Ammonia clearance with haemofiltration in adults with liver disease (original) (raw)
Related papers
Effect of hemodialysis on blood ammonia level among cirrhotic patients undergoing hemodialysis
The Egyptian Journal of Hospital Medicine, 2018
Background: Uremia results in a characteristic breath odor (uremic fetor) which is largely due to its high ammonia content. Earlier studies have shown a strong correlation between breath ammonia and blood urea levels and a 10-fold reduction in breath ammonia after hemodialysis in patients with chronic kidney disease. Potential sources of breath ammonia include: (i) local ammonia production from hydrolysis of urea in the oropharyngeal and respiratory tracts by bacterial flora, and (ii) release of circulating blood ammonia by the lungs. While the effects of uremia and hemodialysis on breath ammonia are well known while their effects on blood ammonia are unknown and were explored here. Methods: Blood samples were obtained from 56 hemodialysis patients (immediately before and after dialysis). Blood levels of ammonia, creatinine, arterial blood gases, and electrolytes were measured. Results: There was significant fall in serum creatinine following hemodialysis with significant increase in...
Ammonia uptake by skeletal muscle in the hyperammonaemic rat
European Journal of Clinical Investigation, 1982
A two-stage surgical occlusion of the portal vein was employed to produce hyperammonaemia in the rat. The procedure resulted in a significant rise of arterial blood ammonia level from 70.5 6.5 pmol/l (mean+SEM, n= 10) to 214.0f 37.7 pmol/l and in a rise of venous blood ammonia from 65.0 f 9.4 pmol/l to 122.2 2 7.4 pmol/l during the first day following the Correspondence: Dr 0. Z. Lernau,
Severe hyperammonaemia in adults not explained by liver disease
Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, 2012
Ammonia is produced continuously in the body. It crosses the blood–brain barrier readily and at increased concentration it is toxic to the brain. A highly integrated system protects against this: ammonia produced during metabolism is detoxified temporarily by incorporation into the non-toxic amino acid glutamine. This is transported safely in the circulation to the small intestine, where ammonia is released, carried directly to the liver in the portal blood, converted to non-toxic urea and finally excreted in urine. As a result, plasma concentrations of ammonia in the systemic circulation are normally very low (<40 μmol/L). Hyperammonaemia develops if the urea cycle cannot control the ammonia load. This occurs when the load is excessive, portal blood from the intestines bypasses the liver and/or the urea cycle functions poorly. By far, the commonest cause is liver damage. This review focuses on other causes in adults. Because they are much less common, the diagnosis may be missed...
Can plasma ammonia be measured in patients with acute liver disease?
Annals of Clinical Biochemistry: International Journal of Laboratory Medicine, 2008
Background Plasma ammonia (PA) measurement is of key importance in the diagnosis and monitoring of some inherited metabolic disorders and to monitor subsequent treatment of hyperammonaemia. Methods Over a six-month period, patients' ammonia concentrations were measured in parallel, using an enzymatic–UV kit (Infinity Ammonia Liquid Stable Reagent, Thermo Electron Corporation, Australia) on an Olympus AU640 analyser (Olympus UK Ltd, Hertfordshire) and on our current dry chemistry system (Vitros 250, Ortho Clinical Diagnostic). Alanine amino transferase (ALT) was added to a human plasma sample to investigate its effect on the assessment of ammonia concentration. Results Both methods correlated well (InfinityTM kit = 1.12 × Vitros 250 + 39, R2 = 0.95, n = 105). However, clinically important discrepancies ranging from 100 to 380 μmol/L were found in patients with acute liver failure. Ammonia concentration measured with the enzymatic Infinity™ kit increased by 137 μmol/L when ALT was...
Gut, 2003
Background and aims: In patients with cirrhosis, hepatic encephalopathy is often precipitated by dehydration. This study tests the hypothesis that volume expansion in cirrhotic patients increases renal ammonia excretion. Patients and methods: Sixteen well compensated cirrhotic patients (mean Pugh score 6.7 (SEM 0.4)) were studied after an overnight fast. One litre of 0.9% saline was administered to patients intravenously over one hour. Plasma and urinary ammonia and sodium, renal plasma flow (RPF), glomerular filtration rate (GFR), plasma renin activity (PRA), and angiotensin II (ANG II) were measured before, during, and two hours after saline infusion. Results: Saline infusion resulted in a significant reduction in plasma ammonia (93 (SEM 7) to 56 (4) µmol/l; p<0.05) and RPF and GFR increased (p<0.05). Urinary ammonia excretion increased (p<0.05) significantly. There was a significant reduction in ANG II and PRA (p<0.05 for each) and the change in ammonia excretion correlated directly with the change in urinary sodium excretion (p<0.007), ANG II (p<0.002), and PRA (p<0.01). The mean increase in urinary ammonia excretion during the observation period was 1.08 mmol. Assuming a volume of distribution of 45 litres, the corresponding change in whole body ammonia during the same period was 1.67 mmol.
The dynamics of ammonia metabolism in man. Effects of liver disease and hyperammonemia
Journal of Clinical …, 1979
cyclotron-produced radionuclide, 13N, was used to label ammonia and to study its metabolism in a group of 5 normal subjects and 17 patients with liver disease, including 5 with portacaval shunts and 11 with encephalopathy. Arterial ammonia levels were 52-264 ,AM. The rate of ammonia clearance from the vascular compartment (metabolism) was a linear function of its arterial concentration: Amol/min = 4.71 [NH3Ia + 3.76, r = +0.85, P < 0.005. Quantitative body scans showed that 7.4+±0.3% of the isotope was metabolized by the brain. The brain ammonia utilization rate, calculated from brain and blood activities, was a function of the arterial ammonia concentration: ,umol/ min per whole brain = 0.375 [NH3]a-3.6, r = +0.93, P < 0.005. Assuming that cerebral blood flow and brain weights were normal, 47 + 3% of the ammonia was extracted from arterial blood during a single pass through the normal brains. Ammonia uptake was greatest in gray matter. The ammonia utilization reaction(s) appears to take place in a compartment, perhaps in astrocytes, that includes <20% of all brain ammonia. In the 11 nonencephalopathic subjects the [NH3Ia was 100±8 ,uM and the brain ammonia utilization rate was 32±3 ,umol/min per whole brain; in the 11 encephalopathic subjects these were respectively elevated to 149±18 AM (P < 0.01), and 53 ± 7 ,umol/min per whole brain (P <0.01). In normal subjects,-50% of the arterial ammonia was metabolized by skeletal muscle. In patients with portal-systemic shunting, muscle may become the most important organ for ammonia detoxification. Muscle atrophy may thereby contribute to the de
…, 1999
Cerebral edema leading to cerebral herniation CHis a common cause of death in acute liver failure ALF. Animal studies have related ammonia with this complication. During liver failure, hepatic ammonia removal can be expected to determine the arterial ammonia level. In patients with ALF, we examined the hypotheses that high arterial ammonia is related to later death by CH, and that impaired removal in the hepatic circulation is related to high arterial ammonia. Twenty-two patients with ALF were studied retrospectively. In addition, prospective studies with liver vein catheterization were performed after development of hepatic encephalopathyHEin 22 patients with ALF and 9 with acute on chronic liver disease AOCLD. Cerebral arterial-venous ammonia difference was studied in 13 patients with ALF. In all patients with ALF n= 44, those who developed CH n = 14 had higher arterial plasma ammonia than the non-CHn = 30patients 230 ± 58 vs. 118 ± 48 μmol/L;P< .001. In contrast, galactose elimination capacity, bilirubin, creatinine, and prothrombin time were not differentNS. Cerebral arterial-venous differences increased with increasing arterial ammonia (P< 001. Arterial plasma ammonia was lower than hepatic venous in ALF 148 ± 73 vs. 203 ± 108 μmol/L;P< .001. In contrast, arterial plasma ammonia was higher than hepatic venous in patients with AOCLD91 ± 26 vs. 66 ± 18 μmol/L;P lt; .05. Net ammonia release from the hepatic-splanchnic region was 6.5 ± 6.4 mmol/h in ALF, and arterial ammonia increased with increasing release. In contrast, there was a net hepatic-splanchnic removal of ammonia 2.8 ± 3.3 mmol/hn patients with AOCLD. We interpret these data that in ALF in humans, vast amounts of ammonia escape hepatic metabolism, leading to high arterial ammonia concentrations, which in turn is associated with increased cerebral ammonia uptake and CH.