Issues of Immunological and Hemodynamic Monitoring Before and During Kidney Transplantation in Sensitized Heart Transplant Recipient.

Previously transplanted highly sensitized patients experience problems with subsequent transplantation. It is also difficult to provide optimal hemodynamic conditions during successive kidney transplantation in heart transplant recipients. PATIENT AND METHODS: We present a case of a 56-year old patient with end-stage renal failure after heart transplantation performed 21 years ago and hemodialyzed using arteriovenous fistula. The patient had 69% panel-reactive antibodies, had been on the active waiting list since 2013, and presented 335 positive crossmatches with deceased donors. He also positively crossmatched with a potential living donor. Detailed examination of anti-HLA antibodies revealed the absence of IgG donor-specific antibodies and negative crossmatch with dithiothreitol-treated serum. The transplantation from his wife was performed with positive crossmatch after 4 plasma exchanges and thymoglobulin induction. Because sympathetic and parasympathetic denervation of the transplanted heart and the presence of arteriovenous fistula induced volume overload of the right heart, we used central venous pressure (CVP) and the PiCCO2 for postsurgical assessment of cardiac output. RESULTS: Monitoring, like CVP and other static exponents of preload obtained by PICCO (extravascular lung water, global end-diastolic volume index) as well as the dynamic parameters obtained by PiCCO2 (pulse pressure variation, stroke volume variation), was not sensitive enough to describe recipient volume status. The immediate graft function was observed, and after 11 months satisfactory estimated glomerular filtration rate is noted with the absence of donor-specific antibodies. CONCLUSION: The history of heart transplantation with existing arteriovenous fistula makes clinical tools such as continuous cardiac output monitoring and CVP parameter inadequate for describing the hemodynamic situation. The high level of panel-reactive antibodies and positive crossmatch possibly caused by IgM antibodies do not have to withdraw the recipient from kidney transplantation.

Continuous positive airway pressure/pressure support pre-oxygenation of morbidly obese patients.

BACKGROUND: Morbidly obese patients are more prone to desaturation of arterial blood during apnea with induction of anesthesia than are non-obese. This study aimed to assess the effect of low-pressure continuous positive airway pressure (CPAP) with pressure support ventilation (PSV) during pre-oxygenation on partial oxygen pressure in arterial blood (PaO2 ) immediately after tracheal intubation (post-intubation PaO2). METHODS: Forty-four adult patients scheduled for laparoscopic gastric bypass surgery were pre-oxygenated with 80% O2 for 2 min, randomized either to CPAP 5 cm H2O + PSV 5 cm H2O (CPAP/PSV, n = 22) or neutral-pressure breathing without CPAP/PSV (control, n = 22). Anesthesia was induced in a rapid-sequence protocol and the trachea was intubated without prior mask ventilation. Arterial blood gases were measured before pre-oxygenation, before induction of anesthesia, and immediately following intubation, before the first positive pressure breath. RESULTS: After pre-oxygenation, partial carbondioxide pressure was significantly lower in the CPAP/PSV group (4.9 ± 0.5 kPa), (mean ± standard deviation) than in the control group (5.2 ± 0.7 kPa) (P = 0.025). Post-preoxygenation PaO2 did not differ between the groups, but post-intubation PaO2 was significantly higher in the CPAP/PSV group (32.2 ± 4.1 kPa) than in the control group (23.8 ± 8.8 kPa) (P < 0.001). In the control group, nadir oxygen saturation was lower (median 98%, range 83-99%) than in the CPAP/PSV group (median 99%, range 97-99%, P = 0.011). CONCLUSIONS: In morbidly obese patients, low-pressure CPAP combined with low-pressure PSV during pre-oxygenation resulted in better oxygenation, compared with neutral-pressure breathing, and prevented desaturation episodes.

Prolonged exposure to inhaled nitric oxide transiently modifies tubular function in healthy piglets and promotes tubular apoptosis.

AIM: Inhaled nitric oxide (iNO) is a selective pulmonary vasodilator. We hypothesized that those piglets exposed to prolonged iNO react with a modified renal function. METHODS: Randomized, placebo-controlled exposure to 40 p.p.m. iNO (30 h) in piglets (n = 20). Plasma and urine were sampled during three periods (first and second 12 h periods, and finally a 6 h period). We measured urine volumes, plasma and urine electrolytes (UNa, UK, UCl), plasma creatinine and urea. We calculated creatinine clearance (Ccr), and fractional excretions of sodium and potassium (FENa, FEK) and urinary excretions of electrolytes (UENa, UEK, UECl). Haemodynamic data were recorded and renal tubular apoptosis detected. RESULTS: For the first 12 h, certain parameters significantly increased in the iNO group (mean +/- SD): UNa (mmol L(-1)), 87.7 (+/-35.0) vs. 39.3 (+/-22.9), UCl (mmol L(-1)) 80.4 (+/-32.8) vs. 48.0 (+/-26.7), FENa (%) 2.1 (+/-0.8) vs. 0.7 (+/-0.5), FEK (%) 31.7 (+/-7.0) vs. 20.7 (+/-12.3), as well as UENa (mmol) 61.0 (+/-21.1) vs. 27.6 (+/-17.9) and UECl (mmol) 57.3 (24.5) vs. 37.6 (29.0). These changes were absent in the second and third periods of the study. Significant differences in percentage of apoptotic cell nuclei in the renal cortex and medulla were found after iNO exposure: 39% vs. 15%. CONCLUSION: Exposure to 40 p.p.m. iNO in healthy anaesthetized piglets has a transient natriuretic effect that disappears after 12 h. We also found evidence of renal tubular apoptosis promotion after 30 h of iNO.