Rhabdomyolysis continues to appear with increasing frequency and represents a medical emergency requiring rapid appropriate treatment. One of the unusual causes of nontraumatic rhabdomyolysis is hypokalemic periodic paralysis without secondary causes. Primary hypokalemic periodic paralysis is a rare genetic disease characterized by episodic attacks of muscle weakness due to decreases in serum potassium. A 30-year-old woman who had 3 episodic attacks of hypokalemic periodic paralysis was admitted in emergency room with sudden onset symmetrical muscle weakness. After several hours, she started to complain myalgia and severe ache in both calves without any changes. Laboratory test showed markedly elevated creatine phosphokinase, lactic dehydrogenase levels with hypokalemia, rhabdomyolysis resulting from hypokalemia was diagnosed. Here, we report an unusual case of rhabdomyolysis caused by severe hypokalemia, which was suggested a result of familial hypokalemic periodic paralysis.

Background: Latent tuberculosis infection (LTBI) is prevalent in end-stage renal disease (ESRD) patients. The risk of tuberculosis activation is also high. The appropriate LTBI screening and treatment is required in this population. Meanwhile, whether hemodialysis adequacy is associated with LTBI in the ESRD population is unclear. In this study, we aimed to investigate the association between hemodialysis adequacy and LTBI in ESRD patients. Methods: In the present cross-sectional study, we reviewed all outpatient-based ESRD patients in our artificial kidney room. Interferon gamma release assay (IGRA) was used for the diagnosis of LTBI. Clinical variables including nutritional adequacy (i.e., normalized protein catabolic rate, nPCR) and dialysis adequacy (i.e., Kt/V) were compared between IGRA-positive and IGRA-negative patients. Results: A total of 90 patients were enrolled, of which 20 (22.2%) had positive IGRA results using the QuantiFERON-TB method. Old fibrotic changes and nPCR (g/kg/day) were significantly different between IGRA-positive and IGRA-negative patients (both p < 0.005), while serum albumin and Kt/V were comparable (p = 0.429 and p = 0.590, respectively). Normalized PCR remained to be significant in a multivariate logistic regression analysis (adjusted hazard ratio, 0.911 (0.861–0.963); p = 0.001). The cutoff nPCR value less than 0.87 g/kg/day had an adjusted hazard ratio of 7.74 (1.77–33.74) for predicting LTBI. Patients with nPCR value less than 0.87 g/kg/day were older and had lower serum hemoglobin, albumin, calcium concentration, and Kt/V levels than those with nPCR value greater than 0.87 g/kg/day. Conclusions: Nutritional adequacy, especially when assessing nPCR value, was associated with LTBI, while dialysis adequacy was not associated with LTBI.

The factors influencing continuous renal replacement therapy (CRRT) duration for critically ill patients with acute kidney injury (AKI) are unclear. Therefore, we investigated the clinical factors that could influence the duration of CRRT for AKI survivors. In this retrospective observational study, the medical records of all hospital survivors who required CRRT for AKI in intensive care units were analyzed. The CRRT duration (median, 6 days) was categorized as short-duration CRRT (≤ 6 days, n = 65) and long-duration CRRT (> 6 days, n = 59), according to the median CRRT duration. A urine output of less than 0.5 mL/kg/h (adjusted odds ratio [OR], 3.4; P = 0.010), mechanical ventilation use (adjusted OR, 7.9; P = 0.001), and extracorporeal membrane oxygenation (ECMO) use (adjusted OR, 6.5; P = 0.010) were independent predictors of long-duration CRRT, whereas serum creatinine and neutrophil gelatinase-associated lipocalin were not significant predictors. A clinical model demonstrated a good discriminatory ability to predict long-duration CRRT (area under the curve, 0.84; 95% confidence interval, 0.76–0.90). The urine output immediately before CRRT initiation and factors associated with disease severity significantly affected the duration of CRRT. Simultaneously considering the urine output, mechanical ventilation use, and ECMO use predicted CRRT duration in AKI survivors.

Postcontrast acute kidney injury (AKI) occurs more frequently in patients with lower estimated glomerular filtration rate. We hypothesized that postcontrast AKI in chronic kidney disease (CKD) patients with distinct risk factors might be associated with accelerated renal progression. We undertook this retrospective cohort study to develop and validate a risk scoring model for predicting renal progression. In a development dataset, 18,278 contrast-enhanced CT scans were performed in 9097 patients with CKD (estimated glomerular filtration rate [eGFR] < 60 mL/min/1.73 m 2 ) who were not undergoing dialysis. Postcontrast AKI was observed in 5.8% (1051/18,278) of all contrast-enhanced CTs with 7.6% (689/9097) of the total CKD patients. We investigated the 1-year renal outcome in 224 eligible patients. A risk scoring model was developed with multivariate regression analysis and was assessed in external validation (independent 154 patients). Among 224 patients, 70 (31.3%) patients had progression of renal dysfunction at 1 year (defined as reduction in estimated GFR ≥25% at 1 year). A risk score of 4, 4, 6, 6, 7, or 6 was assigned to diabetes, baseline estimated GFR < 45 mL/min/1.73 m 2 , hypertension, repeated contrast exposure, congestive heart failure, and persistent renal injury (defined as an elevation of serum creatinine ≥25% at 3 months), respectively. An increasing risk score was associated with renal progression. Of note, persistent renal injury was more prevalent in the progression group than in the non-progression group. The AUROC of the model in the development population was 0.765. In the validation dataset, however, the discriminative power decreased (AUROC = 0.653). Our suggested model provided the risk of renal progression, aiding in predicting prognosis, counseling, and improving outcomes in CKD patients complicated by postcontrast AKI.

BackgroundEvidence suggests that alkaline phosphatase attenuates inflammatory response in sepsis by lipopolysaccharide detoxification and adenosine triphosphate dephosphorylation. We sought to determine changes in alkaline phosphatase (AP) activity during septic acute kidney injury (AKI) and clinical parameters associated with AP activity.MethodsIn this retrospective study, we investigated baseline (when initiating CRRT) and follow-up AP activity on day 3, and associated outcomes in patients who underwent continuous renal replacement therapy (CRRT) due to septic AKI.ResultsWe analyzed the baseline AP activity of 155 patients and day 3 AP activity in 123 patients. Baseline AP activity was not associated with renal or inflammatory biomarkers, or outcomes. It did not significantly differ between the 75 survivors and 80 non-survivors (p = 0.155). AP activity was higher on day 3 than at baseline (105 U/L [interquartile range, 79–156] vs 90 U/L [interquartile range, 59–133]). In particular, liver and bone isoforms increased significantly (p < 0.05), but intestine isoforms did not reach statistical significance (p = 0.367). In addition, day 3 AP activity showed a weak correlation with length of ICU stay (r = 0.213, p = 0.018) and length of hospital stay (r = 0.216, p = 0.017), but not with survival (r = − 0.035, p = 0.698).ConclusionEndogenous AP activity significantly increased in patients with septic AKI. However, neither baseline nor follow-up AP activity was associated with survival.