China
Africa
Explore chapters and articles related to this topic
Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
If stone-forming substances in the urine, such as calcium phosphate, reach high enough concentrations to exceed their solubility, they come out of solution to form stones. Urinary stasis, infection and indwelling catheters all promote stone formation. Citrate, which is present in urine, inhibits stone formation by forming a soluble complex with calcium. Nephrocalcinosis describes diffuse renal calcium deposition, mainly in the medulla, and causes include hyperparathyroidism, distal renal tubular acidosis and medullary sponge kidney.
Urolithiasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Renal tubular acidosis (RTA):Defective distal renal secretion of H+ (Type 1); orDefective proximal HCO3− reabsorption (Type 2).This results in metabolic acidosis, hyperchloraemia, impaired urinary acidification, and urolithiasis.Distal RTA − defect of the apical H+/K+-ATPases of α-intercalated cells:Inability to secrete H+ → serum acidosisAcidic urinary pH does not fall below 5.3.Acidic urine favours CaP precipitation.Increased proximal reabsorption of citrate → lowers urinary citrate → reduces inhibition of urolithiasis
Biochemistry of Buffering Capacity and Ingestion of Buffers In Exercise and Athletic Performance
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Bryan Saunders, Guilherme G. Artioli, Eimear Dolan, Rebecca L. Jones, Joseph Matthews, Craig Sale
There is a perceived lower risk of GI discomfort compared to sodium bicarbonate (91, 95), although side effects still occur with sodium citrate. The most common symptoms include stomach cramps, bloating, nausea, vomiting, urge to defecate, diarrhoea, thirst, and headache (84, 109, 110); essentially the same side effects as sodium bicarbonate. Early studies reported no side effects from sodium citrate doses ranging from 0.1 to 0.5 g·kg−1BM (62, 74, 89), although these investigations failed to adequately record the incidence and severity of side effects, meaning that mild symptoms went unnoticed. Later studies reported side effects with doses of 0.5 g·kg−1BM (83, 84, 110), but GI distress was not experienced by volunteers in all studies (125). Symptom prevalence and severity increase in a dose-dependent manner for intakes of 0.5, 0.7, and 0.9 g·kg−1BM (124). Key moderators of these effects appear to be the volume of fluid supplied with the supplement and the time permitted to consume the fluid; concentrated solutions with a higher osmolality are more likely to result in GI distress (65). Higher doses potentiate these symptoms (124), and lower or staggered doses may reduce symptom prevalence and/or severity (74). Side effects may also have an ergolytic effect on exercise, particularly if sodium citrate is ingested 60–90 minutes pre-exercise, which means that individuals would perform exercise at the moment of the highest risk of GI distress and without reaching peak blood alkalosis (124).
Clinical profile of a Polish cohort of children and young adults with cystinuria
Published in Renal Failure, 2021
Marcin Tkaczyk, Katarzyna Gadomska-Prokop, Iga Załuska-Leśniewska, Kinga Musiał, Jan Zawadzki, Katarzyna Jobs, Tadeusz Porowski, Anna Rogowska-Kalisz, Anna Jander, Merit Kirolos, Adam Haliński, Aleksandra Krzemień, Aleksandra Sobieszczańska-Droździel, Katarzyna Zachwieja, Bodo B. Beck, Przemysław Sikora, Marcin Zaniew
Data on treatment were available for 28 patients (Table 1). The majority (89%) had their fluid intake increased after a clinical diagnosis was made, which is recommended as a standard prevention for stone formation in cystinuria. In 3 patients (10.7%), no dietary restrictions (i.e., a low salt diet and reduced protein intake) were advised. Among pharmacological treatments, potassium citrate was the most commonly prescribed (in 24 patients; 85.7%). Captopril and tiopronin were given to 10 (35.7%) and 4 (14.3%) patients, respectively. Standard initial potassium citrate dosage was 0.5 mEq/kg/day. Parents were instructed to adjust dosage to maintain a high urine pH of 7.7–8.0 at a final dose of 1–1.1 mEq/kg/day. Captoprilum was given at a dosage of 0.5–1.0 mg/kg/day. Triopronin was administered with an initial dose of 15 mg/kg/day dose and finally ranged 300–900 mg (5–30 mg/kg/day).
Effect of endothelial dysfunction on the pathogenesis of urolithiasis in patients with metabolic syndrome
Published in The Aging Male, 2020
Ozgur Yazici, Fehmi Narter, Akif Erbin, Kadriye Aydin, Alper Kafkasli, Kemal Sarica
The pathophysiological mechanisms of urolithiasis are highly complex in patients with MetS and involve both metabolic and environmental factors Although some of these factors have a well-defined role in the etiological pathway, no single pathophysiological theory can properly explain the coexistence of urolithiasis and MetS [28]. Moreover, the causative mechanisms for most patients with urolithiasis are poorly understood, although a number of hypotheses such as the insulin resistance hypothesis and Randall’s Plaque Hypothesis have been proposed. Insulin resistance decreases the production and transport of ammonia, resulting in changes in urine acidification and decreased urine pH [30]. Cupisti et al. found an association between HOMA-IR index and decreased citrate excretion in calcium stone formers [31]. Citrate in urine interacts with calcium particles to form soluble compounds and thus prevent calcium crystal growth in urine. An endoscopic and histological study showed that the majority of calcium oxalate stones (75%) were formed attached to sites of Randall’s plaque in idiopathic calcium oxalate stone formers [32]. These small calcium-containing deposits lie beneath the surface of the collecting system and may act as a “seed”, which leads to the later development of a kidney stone. In addition to calcium oxalate stones, MetS patients are also predisposed to formation of uric acid stones. Increased uric acid excretion is commonly related to insulin resistance, which is closely associated with obesity.
BCG-induced trained immunity in macrophage: reprograming of glucose metabolism
Published in International Reviews of Immunology, 2020
Yuntong Liu, Shu Liang, Ru Ding, Yuyang Hou, Feier Deng, Xiaohui Ma, Tiantian Song, Dongmei Yan
Pyruvate is converted to acetyl-CoA in mitochondria by PDH, then condenses with oxaloacetic acid and enter into TCA cycle to produce citrate. In addition, cells utilize acetyl-CoA, rather than pyruvate, to generate NAD+ in order to inhibit OXPHOS and promote aerobic glycolysis.76 Glutamine metabolism provides the source for LPS-induced increase in succinate generation, via anaplerosis proceeding through α-ketoglutarate (α-KG), as well as via the γ-aminobutyric acid (GABA) shunt.47 Citrate has been shown to be an inflammatory signal, leading to the production of three key pro-inflammatory mediators: NO, ROS and prostaglandins (PGs). Citrate is transported to the cytoplasm and exchange with malate through citrate carrier (CIC). In the cytoplasm, citrate acts as a key regulator of energy metabolism, inhibiting glycolysis and TCA cycle while promoting lipid synthesis and glycosynthesis. It produces oxaloacetic acid and acetyl-CoA. Acetyl-CoA is used for the biosynthesis of fatty acids, and oxanoacetic acid can produce NADPH by generating malate and pyruvate.84 It is known that NADPH participates in NO and ROS production. Studies have shown that long-term activated monocytes in the absence of glucose can enhance their transport activity by acetylating CIC, promoting citrate efflux and maintaining NADPH, which is inadequate supplied by PPP. This process is accompanied by the depletion of malate and the conversion of citrate into glutamate,85 so whether this process can explain the accumulation of glutamate and malate induced by BCG remains to be further studied.