The Experts below are selected from a list of 315 Experts worldwide ranked by ideXlab platform
Curtis R Morris - One of the best experts on this subject based on the ideXlab platform.
-
potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women
The Journal of Clinical Endocrinology and Metabolism, 1997Co-Authors: Lynda A Frassetto, Curtis R MorrisAbstract:Previously we demonstrated that low grade chronic metabolic Acidosis exists normally in humans eating ordinary diets that yield normal net rates of endogenous acid production (EAP), and that the degree of Acidosis increases with age. We hypothesize that such diet-dependent and age-amplifying low grade metabolic Acidosis contributes to the decline in skeletal muscle mass that occurs normally with aging. This hypothesis is based on the reported finding that chronic metabolic Acidosis induces muscle protein breakdown, and that correction of Acidosis reverses the effect. Accordingly, in 14 healthy postmenopausal women residing in a General Clinical Research Center and eating a constant diet yielding a normal EAP rate, we tested whether correcting their "physiological" Acidosis with orally administered potassium bicarbonate (KHCO3; 60-120 mmol/day for 18 days) reduces their urinary nitrogen loss. KHCO3 reduced EAP to nearly zero, significantly reduced the blood hydrogen ion concentration (P < 0.001), and increased the plasma bicarbonate concentration (P < 0.001), indicating that pre-KHCO3, diet-dependent EAP was significantly perturbing systemic acid-base equilibrium, causing a low grade metabolic Acidosis. Urinary ammonia nitrogen, urea nitrogen, and total nitrogen levels significantly decreased. The cumulative reduction in nitrogen excretion was 14.1 +/- 12.3 g (P < 0.001). Renal creatinine clearance and urine volume remained unchanged. We conclude that in postmenopausal women, neutralization of diet-induced EAP with KHCO3 corrects their preexisting diet-dependent low grade metabolic Acidosis and significantly reduces their urinary nitrogen wasting. The magnitude of the KHCO3-induced nitrogen-sparing effect is potentially sufficient to both prevent continuing age-related loss of muscle mass and restore previously accrued deficits.
-
potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women
The Journal of Clinical Endocrinology and Metabolism, 1997Co-Authors: Lynda A Frassetto, Curtis R Morris, Anthony SebastianAbstract:Previously we demonstrated that low grade chronic metabolic Acidosis exists normally in humans eating ordinary diets that yield normal net rates of endogenous acid production (EAP), and that the degree of Acidosis increases with age. We hypothesize that such diet-dependent and age-amplifying low grade metabolic Acidosis contributes to the decline in skeletal muscle mass that occurs normally with aging. This hypothesis is based on the reported finding that chronic metabolic Acidosis induces muscle protein breakdown, and that correction of Acidosis reverses the effect. Accordingly, in 14 healthy postmenopausal women residing in a General Clinical Research Center and eating a constant diet yielding a normal EAP rate, we tested whether correcting their “physiological” Acidosis with orally administered potassium bicarbonate (KHCO3; 60–120 mmol/day for 18 days) reduces their urinary nitrogen loss. KHCO3 reduced EAP to nearly zero, significantly reduced the blood hydrogen ion concentration (P < 0.001), and incre...
Walter H. Dzik - One of the best experts on this subject based on the ideXlab platform.
-
mitochondrial gene sequence variants in children with severe malaria anaemia with or without lactic Acidosis a case control study
Malaria Journal, 2018Co-Authors: Casey Fowler, Aggrey Dhabangi, Christine Csertigazdewich, Charles Musoke, Himanshu Sharma, Sami S Amr, Walter H. DzikAbstract:Background Evolutionary pressure by Plasmodium falciparum malaria is known to have favoured a large number of human gene adaptations, but there is surprisingly little investigation of the effect of malaria on human mitochondrial sequence variation. Plasmodium falciparum infection can cause severe malaria anaemia (SMA) with insufficient tissue oxygenation, lactic Acidosis and death. Despite equal degrees of severe anaemia, some individuals develop lactic Acidosis while others do not. A case–control study design was used to investigate whether differences in host mitochondrial gene sequences were associated with lactic Acidosis in SMA. Full mitochondrial sequences were obtained from 36 subjects with SMA complicated by lactic Acidosis and 37 subjects with SMA without lactic Acidosis. The two groups were matched for age, sex, and degree of anaemia.
-
the effect of blood storage age on treatment of lactic Acidosis by transfusion in children with severe malarial anaemia a pilot randomized controlled trial
Malaria Journal, 2013Co-Authors: Aggrey Dhabangi, Edison Mworozi, Irene R Lubega, Christine Csertigazdewich, Albert Maganda, Walter H. DzikAbstract:Background Severe malarial anaemia requiring blood transfusion is a life-threatening condition affecting millions of children in sub-Saharan Africa. Up to 40% of children with severe malarial anaemia have associated lactic Acidosis. Lactic Acidosis in these children is strongly associated with fatal outcomes and is corrected by blood transfusion. However, it is not known whether the storage age of blood for transfusion affects resolution of lactic Acidosis. The objective of this pilot study was to evaluate the effect of blood storage age on resolution of lactic Acidosis in children with severe malarial anaemia and demonstrate feasibility of conducting a large trial.
-
the effect of blood storage age on treatment of lactic Acidosis by transfusion in children with severe malarial anaemia a pilot randomized controlled trial
Malaria Journal, 2013Co-Authors: Aggrey Dhabangi, Edison Mworozi, Irene R Lubega, Christine Csertigazdewich, Albert Maganda, Walter H. DzikAbstract:Severe malarial anaemia requiring blood transfusion is a life-threatening condition affecting millions of children in sub-Saharan Africa. Up to 40% of children with severe malarial anaemia have associated lactic Acidosis. Lactic Acidosis in these children is strongly associated with fatal outcomes and is corrected by blood transfusion. However, it is not known whether the storage age of blood for transfusion affects resolution of lactic Acidosis. The objective of this pilot study was to evaluate the effect of blood storage age on resolution of lactic Acidosis in children with severe malarial anaemia and demonstrate feasibility of conducting a large trial. Children aged six to 59 months admitted to Acute Care Unit of Mulago Hospital (Kampala, Uganda) with severe malarial anaemia (haemoglobin ≤ 5 g/dL) and lactic Acidosis (blood lactate ≥5 mmol/L), were randomly assigned to receive either blood of short storage age (one to 10 days) or long storage age (21–35 days) by gravity infusion. Seventy-four patients were enrolled and randomized to two equal-sized study arms. Physiological measurements, including blood lactate, oxygen saturation, haemoglobin, and vital signs, were taken at baseline, during and after transfusion. The primary outcome variable was the proportion of children whose lactic Acidosis resolved by four hours after transfusion. Thirty-four of 37 (92%) of the children in the short storage treatment arm compared to 30/37 (81%) in the long storage arm achieved a blood lactate <5 mmol/L by four hours post transfusion (p value = 0.308). The mean time to lactic Acidosis resolution was 2.65 hours (95% CI; 2.25–3.05) in the short storage arm, compared to 3.35 hours (95% CI; 2.60–4.10) in the long storage arm (p value = 0.264). Pilot data suggest that among children with severe malarial anaemia and lactic Acidosis transfused with packed red blood cells, the storage age of blood does not affect resolution of lactic Acidosis. The results support a larger and well-powered study which is under way. clinicaltrials.gov NCT01580111
Lynda A Frassetto - One of the best experts on this subject based on the ideXlab platform.
-
potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women
The Journal of Clinical Endocrinology and Metabolism, 1997Co-Authors: Lynda A Frassetto, Curtis R MorrisAbstract:Previously we demonstrated that low grade chronic metabolic Acidosis exists normally in humans eating ordinary diets that yield normal net rates of endogenous acid production (EAP), and that the degree of Acidosis increases with age. We hypothesize that such diet-dependent and age-amplifying low grade metabolic Acidosis contributes to the decline in skeletal muscle mass that occurs normally with aging. This hypothesis is based on the reported finding that chronic metabolic Acidosis induces muscle protein breakdown, and that correction of Acidosis reverses the effect. Accordingly, in 14 healthy postmenopausal women residing in a General Clinical Research Center and eating a constant diet yielding a normal EAP rate, we tested whether correcting their "physiological" Acidosis with orally administered potassium bicarbonate (KHCO3; 60-120 mmol/day for 18 days) reduces their urinary nitrogen loss. KHCO3 reduced EAP to nearly zero, significantly reduced the blood hydrogen ion concentration (P < 0.001), and increased the plasma bicarbonate concentration (P < 0.001), indicating that pre-KHCO3, diet-dependent EAP was significantly perturbing systemic acid-base equilibrium, causing a low grade metabolic Acidosis. Urinary ammonia nitrogen, urea nitrogen, and total nitrogen levels significantly decreased. The cumulative reduction in nitrogen excretion was 14.1 +/- 12.3 g (P < 0.001). Renal creatinine clearance and urine volume remained unchanged. We conclude that in postmenopausal women, neutralization of diet-induced EAP with KHCO3 corrects their preexisting diet-dependent low grade metabolic Acidosis and significantly reduces their urinary nitrogen wasting. The magnitude of the KHCO3-induced nitrogen-sparing effect is potentially sufficient to both prevent continuing age-related loss of muscle mass and restore previously accrued deficits.
-
potassium bicarbonate reduces urinary nitrogen excretion in postmenopausal women
The Journal of Clinical Endocrinology and Metabolism, 1997Co-Authors: Lynda A Frassetto, Curtis R Morris, Anthony SebastianAbstract:Previously we demonstrated that low grade chronic metabolic Acidosis exists normally in humans eating ordinary diets that yield normal net rates of endogenous acid production (EAP), and that the degree of Acidosis increases with age. We hypothesize that such diet-dependent and age-amplifying low grade metabolic Acidosis contributes to the decline in skeletal muscle mass that occurs normally with aging. This hypothesis is based on the reported finding that chronic metabolic Acidosis induces muscle protein breakdown, and that correction of Acidosis reverses the effect. Accordingly, in 14 healthy postmenopausal women residing in a General Clinical Research Center and eating a constant diet yielding a normal EAP rate, we tested whether correcting their “physiological” Acidosis with orally administered potassium bicarbonate (KHCO3; 60–120 mmol/day for 18 days) reduces their urinary nitrogen loss. KHCO3 reduced EAP to nearly zero, significantly reduced the blood hydrogen ion concentration (P < 0.001), and incre...
Hugh B Carey - One of the best experts on this subject based on the ideXlab platform.
-
recurrent high anion gap metabolic Acidosis secondary to 5 oxoproline pyroglutamic acid
American Journal of Kidney Diseases, 2005Co-Authors: Prayus Tailor, Tuhina Raman, Cheryl L Garganta, Runa Njalsson, Katarina Steen Carlsson, Ellinor Ristoff, Hugh B CareyAbstract:High anion gap metabolic Acidosis in adults is a severe metabolic disorder for which the primary organic acid usually is apparent by clinical history and standard laboratory testing. We report a case of recurrent high anion gap metabolic Acidosis in a 48-year-old man who initially presented with anorexia and malaise. Physical examination was unrevealing. Arterial pH was 6.98, Pco2 was 5 mm Hg, and chemistry tests showed a bicarbonate level of 3 mEq/L (3 mmol/L), anion gap of 32 mEq/L (32 mmol/L), and a negative toxicology screen result, except for an acetaminophen (paracetamol) level of 7.5 μg/mL. Metabolic Acidosis resolved with administration of intravenous fluids. Subsequently, he experienced 5 more episodes of high anion gap metabolic Acidosis during an 8-month span. Methanol, ethylene glycol, acetone, ethanol, d-lactate, and hippuric acid screens were negative. Lactate levels were modestly elevated, and acetaminophen levels were elevated for 5 of 6 admissions. These episodes defied explanation until 3 urinary organic acid screens, obtained on separate admissions, showed striking elevations of 5-oxoproline levels. Inborn errors of metabolism in the γ-glutamyl cycle causing recurrent 5-oxoprolinuria and high anion gap metabolic Acidosis are rare, but well described in children. Recently, there have been several reports of apparent acquired 5-oxoprolinuria and high anion gap metabolic Acidosis in adults in association with acetaminophen use. Acetaminophen may, in susceptible individuals, disrupt regulation of the γ-glutamyl cycle and result in excessive 5-oxoproline production. Suspicion for 5-oxoproline-associated high anion gap metabolic Acidosis should be entertained when the cause of high anion gap metabolic Acidosis remains poorly defined, the anion gap cannot be explained reasonably by measured organic acids, and there is concomitant acetaminophen use.
Daniel Guido Fuster - One of the best experts on this subject based on the ideXlab platform.
-
furosemide fludrocortisone test and clinical parameters to diagnose incomplete distal renal tubular Acidosis in kidney stone formers
Clinical Journal of The American Society of Nephrology, 2017Co-Authors: Nasser Dhayat, Michael W. Gradwell, Ganesh Pathare, Manuel Anderegg, Lisa Schneider, David Luethi, Cedric Mattmann, Orson W. Moe, Bruno Vogt, Daniel Guido FusterAbstract:Background and objectives Incomplete distal renal tubular Acidosis is a well known cause of calcareous nephrolithiasis but the prevalence is unknown, mostly due to lack of accepted diagnostic tests and criteria. The ammonium chloride test is considered as gold standard for the diagnosis of incomplete distal renal tubular Acidosis, but the furosemide/fludrocortisone test was recently proposed as an alternative. Because of the lack of rigorous comparative studies, the validity of the furosemide/fludrocortisone test in stone formers remains unknown. In addition, the performance of conventional, nonprovocative parameters in predicting incomplete distal renal tubular Acidosis has not been studied. Design, setting, participants, & measurements We conducted a prospective study in an unselected cohort of 170 stone formers that underwent sequential ammonium chloride and furosemide/fludrocortisone testing. Results Using the ammonium chloride test as gold standard, the prevalence of incomplete distal renal tubular Acidosis was 8%. Sensitivity and specificity of the furosemide/fludrocortisone test were 77% and 85%, respectively, yielding a positive predictive value of 30% and a negative predictive value of 98%. Testing of several nonprovocative clinical parameters in the prediction of incomplete distal renal tubular Acidosis revealed fasting morning urinary pH and plasma potassium as the most discriminative parameters. The combination of a fasting morning urinary threshold pH 3.8 mEq/L yielded a negative predictive value of 98% with a sensitivity of 85% and a specificity of 77% for the diagnosis of incomplete distal renal tubular Acidosis. Conclusions The furosemide/fludrocortisone test can be used for incomplete distal renal tubular Acidosis screening in stone formers, but an abnormal furosemide/fludrocortisone test result needs confirmation by ammonium chloride testing. Our data furthermore indicate that incomplete distal renal tubular Acidosis can reliably be excluded in stone formers by use of nonprovocative clinical parameters.
-
incomplete drta in kidney stone formers diagnostic performance of furosemide fludrocortisone testing and non provocative clinical parameters
2017Co-Authors: Nasser Dhayat, Ganesh Pathare, Manuel Anderegg, Bruno Vogt, Daniel Guido FusterAbstract:Background and objectives: Incomplete distal renal tubular Acidosis is a well-known cause of calcareous nephrolithiasis but the prevalence is unknown, mostly due to lack of accepted diagnostic tests and criteria. The ammonium chloride test is considered as gold standard for the diagnosis of incomplete distal renal tubular Acidosis, but the furosemide/fludrocortisone test was recently proposed as an alternative. Due to the lack of rigorous comparative studies, the validity of the furosemide/fludrocortisone test in stone formers remains unknown. In addition, the performance of conventional, non-provocative parameters in predicting incomplete distal renal tubular Acidosis has not been studied. Design, setting, participants, and measurements: We conducted a prospective study in an unselected cohort of 170 stone formers that underwent sequential ammonium chloride and furosemide/fludrocortisone testing. Results: Using the ammonium chloride test as gold standard, the prevalence of incomplete distal renal tubular Acidosis was 7.78 %. Sensitivity and specificity of the furosemide/fludrocortisone test FF test were 77 % and 85 %, respectively, yielding a positive predictive value of 30 % and a negative predictive value of 98 %. Testing of several non-provocative clinical parameters in the prediction of incomplete distal renal tubular Acidosis revealed fasting morning urinary pH and plasma potassium as the most discriminative parameters. The combination of a fasting morning urinary threshold pH <5.3 with a plasma potassium threshold >3.8 mmolmEq/l yielded a negative predictive value of 98 % with a sensitivity of 85 % and a specificity of 77 % for the diagnosis of incomplete distal renal tubular Acidosis. Conclusions: The furosemide/fludrocortisone test can be used for incomplete distal renal tubular Acidosis screening in stone formers, but an abnormal furosemide/fludrocortisone test result needs confirmation by ammonium chloride testing. Our data furthermore indicate that incomplete distal renal tubular Acidosis can reliably be excluded in stone formers by use of non-provocative clinical parameters.
