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Actas Urologicas Espanolas May 2023Urine contact with the mucosa of the urinary diversion (UD) after radical cystectomy (RC) produces different ion exchanges that favor the development of metabolic... (Review)
Review
Urine contact with the mucosa of the urinary diversion (UD) after radical cystectomy (RC) produces different ion exchanges that favor the development of metabolic acidosis (MA). This phenomenon is a frequent cause of hospital readmission and short/long-term complications. We performed a systematic review of MA in RCs with ileal UD, analyzing its prevalence, diagnosis, risk factors and treatment. We systematically searched Pubmed® and Cochrane Library for original articles published before May 2022 according to PRISMA guidelines. A total of 421 articles were identified. We selected 25 studies that met the inclusion criteria involving 5811 patients. Obtaining precise data on the prevalence of MA is difficult, largely due to the heterogeneity of the diagnostic criteria used given the diversity of studies analyzed. Development of MA is multifactorial. In the early period, MA is more prevalent in patients with UD with longer ileal segments, better urinary continence, and impaired renal function. Age and diabetes are risk factors associated with MA in later periods. MA is the most common cause of second or more hospital readmissions. Prophylaxis with oral bicarbonate for three months in patients at risk could improve these results. Although MA after ileal UD is a well-known condition, this review highlights the need to implement homogeneous criteria for the diagnosis, follow-up, and treatment, in addition to protocolizing prevention/prophylaxis strategies in patients at risk.
Topics: Humans; Cystectomy; Urinary Bladder Neoplasms; Urinary Bladder; Urinary Diversion; Acidosis
PubMed: 36427800
DOI: 10.1016/j.acuroe.2022.11.005 -
Critical Care (London, England) Feb 2021Metabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic... (Observational Study)
Observational Study
BACKGROUND
Metabolic acidosis is a major complication of critical illness. However, its current epidemiology and its treatment with sodium bicarbonate given to correct metabolic acidosis in the ICU are poorly understood.
METHOD
This was an international retrospective observational study in 18 ICUs in Australia, Japan, and Taiwan. Adult patients were consecutively screened, and those with early metabolic acidosis (pH < 7.3 and a Base Excess < -4 mEq/L, within 24-h of ICU admission) were included. Screening continued until 10 patients who received and 10 patients who did not receive sodium bicarbonate in the first 24 h (early bicarbonate therapy) were included at each site. The primary outcome was ICU mortality, and the association between sodium bicarbonate and the clinical outcomes were assessed using regression analysis with generalized linear mixed model.
RESULTS
We screened 9437 patients. Of these, 1292 had early metabolic acidosis (14.0%). Early sodium bicarbonate was given to 18.0% (233/1292) of these patients. Dosing, physiological, and clinical outcome data were assessed in 360 patients. The median dose of sodium bicarbonate in the first 24 h was 110 mmol, which was not correlated with bodyweight or the severity of metabolic acidosis. Patients who received early sodium bicarbonate had higher APACHE III scores, lower pH, lower base excess, lower PaCO, and a higher lactate and received higher doses of vasopressors. After adjusting for confounders, the early administration of sodium bicarbonate was associated with an adjusted odds ratio (aOR) of 0.85 (95% CI, 0.44 to 1.62) for ICU mortality. In patients with vasopressor dependency, early sodium bicarbonate was associated with higher mean arterial pressure at 6 h and an aOR of 0.52 (95% CI, 0.22 to 1.19) for ICU mortality.
CONCLUSIONS
Early metabolic acidosis is common in critically ill patients. Early sodium bicarbonate is administered by clinicians to more severely ill patients but without correction for weight or acidosis severity. Bicarbonate therapy in acidotic vasopressor-dependent patients may be beneficial and warrants further investigation.
Topics: APACHE; Acidosis; Aged; Australia; Female; Humans; Incidence; Intensive Care Units; Internationality; Japan; Male; Middle Aged; Retrospective Studies; Sodium Bicarbonate; Taiwan
PubMed: 33531020
DOI: 10.1186/s13054-020-03431-2 -
American Journal of Nephrology 2022In metabolic acidosis, a negative calcium balance is induced by decreased renal tubular calcium reabsorption. This occurs independently of the action of parathyroid... (Review)
Review
BACKGROUND
In metabolic acidosis, a negative calcium balance is induced by decreased renal tubular calcium reabsorption. This occurs independently of the action of parathyroid hormone or vitamin D and was attributed to a direct action of metabolic acidosis on the renal tubular cells. The latter has been verified by recent studies on the molecular levels in the kidney.
SUMMARY
Whereas the regulatory role of urinary calcium excretion was traditionally assigned to the transcellular calcium transport in the distal convoluted tubule (DCT) and connecting tubule (CNT), most of the calcium reabsorption from the glomerular filtrate paracellularly occurs through the tight junctions in the proximal tubule (PT) and the thick ascending limb (TAL) of Henle's loop. Interestingly, all these nephron segments participate in producing hypercalciuria caused by metabolic acidosis. Claudin-2 is the major route of paracellular calcium transport in the PT and was downregulated in rats with 5 days' NH4Cl loading. In the TAL, the lumen-positive voltage produced by apical K+ recycling drives paracellular reabsorption of Ca2+ and Mg2+ via the claudin-16/19 complex. Activation of calcium-sensing receptor (CaSR) by extracellular calcium upregulates claudin-14, which in turn interacts with the claudin-16/19 complex and inhibits its cation permeability. This TAL CaSR-claudins axis was activated by chronic NH4Cl loading in rats. Finally, the major transcellular calcium transporters TRPV5 and 28K calcium-binding protein in the DCT-CNT were also downregulated by NH4Cl or acetazolamide administration in mice.
KEY MESSAGES
Both paracellular and transcellular calcium transport pathways in the kidney are regulated by metabolic acidosis and lead to renal calcium wasting. In the PT, claudin-2 is downregulated by acidic pH. In the TAL of Henle's loop, CaSR is stimulated by the ionized calcium released from bone and upregulates claudin-14, which in turn inhibits the claudin-16/19 complex and leads to calcium and magnesium wasting. Finally, the transcellular calcium transporters, TRPV5 and calbindin-D28K, are downregulated by metabolic acidosis in the DCT and CNT.
Topics: Mice; Rats; Animals; Calcium; Hypercalciuria; Claudin-2; Claudins; Kidney; Acidosis
PubMed: 36450225
DOI: 10.1159/000528089 -
Pflugers Archiv : European Journal of... Aug 2022Kidneys are central in the regulation of multiple physiological functions, such as removal of metabolic wastes and toxins, maintenance of electrolyte and fluid balance,... (Review)
Review
Kidneys are central in the regulation of multiple physiological functions, such as removal of metabolic wastes and toxins, maintenance of electrolyte and fluid balance, and control of pH homeostasis. In addition, kidneys participate in systemic gluconeogenesis and in the production or activation of hormones. Acid-base conditions influence all these functions concomitantly. Healthy kidneys properly coordinate a series of physiological responses in the face of acute and chronic acid-base disorders. However, injured kidneys have a reduced capacity to adapt to such challenges. Chronic kidney disease patients are an example of individuals typically exposed to chronic and progressive metabolic acidosis. Their organisms undergo a series of alterations that brake large detrimental changes in the homeostasis of several parameters, but these alterations may also operate as further drivers of kidney damage. Acid-base disorders lead not only to changes in mechanisms involved in acid-base balance maintenance, but they also affect multiple other mechanisms tightly wired to it. In this review article, we explore the basic renal activities involved in the maintenance of acid-base balance and show how they are interconnected to cell energy metabolism and other important intracellular activities. These intertwined relationships have been investigated for more than a century, but a modern conceptual organization of these events is lacking. We propose that pH homeostasis indissociably interacts with central pathways that drive progression of chronic kidney disease, such as inflammation and metabolism, independent of etiology.
Topics: Acid-Base Equilibrium; Acidosis; Homeostasis; Humans; Kidney; Renal Insufficiency, Chronic
PubMed: 35513635
DOI: 10.1007/s00424-022-02696-6 -
Praxis Sep 2020Lactic Acidosis and Other Misunderstandings Lactic acidosis is a frequently encountered clinical problem in intensive care medicine. Nevertheless, many of the...
Lactic Acidosis and Other Misunderstandings Lactic acidosis is a frequently encountered clinical problem in intensive care medicine. Nevertheless, many of the underlying biochemical processes are insufficiently understood, which leads to various misconceptions. Physiologically, lactate is an important, continuously produced carrier of energy and by no means a metabolic 'waste product'. Lactate is the corresponding base to lactic acid and is produced directly from pyruvate. In this reaction H is consumed and therefore lactate production itself cannot be directly responsible for the simultaneously arising acidosis. An elevated lactate level allows no conclusions about the underlying pathophysiological process, and, more importantly, it is not an appropriate marker for tissue oxygenation.
Topics: Acidosis; Acidosis, Lactic; Biomarkers; Critical Care; Humans; Lactic Acid
PubMed: 32933388
DOI: 10.1024/1661-8157/a003508 -
Giornale Italiano Di Nefrologia :... Dec 2022In patients on hemodialysis, the reduced alkali urinary loss makes metabolic acidosis less severe. Unexpected is the large occurrence of respiratory alkalosis and... (Review)
Review
In patients on hemodialysis, the reduced alkali urinary loss makes metabolic acidosis less severe. Unexpected is the large occurrence of respiratory alkalosis and acidosis. During the therapy, the convective/diffusive inward fluxes of CO2 and bicarbonate and the loss of organic anions affect acid-base homeostasis. In bicarbonate-dialysis, the neutralization of acids by bicarbonate and gain of gaseous CO from the dialysate cause an increase of CO2 content in the body water, which requires an increase in lung ventilation (>10%) to prevent hypercapnia. In on-line hemodiafiltration, the infusate drags additional CO2 into bloodstream, while in acetate - free biofiltration the dialysate is CO2 - free and this prevents any addition of CO2. Bicarbonate and acetate diffuse into extracellular fluid according to their bath-to-blood concentration gradients. The initially large bicarbonate flux decreases rapidly because of the rapid increase in blood concentration. The smallest acetate flux is instead constant with time providing a constant source of alkali. Rapid alkalinization elicits H+ mobilization that consumes most of the bicarbonate added. Some H+ are originated by back-titration of body buffers, but others are originated by new organic acid production, a maladaptive event that wastes metabolic energy. In addition, organic anions diffuse into dialysate causing a substantial increase in net acid production. A novel dialysis protocol prescribes a low initial bath bicarbonate concentration and a stepwise increase during the therapy. Such a staircase protocol ensures a smoother increase of blood bicarbonate concentration avoiding the initial rapid growth and reducing the rate of organic acid production, thus making the treatment more effective.
Topics: Humans; Renal Dialysis; Acid-Base Equilibrium; Bicarbonates; Carbon Dioxide; Acidosis; Dialysis Solutions; Acetates; Alkalies
PubMed: 36655830
DOI: No ID Found -
Revista Medica de Chile Sep 2022Severe metabolic acidosis is defined by a pH < 7.2 with HCO3- < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces... (Review)
Review
Severe metabolic acidosis is defined by a pH < 7.2 with HCO3- < 8 mE- q/L in plasma. Its best treatment is to correct the underlying cause. However, acidemia produces multiple complications such as resistance to the action of catecholamines, pulmonary vasoconstriction, impaired cardiovascular function, hyperkalemia, immunological dysregulation, respiratory muscle fatigue, neurological impairment, cellular dysfunction, and finally, it contributes to multisystemic failure. Intravenous NaHCO3 buffers severe acidemia, preventing the associated damage and gains time while the causal disease is corrected. Its indication requires a risk-benefit assessment, considering its complications. These are hypernatremia, hypokalemia, ionic hypocalcemia, rebound alkalosis, and intracellular acidosis. For this reason, therapy must be "adapted" and administered judiciously. The patient will require monitoring with serial evaluation of the internal environment, especially arterial blood gases, plasma electrolytes, and ionized calcium. Isotonic solutions should be preferred instead of hypertonic bicarbonate. The development of hypernatremia must be prevented, calcium must be provided for hypocalcemia to improve cardiovascular function. Furthermore, in mechanically ventilated patients, a respiratory response similar to the one that would develop physiologically, must be established to be able to extract excess CO2 and thus avoid intracellular acidosis. It is possible to estimate the bicarbonate deficit, speed, and volume of its infusion. However, the calculations are only for reference. More important is to start intravenous NaHCO3 when needed, administer it judiciously, manage its side effects, and continue it to a safe goal. In this review we address all the necessary elements to consider in the administration of intravenous NaHCO3, highlighting why it is the best buffer for the management of severe metabolic acidosis.
Topics: Humans; Acidosis; Sodium Bicarbonate; Administration, Intravenous; Risk Assessment; Severity of Illness Index
PubMed: 37358132
DOI: 10.4067/S0034-98872022000901214 -
Open Heart Sep 2021
Topics: Acidosis; Female; Humans; Insulin Resistance; Male; Metabolic Syndrome; Middle Aged
PubMed: 34497064
DOI: 10.1136/openhrt-2021-001788 -
Journal of Molecular Histology Dec 2020The kidney controls body fluids, electrolyte and acid-base balance. Previously, we demonstrated that hyperpolarization-activated and cyclic nucleotide-gated (HCN) cation...
The kidney controls body fluids, electrolyte and acid-base balance. Previously, we demonstrated that hyperpolarization-activated and cyclic nucleotide-gated (HCN) cation channels participate in ammonium excretion in the rat kidney. Since acid-base balance is closely linked to potassium metabolism, in the present work we aim to determine the effect of chronic metabolic acidosis (CMA) and hyperkalemia (HK) on protein abundance and localization of HCN3 in the rat kidney. CMA increased HCN3 protein level only in the outer medulla (2.74 ± 0.31) according to immunoblot analysis. However, immunofluorescence assays showed that HCN3 augmented in cortical proximal tubules (1.45 ± 0.11) and medullary thick ascending limb of Henle's loop (4.48 ± 0.45) from the inner stripe of outer medulla. HCN3 was detected in brush border membranes (BBM) and mitochondria of the proximal tubule by immunogold electron and confocal microscopy in control conditions. Acidosis did not alter HCN3 levels in BBM and mitochondria but augmented them in lysosomes. HCN3 was also immuno-detected in mitoautophagosomes. In the distal nephron, HCN3 was expressed in principal and intercalated cells from cortical to medullary collecting ducts. CMA did not change HCN3 abundance in these nephron segments. In contrast, HK doubled HCN3 level in cortical collecting ducts and favored its basolateral localization in principal cells from the inner medullary collecting ducts. These findings further support HCN channels contribution to renal acid-base and potassium balance.
Topics: Acidosis; Animals; Biomarkers; Chronic Disease; Epithelial Cells; Fluorescent Antibody Technique; Gene Expression; Hyperkalemia; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels; Kidney Tubules, Proximal; Loop of Henle; Nephrons; Potassium Channels; Rats
PubMed: 33070272
DOI: 10.1007/s10735-020-09916-2 -
Journal of Ayub Medical College,... 2020Blood gases can provide information about the perinatal, natal and postnatal condition of newborn. Severity of metabolic acidosis has deleterious effect on the outcome...
BACKGROUND
Blood gases can provide information about the perinatal, natal and postnatal condition of newborn. Severity of metabolic acidosis has deleterious effect on the outcome of babies. When the cord blood gases are not available the arterial blood gases are used for interpreting the status of newborn. The purpose of study was to determine the relationship between severity of metabolic acidosis at admission with the stage of hypoxic ischemic encephalopathy, and its outcome in asphyxiated neonates.
METHODS
This was descriptive cross-sectional study of 384 neonates born at ≥35 weeks to <42 weeks from June to December 2018, admitted in Neonatology department of the Children's hospital & the Institute of Child Health, Lahore within first 6 hours of birth. The neonates with history of delayed cry at birth and arterial pH ≤7.30 and base deficit ≥10 were included in the study. The pH and base deficit of babies was analyzed in relation to the stage of HIE, duration of stay and death or discharge of the babies using SPSS-20. The p-value was calculated using chi-square test.
RESULTS
Total of 470 neonates were eligible. Eighty-four neonates were excluded. Finally, 384 neonates were included and analyzed for the outcome variables. With severe metabolic acidosis pH <7.01, all the babies developed HIEII/III. Majority (82.1%) of the babies expired and 27.9% had prolonged hospital stay.
CONCLUSIONS
Increasing severity of metabolic acidosis at admission increases the likelihood of adverse outcome in asphyxiated neonates.
Topics: Acidosis; Asphyxia Neonatorum; Cross-Sectional Studies; Humans; Infant, Newborn; Patient Admission; Treatment Outcome
PubMed: 32583992
DOI: No ID Found