA-RRT.

Abstract Background Acute kidney injury (AKI) places a heavy burden on the healthcare system in China and is usually misdiagnosed. However, there are limited studies that have described the epidemiology and diagnosis of AKI in China. The aim of this study was to describe the incidence and diagnosis of AKI in hospitalized adult patients in a tertiary teaching hospital in southeast China. Methods All adult patients hospitalized from October 1, 2013 to September 30, 2014 in the First Affiliated Hospital of Nanjing Medical University were screened using the Lab Administration Network. AKI definition and staging were based on the KDIGO AKI criteria. Demographic characteristics, laboratory examination, clinical data, and clinical outcomes of AKI patients were recorded and analyzed. Results The incidence of AKI was 1.6% (1401/87196). The 30-day mortality was 35.3%. AKI stage 1, 2, 3 and RRT accounted for 38.0% (532/1401), 22.0% (309/1401), 40.0% (560/1401), and 16.3% (228/1401) of patients, respectively. The Renal, other Internal Medicine, Surgery, and ICU Departments accounted for 7.4%, 37.1%, 30.1%, and 25.4% of AKI patients, respectively. The timely diagnosis rate, delayed diagnosis rate, and missed diagnosis rate were 44% (616/1401), 3.3% (46/1401), and 52.7% (739/1401), respectively. Patients hospitalized in the Renal Department had the highest AKI diagnosis rate (89.3%, 88/103), while missed diagnosis rate of the surgical patients was as high as 75.1% (317/422). Multivariable logistic regression analysis indicated that presence of tumors, higher serum albumin, and AKI stage 1 were associated with failure to timely diagnose AKI, whereas presence of chronic kidney disease, oliguria, higher blood urea nitrogen, and greater number of organ failures correlated with earlier diagnosis. Conclusions AKI was characterized by a high incidence, high short-term mortality, and high missed diagnosis rate in hospitalized adult patients in our hospital. Interventions for improving diagnosis of AKI are urgently needed.