The elevation of the anion gap in steady state chronic kidney disease may be less prominent than generally accepted.

Background: A presumed cause of metabolic acidosis in chronic kidney disease (CKD) is accumulation of unmeasured anions, leading to a high anion gap (AG). In patients with CKD with a high AG, only minor increases are expected. The aim of this study is to evaluate the magnitude of the AG in documented steady state CKD to examine the effect of CKD on a high-AG metabolic acidosis (HAGMA). Methods: In this cross-sectional study the AG, bicarbonate, and chloride were evaluated in 1045 blood and urine samples of 501 patients with steady state CKD in the outpatient clinic. The influence of phosphate, albumin and potassium on the AG were evaluated. Results: The mean AG increased from 8.8 mEq/l (±1.57) in CKD stage 1 to 11.2 mEq/l (±2.22) in CKD stage 5 (P < 0.001). Correction for albumin or phosphate did not influence the magnitude of the AG. Correction for potassium did alter the prevalence of HAGMA, but not the severity. [HCO3-] decreased between CKD stages 1 and 5 by 5.1 mEq/l. The [Cl-] increased by 2.6 mEq/l between CKD stages 1 and 5. Conclusions: The elevation of the AG in patients with steady state CKD is limited and less pronounced than the decrease in [HCO3-]. Normal AG metabolic acidosis seems to be more important in CKD than HAGMA. The CKD stage and the magnitude of the AG should be taken into account when evaluating a patient with HAGMA. This study suggests that an AG >15 mEq/l is rarely due to renal failure alone.

Oxalate nephropathy in an elderly patient with newly diagnosed celiac disease - a case report.

Oxalate nephropathy, due to secondary hyperoxaluria has widely been described in gastrointestinal diseases. However, reports of oxalate nephropathy in newly diagnosed celiac disease are rare. A 72-year-old Caucasian male presented to the hospital with abdominal discomfort and acute renal insufficiency with a creatinine of 290 µmol/L. The clinical course, laboratory results and urinalysis were suspect for tubular injury. Renal biopsy showed calcium oxalate depositions. Elevated plasma and urine oxalate levels established the diagnosis oxalate nephropathy. The abdominal complaints with steatorrhea and positive anti-tissue transglutaminase antibodies were diagnosed as celiac disease, which was confirmed after duodenal biopsies. Treatment with prednisone, and gluten-free, low oxalate and normal calcium diet, lowered the plasma oxalate levels and improved his renal function. Decreased absorption of free fatty acids can lead to increased free oxalate in the colon due to the binding of free fatty acids to calcium, preventing the formation of the less absorbable calcium oxalate in the colon. Oxalate dispositions in the kidney can lead to acute tubular injury and chronic renal insufficiency. Celiac disease is therefore one of the intestinal diseases that can lead to hyperoxaluria and oxalate nephropathy.

Differences in capillary recruitment between cardiac surgery and septic patients after fluid resuscitation.

BACKGROUND: Clinical evaluation of the effects of fluid therapy remains cumbersome and strategies are based on the assumption that normalization of macrohemodynamic variables will result in parallel improvement in organ perfusion. Recently, we and others suggested the use of direct in-vivo observation of the microcirculation to evaluate the effects of fluid therapy. METHODS: A single-centre observational study, using in-vivo microscopy to assess total vessel density (TVD) in two subsets of ICU patients. RESULTS: After fluid resuscitation TVD showed no difference between sepsis patients (N = 47) and cardiac surgery patients (N = 52): 18.4[16.8-20.8] vs 18.7[16.8-20.9] mm/mm2, p = 0.59. In cardiac surgery patients there was a significant correlation between the amount of fluids administered and TVD, with an optimum in the third quartile. However, such correlation was absent in septic patients. CONCLUSIONS: TVD after fluid administration is not different between 2 subtypes of intensive care patients. However, only in septic patients we observed a lack of coherence between the amount of fluids administered and TVD. Further research is needed to determine if TVD may serve as potential endpoint for fluid administration.

The reliability and validity of passive leg raise and fluid bolus to assess fluid responsiveness in spontaneously breathing emergency department patients.

PURPOSE: We investigated the reproducibility of passive leg raise (PLR) and fluid bolus (BOLUS) using the Non-Invasive Cardiac Output Monitor (NICOM; Cheetah Medical, Tel Aviv, Israel) for assessment of fluid responsiveness (FR) in spontaneously breathing emergency department (ED) patients. METHODS: Prospective, observational study of a convenience sample of adult ED patients receiving intravenous fluid bolus. We assessed stroke volume (SV) using NICOM and obtained results from PLR, where the head of the bed was changed from semirecumbent to supine while the patients' legs raised to 45° for 3 minutes. Fluid bolus was defined as 5 mL/kg normal saline infusion. Maximal increase in SV was recorded. Fluid responsiveness was defined as an increase of SV greater than 10% from baseline. We obtained 4 consecutive responses for each patient; PLR1, PLR2, BOLUS1 separated each by 10 minutes, and BOLUS2 initiated immediately after the end of BOLUS1. We calculated κ statistics, correlation coefficients, and odds ratios with 95% confidence interval and Bland-Altman plots. RESULTS: We enrolled 109 patients enrolled in this study. The 2 PLRs were significantly correlated (r = 0.78, P < .001) with κ = 0.46 for FR (P < .001). The 2 BOLUSES less strongly correlated (r = 0.14, P = .001) and κ = 0.06 for FR (P < .001). Patients who were responsive to PLR1 had 9.5 (3.6-25) odds of being FR for PLR2, whereas those responsive to BOLUS1 had a 1.8 (0.76-4.3) increased odds of FR for BOLUS2. CONCLUSION: In conclusion, we have found PLR as measured by the NICOM to be a promising tool for the evaluation of SV responsiveness. It was feasible for use in the ED, and the data suggest that the PLR technique may be more reproducible than the fluid bolus technique for assessing volume responsiveness.