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Pediatric Nephrology (Berlin, Germany) Mar 2023The clinical manifestations of primary distal renal tubular acidosis usually begin in childhood, but the disease is caused by a genetic defect that persists throughout... (Review)
Review
The clinical manifestations of primary distal renal tubular acidosis usually begin in childhood, but the disease is caused by a genetic defect that persists throughout life. This review focuses on the complications of distal tubular acidosis that occur or remain long-term such as nephrocalcinosis and urolithiasis, growth impairment, bone mineralization, severe hypokalemia, kidney cysts, and progressive kidney failure, as well as other persistent manifestations that occur independent of acidosis but are associated with some inherited forms of the disease. The pathogenic factors responsible for kidney failure are discussed in particular because it is a complication to which different publications have recently drawn attention and which affects a high percentage of adults with primary distal renal tubular acidosis. The need to maintain optimal metabolic control of the disease and scheduled clinical follow-up throughout life and the importance of organizing protocols for the transition of patients to adult nephrology services are emphasized.
Topics: Adult; Humans; Acidosis, Renal Tubular; Hypokalemia; Acidosis; Nephrocalcinosis; Renal Insufficiency
PubMed: 35543873
DOI: 10.1007/s00467-022-05546-w -
Nutrients May 2018Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets... (Review)
Review
Recent epidemiological findings suggest that high levels of dietary acid load can affect insulin sensitivity and glucose metabolism. Consumption of high protein diets results in the over-production of metabolic acids which has been associated with the development of chronic metabolic disturbances. Mild metabolic acidosis has been shown to impair peripheral insulin action and several epidemiological findings suggest that metabolic acid load markers are associated with insulin resistance and impaired glycemic control through an interference intracellular insulin signaling pathways and translocation. In addition, higher incidence of diabetes, insulin resistance, or impaired glucose control have been found in subjects with elevated metabolic acid load markers. Hence, lowering dietary acid load may be relevant for improving glucose homeostasis and prevention of type 2 diabetes development on a long-term basis. However, limitations related to patient acid load estimation, nutritional determinants, and metabolic status considerably flaws available findings, and the lack of solid data on the background physiopathology contributes to the questionability of results. Furthermore, evidence from interventional studies is very limited and the trials carried out report no beneficial results following alkali supplementation. Available literature suggests that poor acid load control may contribute to impaired insulin sensitivity and glucose homeostasis, but it is not sufficiently supportive to fully elucidate the issue and additional well-designed studies are clearly needed.
Topics: Acid-Base Equilibrium; Acidosis; Blood Glucose; Diabetes Mellitus, Type 2; Diet; Diet, High-Protein; Homeostasis; Humans; Insulin; Insulin Resistance; Muscle, Skeletal; Randomized Controlled Trials as Topic
PubMed: 29762478
DOI: 10.3390/nu10050618 -
Molecular and Cellular Biochemistry Aug 2020Diabetic nephropathy and cardiomyopathy are two major causes of mortality among patients with diabetes mellitus (DM). Since current diabetic medications are associated...
Diabetic nephropathy and cardiomyopathy are two major causes of mortality among patients with diabetes mellitus (DM). Since current diabetic medications are associated with various side effects, the naturally occurring plant-derived compounds are in demand. Bioflavonoids originating from vegetables and medicinal plants have beneficial effects on diabetes by improving glycemic control, lipid metabolism, and anti-oxidant status. The present study is focused on the effect of rutin against alloxan induced diabetic nephropathy and cardiomyopathy. Male albino Wistar rats were divided into four groups, each of six rats. Group I control rats received 0.9% saline as a single dose intraperitoneally. Group II rats were induced diabetes with a single dose of alloxan monohydrate (150 mg/kg body weight in 0.9% saline) intraperitoneally. Group III rats received 0.28 M of NHCl in drinking water for 3 days for the experimental induction of metabolic acidosis. Group IV rats were injected with a single dose of alloxan monohydrate (150 mg/kg bodyweight) and administered rutin hydrate (100 mg/kg) for a period of 4 weeks by oral gavage. Administration of rutin prevented urinary ketone body formation and decreased serum creatinine and urea levels in alloxan induced diabetic rats. Rutin supplementation reduced the levels of serum triglycerides and cholesterol in diabetic rats. Gene expression profiling of metabolic acidosis related genes (AQP2, AQP3 and V2R) and also histopathological results demonstrated the protective effect of rutin against diabetic ketoacidodis and fibrosis. The results of the present study revealed rutin administration prevents the progression of diabetic nephropathy and cardiomyopathy through amelioration of fibrosis and metabolic acidosis.
Topics: Acidosis; Alloxan; Animals; Antioxidants; Blood Glucose; Cardiomyopathies; Diabetes Mellitus, Experimental; Diabetic Nephropathies; Fibrosis; Male; Oxidative Stress; Rats; Rats, Wistar; Rutin
PubMed: 32529498
DOI: 10.1007/s11010-020-03758-y -
Clinical Nephrology Oct 2022Continuous renal replacement therapy (CRRT) is a dialysis modality used in critically ill patients with acute kidney injury (AKI). Although most dialysate and...
Continuous renal replacement therapy (CRRT) is a dialysis modality used in critically ill patients with acute kidney injury (AKI). Although most dialysate and replacement fluids are dextrose-containing, CRRT-associated hypophosphatemia sometimes warrants the use of phosphorus-containing solutions which are dextrose free. The other less commonly used dextrose-free dialysate solutions are certain formulations of Prismasol and Prismasate. As glucose is a small molecule, which is readily cleared with dialysis, use of these solutions can result in increased caloric loss, net glucose deficit, and shifting of the metabolic pathway towards gluconeogenesis and ketogenesis. Starvation ketosis is usually a benign entity, however when combined with factors such as stress of critical illness, can produce metabolic acidosis which at times can be severe. We describe five patients who developed worsening metabolic acidosis despite adequate clearance from CRRT and were diagnosed with CRRT-associated ketoacidosis. Administration of dextrose-containing fluids or tube feeds promptly resulted in resolution of ketonemia and acidosis. Recognition of this entity is of great importance as the reflexive reaction to increase the prescribed dose of CRRT to improve the acidosis, in fact worsens the problem.
Topics: Acidosis; Acute Kidney Injury; Continuous Renal Replacement Therapy; Critical Illness; Dialysis Solutions; Glucose; Humans; Ketosis; Phosphorus; Renal Replacement Therapy
PubMed: 34142948
DOI: 10.5414/CN110460 -
Nutrients Jul 2021Metabolic acidosis is a severe complication of chronic kidney disease (CKD) which is associated with nefarious impairments such as bone demineralization, muscle wasting,... (Review)
Review
Metabolic acidosis is a severe complication of chronic kidney disease (CKD) which is associated with nefarious impairments such as bone demineralization, muscle wasting, and hormonal alterations, for example, insulin resistance. Whilst it is possible to control this condition with alkali treatment, consisting in the oral administration of sodium citrate or sodium bicarbonate, this type of intervention is not free from side effects. On the contrary, opting for the implementation of a targeted dietetic-nutritional treatment for the control of CKD metabolic acidosis also comes with a range of additional benefits such as lipid profile control, increased vitamins, and antioxidants intake. In our review, we evaluated the main dietary-nutritional regimens useful to counteract metabolic acidosis, such as the Mediterranean diet, the alkaline diet, the low-protein diet, and the vegan low-protein diet, analyzing the potentialities and limits of every dietary-nutritional treatment. Literature data suggest that the Mediterranean and alkaline diets represent a valid nutritional approach in the prevention and correction of metabolic acidosis in CKD early stages, while the low-protein diet and the vegan low-protein diet are more effective in CKD advanced stages. In conclusion, we propose that tailored nutritional approaches should represent a valid therapeutic alternative to counteract metabolic acidosis.
Topics: Acid-Base Equilibrium; Acidosis; Diet; Diet, Mediterranean; Diet, Protein-Restricted; Diet, Vegan; Humans; Nutrition Therapy; Renal Insufficiency, Chronic
PubMed: 34444694
DOI: 10.3390/nu13082534 -
PloS One 2017It is currently recognized that an optimized nutritional approach, consisting of an early and substantial supply of protein and energy by parenteral route, may be... (Observational Study)
Observational Study
BACKGROUND
It is currently recognized that an optimized nutritional approach, consisting of an early and substantial supply of protein and energy by parenteral route, may be beneficial for very low birth weight infants and recent guidelines endorse this strategy. However, the impact of the enhanced parenteral nutrition (PN) on acid-basic balance has never been investigated. The aim of the present study is to assess the effect of nutrient intake on acid-base homeostasis in a large population of preterm infants on PN.
METHODS
This observational study described the acid-base profile of very preterm infants (≤29 week's gestation) receiving PN during the first week of life. For this purpose three different cohorts of infants who received increasing (group 1 to group 3) nutritional intakes were considered. Nutrition data were recorded daily and correlated to acid-base data (pH, base excess, and lactate). The outcome measure to assess metabolic acidosis was the base excess (BE).
RESULTS
161 infants were included. 1127 daily nutritional records and 795 blood gas data were analyzed. The three groups were different with regard to nutritional intravenous intakes. Group 3 in particular had a higher mean intake of both amino acids (3.3 ± 0.8 g/kg/d) and lipids (2.8 ± 1.4 g/kg/d) during the first week of life. Metabolic acidosis was more severe in the group with the highest parenteral intake of amino acids and lipids: mean BE = -8.7 ± 3.4 (group 3); -6.4 ± 3.4 (group 2); -5.1 ± 3.0 (group 1)]. At the multivariate analysis the significant risk factors for metabolic acidosis were: gestational age, initial base excess, amino acid and lipid intravenous intakes.
DISCUSSION
Acid-base homeostasis was influenced by the nutritional intake. Earlier and higher intravenous amino acid and lipid intakes particularly increased the risk of metabolic acidosis. The nutritional tolerance was different depending on gestational age, and the smaller infants (24-26 week's gestation) displayed greater acidotic disequilibrium and a higher need of bicarbonate.
Topics: Acid-Base Equilibrium; Acidosis; Amino Acids; Gestational Age; Humans; Hydrogen-Ion Concentration; Infant, Newborn; Infant, Premature; Lipids; Multivariate Analysis; Parenteral Nutrition
PubMed: 29176758
DOI: 10.1371/journal.pone.0186936 -
Nephrology, Dialysis, Transplantation :... May 2016Chronic metabolic acidosis (CMA) is a common complication of the more advanced stages of chronic kidney diseases (CKD), and is associated with morbidity and mortality of... (Review)
Review
Chronic metabolic acidosis (CMA) is a common complication of the more advanced stages of chronic kidney diseases (CKD), and is associated with morbidity and mortality of CKD patients and possibly with the progression of renal disease. Nevertheless, there is limited evidence or information on the prevalence, the potential causal factors, the clinical impact and the effects of correction of CMA in kidney transplant recipients. In this review, we briefly look at the more relevant, though scanty, studies which have, over time, addressed the above-mentioned points, with the hope that in the future the interest of transplant nephrologists and surgeons will grow towards this unreasonably neglected issue.
Topics: Acidosis; Humans; Kidney Diseases; Kidney Transplantation
PubMed: 25934992
DOI: 10.1093/ndt/gfv098 -
Pediatric Nephrology (Berlin, Germany) Jun 2015Metabolic acidosis (MA) is relatively common in patients with chronic kidney disease (CKD) particularly in stages 4 and 5. It is assumed to play a contributory role in... (Review)
Review
Metabolic acidosis (MA) is relatively common in patients with chronic kidney disease (CKD) particularly in stages 4 and 5. It is assumed to play a contributory role in the development of several complications including bone disease, skeletal muscle wasting, altered protein synthesis, and degradation. Recent evidence also suggests that even mild acidosis might play a role in progressive glomerular filtration rate loss. Experimental and clinical studies suggest that correction of acidosis by alkali therapy attenuates these complications and improves quality of life. Despite several recent small and single-center studies supporting this notion, more robust evidence is required with regard to the long-term benefits of alkali therapy, type of alkali supplements, and the optimal level of serum bicarbonate.
Topics: Acidosis; Age Factors; Alkalies; Animals; Disease Progression; Humans; Hydrogen-Ion Concentration; Quality of Life; Renal Insufficiency, Chronic; Risk Factors; Sodium Bicarbonate; Treatment Outcome
PubMed: 25085611
DOI: 10.1007/s00467-014-2873-9 -
Best Practice & Research. Clinical... Jan 2016ST-analysis of the fetal electrocardiogram (ECG) (STAN(®)) combined with cardiotocography (CTG) for intrapartum fetal monitoring has been developed following many years... (Review)
Review
ST-analysis of the fetal electrocardiogram (ECG) (STAN(®)) combined with cardiotocography (CTG) for intrapartum fetal monitoring has been developed following many years of animal research. Changes in the ST-segment of the fetal ECG correlated with fetal hypoxia occurring during labor. In 1993 the first randomized controlled trial (RCT), comparing CTG with CTG + ST-analysis was published. STAN(®) was introduced for daily practice in 2000. To date, six RCTs have been performed, out of which five have been published. Furthermore, there are six published meta-analyses. The meta-analyses showed that CTG + ST-analysis reduced the risks of vaginal operative delivery by about 10% and fetal blood sampling by 40%. There are conflicting results regarding the effect on metabolic acidosis, much because of controveries about which RCTs should be included in a meta-analysis, and because of differences in methodology, execution and quality of the meta-analyses. Several cohort studies have been published, some showing significant decrease of metabolic acidosis after the introduction of ST-analysis. In this review, we discuss not only the scientific evidence from the RCTs and meta-analyses, but also the limitations of these studies. In conclusion, ST-analysis is effective in reducing operative vaginal deliveries and fetal blood sampling but the effect on neonatal metabolic acidosis is still under debate. Further research is needed to determine the place of ST-analysis in the labor ward for daily practice.
Topics: Acidosis; Cardiotocography; Delivery, Obstetric; Electrocardiography; Extraction, Obstetrical; Female; Fetal Blood; Fetal Hypoxia; Fetal Monitoring; Heart Rate, Fetal; Humans; Labor, Obstetric; Pregnancy
PubMed: 26206514
DOI: 10.1016/j.bpobgyn.2015.05.007 -
International Urology and Nephrology Dec 2020Chronic kidney disease is prevalent, affecting more than one in ten adults. In this population, metabolic acidosis is considered a key underlying pathophysiological... (Review)
Review
Chronic kidney disease is prevalent, affecting more than one in ten adults. In this population, metabolic acidosis is considered a key underlying pathophysiological feature, tying together bone mineral disorders, sarcopenia, insulin resistance, vascular calcification, pro-inflammatory and pro-thrombotic states. This review aims to address the paucity of literature on alkalinizing agents, a promising treatment option that has known adverse effects.
Topics: Acidosis; Antacids; Humans; Renal Insufficiency, Chronic
PubMed: 32661618
DOI: 10.1007/s11255-020-02563-2