scholarly journals Potassium Citrate is Better in Reducing Salt and Increasing Urine pH than Oral Intake of Lemonade: A Cross-Over Study

2018 ◽  
Vol 24 ◽  
pp. 1924-1929
Author(s):  
Jing Shen ◽  
Xicheng Zhang
Author(s):  
Michel Daudon ◽  
Paul Jungers

Cystinuria, an autosomal recessive disease (estimated at 1:7000 births worldwide), results from the defective reabsorption of cystine and dibasic amino acids (also ornithine, arginine, lysine, COAL) by epithelial cells of renal proximal tubules, leading to an abnormally high urinary excretion of these amino acids. Due to the poor solubility of cystine at the usual urine pH, formation of cystine crystals and stones ensues. Incidence of homozygotes is estimated at 1 in 7000 births worldwide, but is lower in European countries and much higher in populations with frequent consanguinity. Cystine stones represent 1–2% of all stones in adults and 5–8% in paediatric patients, with an equal distribution between males and females.Cystinuria is caused by inactivating mutations in the gene SLC3A1 or SLC7A9, both encoding proteins contributing to the function of the heterodimeric transport system of cystine.Cystine nephrolithiasis may present in infants, most frequently in adolescents or young adults, sometimes later. Cystine calculi are weakly radio-opaque. Stone analysis using infrared spectroscopy (or X-ray diffraction) allows immediate and accurate diagnosis. Urinary amino acid chromatography quantifies urinary cystine excretion, needed to define the therapeutic strategy.Urological treatment of cystine stones currently uses extracorporeal stone wave lithotripsy or flexible ureterorenoscopy with Holmium laser, that is, minimally invasive techniques. However, as cystine stones are highly recurrent, preventive therapy is essential.Medical treatment combines reduced methionine and sodium intake, to lower cystine excretion; hyperdiuresis (> 3 L/day) to reduce cystine concentration; and active alkalinization preferably using potassium citrate (40–80 mEq/day) to increase cystine solubility by rising urine pH up to 7.5–8. If these measures are insufficient to prevent recurrent stone formation, a thiol derivative (D-penicillamine or tiopronin), which converts cystine into a more soluble disulphide, should be added. Close monitoring and adherence of the patient to the therapeutic programme are needed to ensure life-long compliance, the key for successful prevention in the long term.


2019 ◽  
Vol 60 (1) ◽  
Author(s):  
Leonardo Santos Hoff ◽  
Claudia Goldenstein-Schainberg ◽  
Ricardo Fuller

Abstract Background The aims of this article were to assess the prevalence of nephrolithiasis and the factors associated with nephrolithiasis in Brazilian patients with primary gout. Methods One hundred twenty-three patients with primary gout were recruited from a tertiary referral hospital in São Paulo, Brazil. All patients underwent ultrasonography and had their clinical and laboratory characteristics assessed. Results One hundred fifteen (93.5%) patients were male, with a mean age of 62.9 ± 9.4 years. Twenty-three (18.7%) patients had asymptomatic nephrolithiasis (detected only by ultrasonography), 7 (6.0%) had symptomatic nephrolithiasis (detected by ultrasonography and a positive clinical history), and 13 (10.0%) had a history of kidney stones, but ultrasonography at evaluation did not show nephrolithiasis. Therefore, 35.0% of the patients had nephrolithiasis (detected either by ultrasonography and/or a positive clinical history). Nephrolithiasis was associated with male gender (43 [100%] vs 72 [90%], p = 0.049), the use of potassium citrate (13 [30.2%] vs 0, p <  0.001) and the use of medications for diabetes (10 [23.3%] vs 8 [10%], p = 0.047) and dyslipidemia (15 [34.9%] vs 10 [12.5%], p = 0.003); benzbromarone had an inverse association with nephrolithiasis (21 [48.8%] vs 55 [68.8%], p = 0.030). In patients with and without nephrolithiasis, no differences were found in the laboratory and ultrasonography characteristics, including serum uric acid levels, urinary uric acid excretion and urine pH. Conclusions The prevalence of nephrolithiasis in primary gout was 35.0%, and 18.7% of the patients were asymptomatic. Nephrolithiasis was associated with male gender, diabetes and dyslipidemia. A positive history of nephrolithiasis probably biased the prescription of potassium citrate and benzbromarone.


2018 ◽  
Author(s):  
Dustin Whitaker ◽  
Ava Saidian ◽  
Jacob Britt ◽  
Carter Boyd ◽  
Kyle Wood ◽  
...  

Uric acid is the third most common stone composition and comprises 7 to 10% of all kidney stones sent for analysis. These stones are more common with increasing age and in men. Uric acid stone disease is associated with conditions such as the metabolic syndrome and type 2 diabetes mellitus. Uric acid is produced by the enzyme, xanthine oxidase and is the final product of purine metabolism in humans. Three main factors contribute to the formation of uric acid stones: low urine pH (the most important), hyperuricosuria (rare, includes conditions such as myeloproliferative disorders and Lesch-Nyhan syndrome), and low urine volume. Uric acid stones appear radiolucent on plain radiographs and are ultimately diagnosed via stone analysis. These stones may be treated with medical expulsive therapy, dissolution therapy, or surgical intervention depending on the size, location, and clinical presentation. Urine pH manipulation therapy with potassium citrate is the first-line treatment for the prevention of uric acid stones and attempts at dissolution. Allopurinol should not be offered as the first-line therapy for uric acid stones.  This review contains 3 figures, 1 table and 38 references Key Words: ammonium, diabetes mellitus, epidemiology, management, metabolic syndrome, nephrolithiasis, pathophysiology, potassium citrate, uric acid, urine pH


Urology ◽  
2007 ◽  
Vol 69 (6) ◽  
pp. 1013-1016 ◽  
Author(s):  
Stacey G. Koff ◽  
Edmond L. Paquette ◽  
Jenny Cullen ◽  
Kevin K. Gancarczyk ◽  
Paulette R. Tucciarone ◽  
...  

2007 ◽  
Vol 98 (1) ◽  
pp. 72-77 ◽  
Author(s):  
Houda Sabboh ◽  
Véronique Coxam ◽  
Marie-Noëlle Horcajada ◽  
Christian Rémésy ◽  
Christian Demigné

Potassium (K) organic anion salts, such as potassium citrate or potassium malate in plant foods, may counteract low-grade metabolic acidosis induced by western diets, but little is known about the effect of other minor plant anions. Effects of K salts (chloride, citrate, galacturonate or tartrate) were thus studied on the mineral balance and digestive fermentations in groups of 6-week-old rats adapted to an acidogenic/5 % inulin diet. In all diet groups, substantial amounts of lactate and succinate were present in the caecum, besides SCFA. SCFA were poorly affected by K salts conditions. The KCl-supplemented diet elicited an accumulation of lactate in the caecum; whereas the lactate caecal pool was low in rats fed the potassium tartrate-supplemented (K TAR) diet. A fraction of tartrate (around 50 %) was recovered in urine of rats fed the K TAR diet. Potassium citrate and potassium galacturonate diets exerted a marked alkalinizing effect on urine pH and promoted a notable citraturia (around 0·5 μmol/24 h). All the K organic anion salts counteracted Ca and Mg hyperexcretion in urine, especially potassium tartrate as to magnesuria. The present findings indicate that K salts of unabsorbed organic anions exert alkalinizing effects when metabolizable in the large intestine, even if K and finally available anions (likely SCFA) are not simultaneously bioavailable. Whether this observation is also relevant for a fraction of SCFA arising from dietary fibre breakdown (which represents the major organic anions absorbed in the digestive tract in man) deserves further investigation.


Urolithiasis ◽  
2020 ◽  
Vol 48 (6) ◽  
pp. 501-507
Author(s):  
Arman Tsaturyan ◽  
Elizaveta Bokova ◽  
Piet Bosshard ◽  
Olivier Bonny ◽  
Daniel G. Fuster ◽  
...  

AbstractDespite the possible benefit from avoiding stone surgery with all its possible complications, oral chemolysis is rarely performed in patients with urinary stones suspected of uric acid content. Among the reasons for its limited use is the sparse and low-quality data on its efficacy and the lack of reliable factors predicting its outcome. We thus performed a retrospective single-center cohort study of 216 patients (median patient age 63 years) with 272 renal (48%) and/or ureteral (52%) stones treated with oral chemolysis from 01/2010 to 12/2019. Patients with low urine pH (< 6), low stone density upon non-contrast enhanced computed tomography (NCCT), radiolucent urinary stones on plain radiography, and/or a history of uric acid urolithiasis were included. Potassium citrate and/or sodium/magnesium bicarbonate were used for alkalization (target urine pH 6.5–7.2). Median stone size was 9 mm, median stone density 430 Hounsfield Units. Patients with ureteral stones < 6 mm were excluded since stones this small are very likely to pass spontaneously. The stone-free status of each patient was evaluated after 3 months using NCCT. Oral chemolysis was effective with a complete and partial response rate of stones at 3 months of 61% and 14%, respectively; 25% of stones could not be dissolved. Lower stone density (OR = 0.997 [CI 0.994–0.999]; p = 0.008) and smaller stone size (OR = 0.959 [CI 0.924–0.995]; p = 0.025) significantly increased the success rate of oral chemolysis in multivariate logistic regression analysis. More precise stone diagnostics to exclude non-uric-acid stones could further improve outcome.


2007 ◽  
Vol 177 (4S) ◽  
pp. 450-450
Author(s):  
Mamie R. Robinson ◽  
Victor A. Leitao ◽  
Charles D. Scales ◽  
George E. Haleblian ◽  
Aravind Chandrashekar ◽  
...  
Keyword(s):  

2000 ◽  
Vol 61 (4) ◽  
pp. 430-435 ◽  
Author(s):  
Abigail E. Stevenson ◽  
David J. Wrigglesworth ◽  
Brigitte H. E. Smith ◽  
Peter J. Markwell

Author(s):  
Michel Daudon ◽  
Paul Jungers

Uric acid (UA) stones are typically red-orange and often appear as sand/ gravel though they may be large. They are totally radiolucent. They account for about 10% of all kidney stones in most countries, and up to 20% in some populations. It is twice as frequent in males, prevalence increases with age, and it is two to three times higher in patients with type 2 diabetes or with features of the metabolic syndrome. Factors that induce the formation of UA stones are a low urine volume, hyperuricosuria, and, more importantly, a permanently low urine pH (< 5). Indeed, below its pKa of 5.35 at 37°C, UA is in non-dissociated form, whose solubility is at best 100 mg/L, whereas urinary UA excretion normally exceeds 600 mg/day and may exceed 1g/day.Because UA solubility increases up to approximately 500 mg/L at urine pH > 6, urine alkalinization, with a target pH of 6.5–7, is the cornerstone of medical treatment. This most often allows dissolution of existing stones and prevention of recurrent stone formation so that urological intervention is infrequently needed. The preferred agent for alkalinization is potassium citrate (30–60 mEq/day in divided doses), because potassium urate is twice more soluble than sodium urate. However, in patients with poor gastric tolerance to potassium citrate or contraindication to potassium supplements, sodium bicarbonate is an acceptable alternative. Limitation of animal proteins, purine-rich foods (including beer), alcoholic drinks and acidified beverages (sodas) are useful measures, together with large fluid intake (> 2–2.5 L/day). Allopurinol may be indicated in cases of symptomatic hyperuricaemia. Regular observance of alkalinisation, with periodic controls of urine pH by the patient, is needed to prevent the rapid formation of UA stones. Patients affected by UANL, especially if overweight, should be evaluated for type 2 diabetes or glucose intolerance and managed accordingly.


1984 ◽  
Vol 51 (03) ◽  
pp. 358-361 ◽  
Author(s):  
H Bechtold ◽  
K Andrassy ◽  
E Jähnchen ◽  
J Koderisch ◽  
H Koderisch ◽  
...  

SummaryIn 8 patients on no oral intake and with parenteral alimentation, administration of cephalosporins with N-methyl-thiotetrazole side chain (moxalactam, cefamandole), was associated with prolongation of prothrombin time, appearance in the circulation of descarboxy-prothrombin (counter immunoelectrophoresis and echis carinatus assay) and diminution of protein C. Acute administration of 10 mg vitamin Ki was followed by the transient appearance of vitamin K1 2,3-epoxide, indicating an impaired hepatocellular regeneration of vitamin K1 from the epoxide. Impaired hepatic vitamin K1 metabolism, tentatively ascribed to the N-methyl-thiotetrazole group, is one (but possibly not the only) cause of bleeding complications and depression of vitamin K1dependent procoagulants in patients treated with the new class of cephalosporins.


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