AMINO ACID REMOVAL DURING HEMODIALYSIS OF PATI-ENTS WHO HAD UNDERGONE INTRADIALYTIC PAR-ENTERAL NUTRITION.

Hemodialysis removes solutes uniformly according to their molecular weight. During each hemodialysis session, 6–8 g of amino acids are reportedly removed into the dialysate. Little is known about the amount of amino acids removed from those who have undergone intradialytic parenteral nutrition (IDPN). Objective: We measured amino acid amounts prospectively during hemodialysis treatment. Methods: We used 200 ml of 7.2% amino acid solution (KidminTM), 200 ml of 50% glucose, and 20% of lipid emulsion as IDPN fluid. Blood samples were collected at the beginning and end of each session. The dialysate portion was also collected. Results: Six patients were included in this study after providing written informed consent. The amount of amino acids removed during hemodialysis sessions was calculated as 9.1±1.4 g, which was less than that infused as IDPN. The profiles of the removed amino acids showed that the amount removed was less than that within IDPN. However, for tyrosine and alanine, hemodialysis treatment removed more amino acids than that infused as IDPN, as well as amino acids that were not IDPN solution constituents. During a 2-week follow-up period, no significant change in amino acid profiles was observed. Conclusions: IDPN entirely supplemented the removed amino acids, although some amino acids were not restored

A case of refeeding syndrome during intradialytic parenteral nutrition

Abstract Background Refeeding syndrome is a potentially fatal electrolyte shift in patients with rapid feeding after low-calorie intake. Although the key to diagnosing refeeding syndrome is hypophosphatemia after feeding, renal dysfunction might hide refeeding hypophosphatemia, especially in maintenance hemodialysis patients. Intradialytic parenteral nutrition (IDPN) is a therapeutic approach used to treat malnourished patients with maintenance hemodialysis. No earlier report describes a study of refeeding syndrome complicated with IDPN. Case presentation We present a case of a 77-year-old man undergoing maintenance hemodialysis for 17 years. While IDPN was administered after 10 days fasting, ventricular tachycardia (VT) occurred, possibly because of a rapid intracellular shift of potassium mainly explained as refeeding syndrome in addition to potassium removal by hemodialysis. A greater decline of serum phosphate concentrations during hemodialysis on that day compared with that during usual hemodialysis session supports our inference of the contribution of refeeding syndrome to VT complicated with hypokalemia. Conclusion Physicians should know that IDPN can induce refeeding hypophosphatemia and rapid intracellular shift of potassium. Synergic lowering effects of serum potassium both with intracellular shift caused by refeeding syndrome and potassium removal by hemodialysis might cause lethal arrhythmia in patients treated with IDPN. Before treating malnourished patients with IDPN, the risk of refeeding syndrome should be assessed in patients with high risk of refeeding syndrome

The Longitudinal Study of Liver Cysts in Patients With Autosomal Dominant Polycystic Kidney Disease and Polycystic Liver Disease

Although polycystic liver disease (PCLD) is one of the extrarenal complications in patients with autosomal dominant polycystic kidney disease (ADPKD), longitudinal changes and the association with total liver volume (TLV) have not been clearly elucidated yet. Methods: Patients with ADPKD were chosen who underwent computed tomography or magnetic resonance imaging twice or more during August 2003 through December 2015. TLV, each cyst volume, and the proportion of parenchyma were measured. The natural history of liver cysts and the association between TLV and liver cysts were evaluated. To compare with liver cysts in ADPKD patients with PCLD, simple liver cysts in patients without ADPKD were also evaluated. Results: TLV at baseline and its growth rate in all the patients with ADPKD, whose serum creatinine, estimated glomerular filtration rate, and total kidney volume were 1.45 mg/dl (0.76–2.32 mg/dl), 38.5 ml/min per 1.73 m2 (18.7–57.9 ml/min per 1.73 m2), and 1394 ml (773–2861 ml), were 1431 ml (1062–1749 ml) and −0.95%/yr (−3.16 to 4.94%/yr), respectively, in the observation period (median, 1063 days). Neither TLV nor its growth rate was significantly different between ADPKD patients with PCLD and those without PCLD. The growth rate of 79 liver cysts was 39.5%/yr (17.5–80.8%/yr) in PCLD patients with ADPKD. It was significantly larger than that of 60 simple liver cysts in the non-ADPKD group, 11.0%/yr (−2.2 to 33.1%/yr). Moreover, the proportion of parenchyma reduced, whereas that of total cyst volume increased significantly (P = 0.001). Discussion: The reduction of parenchyma was accompanied by the growth of liver cysts during time course in PCLD patients with ADPKD

Different Biomarker Kinetics in Critically Ill Patients with High Lactate Levels

We evaluated the association of the kinetics of interleukin-6 (IL-6), neutrophil gelatinase-associated lipocalin (NGAL), and high-mobility group box 1 (HMGB1) with intensive care unit (ICU) mortality in critically ill patients with hyperlactatemia. This proof-of-concept study was conducted with prospectively enrolled patients admitted to a medical/surgical ICU with hyperlactatemia (lactate levels >4 mmol/L). Blood lactate, IL-6, NGAL, and HMGB1 were measured every 2 h until 6 h post ICU admission. The primary outcome was ICU mortality. Of thirty patients in this study, 14 patients (47%) had sepsis, and the ICU mortality was 47%. IL-6 and NGAL levels were significantly higher in septic patients than in non-septic patients. On kinetic analysis, the lactate levels were significantly decreased in survivors, and the NGAL levels were significantly increased in non-survivors. Among septic patients, a decline in IL-6 levels were observed in survivors. The HMGB1 levels were unchanged in survivors and non-survivors regardless of sepsis complication. Non-septic patients with higher reduction rate of lactate and HMGB1 had the lowest mortality than the others. ICU patients exhibited different kinetic patterns in lactate, NGAL, and IL-6, but HMGB1 did not seem to change over the 6-h duration. Further studies are necessary to evaluate the efficacy of the combination of the inflammatory biomarkers with lactate

Different Biomarker Kinetics in Critically Ill Patients with High Lactate Levels

We evaluated the association of the kinetics of interleukin-6 (IL-6), neutrophil gelatinase-associated lipocalin (NGAL), and high-mobility group box 1 (HMGB1) with intensive care unit (ICU) mortality in critically ill patients with hyperlactatemia. This proof-of-concept study was conducted with prospectively enrolled patients admitted to a medical/surgical ICU with hyperlactatemia (lactate levels >4 mmol/L). Blood lactate, IL-6, NGAL, and HMGB1 were measured every 2 h until 6 h post ICU admission. The primary outcome was ICU mortality. Of thirty patients in this study, 14 patients (47%) had sepsis, and the ICU mortality was 47%. IL-6 and NGAL levels were significantly higher in septic patients than in non-septic patients. On kinetic analysis, the lactate levels were significantly decreased in survivors, and the NGAL levels were significantly increased in non-survivors. Among septic patients, a decline in IL-6 levels were observed in survivors. The HMGB1 levels were unchanged in survivors and non-survivors regardless of sepsis complication. Non-septic patients with higher reduction rate of lactate and HMGB1 had the lowest mortality than the others. ICU patients exhibited different kinetic patterns in lactate, NGAL, and IL-6, but HMGB1 did not seem to change over the 6-h duration. Further studies are necessary to evaluate the efficacy of the combination of the inflammatory biomarkers with lactate

Patency with antiplatelet treatment after vascular access intervention therapy: a retrospective observational study

Abstract Background Vascular access (VA) intervention therapy (VAIVT) has been increasingly used for treating VA failure (VAF) in patients undergoing hemodialysis; however, clinical evidence demonstrating the efficacy of prevention of VAF after VAIVT is limited. Therefore, we aimed to assess characteristics of patients developing VAF after VAIVT and analyze risk factors for VAF after VAIVT. Methods This retrospective study included 96 patients with VAF who underwent ultrasound-guided VAIVT by interventional nephrologists between January 2013 and March 2018 at the Department of Nephrology, University of Tokyo Hospital, Japan. Patient information included age, sex, medication history, and comorbidities that could potentially affect VAF onset. Patients were categorized into two groups based on antiplatelet treatment. Multivariate Cox regression analysis was performed for evaluating effect of various factors on VAF after VAIVT. Results Median age of patients at the time of VAIVT was 71 years (interquartile range 63–79); the most prevalent etiology underlying end-stage renal disease was diabetic nephropathy (40.7%). Comparison between the antiplatelet and non-antiplatelet groups revealed that the incidence of VAF was significantly lower in the antiplatelet group. Multivariate analysis revealed that antiplatelet treatment was associated with a lower risk of VAF after VAIVT. Conclusion Administration of antiplatelet agents was associated with a significant reduction in VAF risk after VAIVT

Urinary fatty acid-binding protein 1: an early predictive biomarker of kidney injury

In the development of novel therapeutic strategies for kidney disease, new renal biomarkers for early detection and accurate evaluation of renal injury are urgently required for both acute kidney injury (AKI) and chronic kidney disease (CKD). Fatty acid-binding protein 1 (FABP1) is expressed in renal proximal tubule cells and shed into urine in response to hypoxia caused by decreased peritubular capillary blood flow. To clarify the role of urinary FABP1 in kidney disease, we established human FABP1 transgenic mice and evaluated the responses of FABP1 to several AKI and CKD models. Moreover, there are accumulating clinical data that urinary FABP1 can detect human AKI earlier than serum creatinine and can distinguish the risk population for AKI. Investigation with “humanized” FABP1 transgenic mice and measurement of clinical samples allowed us to develop urinary FABP1 as a new renal biomarker. Further clinical studies are necessary to confirm the potential of urinary FABP1 for clinical application

Mild elevation of urinary biomarkers in prerenal acute kidney injury

Prerenal acute kidney injury (AKI) is thought to be a reversible loss of renal function without structural damage. Although prerenal and intrinsic AKI frequently coexist in clinical situations, serum creatinine and urine output provide no information to support their differentiation. Recently developed biomarkers reflect tubular epithelial injury; therefore, we evaluated urinary biomarker levels in an adult mixed intensive care unit (ICU) cohort of patients who had been clinically evaluated as having prerenal AKI. Urinary L-type fatty acid–binding protein (L-FABP), neutrophil gelatinase–associated lipocalin (NGAL), interleukin-18 (IL-18), N-acetyl-β-D-glucosaminidase (NAG), and albumin in patients with prerenal AKI showed modest but significantly higher concentrations than in patients with non-AKI. We also conducted a proof-of-concept experiment to measure urinary biomarker excretion in prerenal AKI caused by volume depletion. Compared with cisplatinum and ischemia–reperfusion models in mice, volume depletion in mice caused a modest secretion of L-FABP and NGAL into urine with more sensitive response of L-FABP than that of NGAL. Although no histological evidence of structural damage was identified by light microscopy, partial kidney hypoxia was found by pimonidazole incorporation in the volume depletion model. Thus, our study suggests that new AKI biomarkers can detect mild renal tubular damage in prerenal acute kidney injury