DOES RISING URINE PH INCREASE THE STONE FORMATION RATE?

2009 ◽  
Vol 181 (4S) ◽  
pp. 521-522 ◽  
Author(s):  
Marnie R Robinson ◽  
Charles D Scales ◽  
Benjamin D Lack ◽  
Michael N Ferrandino ◽  
Dorit E Zilberman ◽  
...  
Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 528
Author(s):  
Roswitha Siener ◽  
Norman Bitterlich ◽  
Hubert Birwé ◽  
Albrecht Hesse

Despite the importance of dietary management of cystinuria, data on the contribution of diet to urinary risk factors for cystine stone formation are limited. Studies on the physiological effects of diet on urinary cystine and cysteine excretion are lacking. Accordingly, 10 healthy men received three standardized diets for a period of five days each and collected daily 24 h urine. The Western-type diet (WD; 95 g/day protein) corresponded to usual dietary habits, whereas the mixed diet (MD; 65 g/day protein) and lacto-ovo-vegetarian diet (VD; 65 g/day protein) were calculated according to dietary reference intakes. With intake of the VD, urinary cystine and cysteine excretion decreased by 22 and 15%, respectively, compared to the WD, although the differences were not statistically significant. Urine pH was significantly highest on the VD. Regression analysis showed that urinary phosphate was significantly associated with cystine excretion, while urinary sulfate was a predictor of cysteine excretion. Neither urinary cystine nor cysteine excretion was affected by dietary sodium intake. A lacto-ovo-vegetarian diet is particularly suitable for the dietary treatment of cystinuria, since the additional alkali load may reduce the amount of required alkalizing agents.


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.


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

2013 ◽  
Vol 6 (2) ◽  
pp. 108-109
Author(s):  
Santosh Kumar Swain ◽  
Jayaprakash Russell Ravan ◽  
Ranjita Acharya

ABSTRACT Topiramate is a neuromodulatory drug widely used for refractory seizures, migraine and alcohol dependence. Chronic use of this medication can cause metabolic acidosis in patients secondary to inhibition of carbonic anhydrase. It impairs the normal compensatory drop in urine pH. These factors can lead to nephrolithiasis. Although it is difficult to get an exact mechanism for stone formation in other organ of the body, we report a case of topiramate-induced nephrolithiasis along with nasal stone which is rare in medical literature. How to cite this article Swain SK, Ravan JR, Acharya R. Rhinolith with Nephrolithiasis following Prolonged use of Topiramate: A Rare Incidence. Clin Rhinol An Int J 2013;6(2): 108-109.


2012 ◽  
Vol 4 (2) ◽  
pp. 58-65 ◽  
Author(s):  
Christos Paliouras ◽  
Eirini Tsampikaki ◽  
Polichronis Alivanis ◽  
Georgios Aperis

The incidence of nephrolithiasis has risen over the last twenty years and continues to rise. Although it is often referred to as a disease, recent advances in the understanding of the pathophysiology suggest that it is a systemic disorder. We conducted a PubMed based literature review on the recent advances in the pathophysiology of kidney stone formation. There is a link between diabetes, metabolic syndrome, obesity, insulin resistance and nephrolithiasis. Along with the aging population and a Western diet, these are the main reasons for the rising incidence and prevalence of nephrolithiasis. Different theories as to the pathophysiological mechanisms of lithogenesis have been proposed, including the free and fixed particle theories, and Randal's plaque hypothesis. Among the different types of kidney stones, those containing calcium are the most common, followed by those containing uric acid, struvite and cystine. Supersaturated urine, acidic urine pH and reductions in kidney stone inhibitors in the urine are the main recognized causes that contribute to the formation of all these stone-types. Nephrolithiasis is considered a systemic pathology that may lead to end-stage renal disease. Although much progress has been made, the underlying pathophysiological mechanisms of kidney stone formation are still not fully understood.


Electronics ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2180
Author(s):  
Wen-Yaw Chung ◽  
Roozbeh Falah Ramezani ◽  
Angelito A. Silverio ◽  
Vincent F. Tsai

In this paper, we present an Internet of things (IoT)-based data collection system for the risk assessment of urinary stone formation, or urolithiasis, by the measurement and storage of four parameters in urine: pH, concentrations of ionized calcium (Ca2+), uric acid and total dissolved solids. The measurements collected by the system from patients and healthy individuals grouped by age and gender will be stored in a cloud database. These will be used in the training phase of an artificial intelligence (AI) machine learning process utilizing the logistics regression model. The trained model provides a binary risk assessment, indicating if the end user is either a stone-former or not. For system validation, standard chemical solutions were used. Preliminary results indicated a sufficient measurement range, falling within the physiological range, and resolution for pH (2.0–10.0, +/−0.1), Ca2+(0.1–3.0 mmol/l, +/−0.05), uric acid (20–500 ppm, +/−1) and conductivity (1.0–40.0 mS/cm, +/−0.1), exhibiting high correlation with standard instruments. We intend to deploy this system in few hospitals in Taiwan to collect the data of patients’ urine, with analysis aided by urologist assessments for the risk of urolithiasis. The modularized design allows future modification and expansion to accommodate other sensing analytes.


Author(s):  
Jyothi Sujatha Shibulal ◽  
Chidambaram Dhandapani ◽  
Kuppurajan Narayanasamy

ABSTRACTObjective: Renal stone disease has become an important clinical condition worldwide, and it results from a combination of several factors whichare biochemical, epidemiologic, and genetic in origin. Preventive measures are very important concerning stone disease and these measures greatlydepend on the type of stones. Performing a metabolic evaluation of stone patients to identify metabolic abnormality, if any, and treating the same helpsreduce the recurrence of stones. To identify and correct the metabolic risk factors of patients presenting with either recurrent, bilateral, or multiplestones and thereby reduce the recurrence of stones.Methods: A hospital-based prospective observational study, including collection of essential data of 100 patients and analyzing them for any metabolicabnormality.Results: Out of the 100 patients, 73 were males and 27 were females. The frequency of stone formation was high in the age group 51-60, eventhough age is not a significant factor. Only 55 patients underwent metabolic evaluation, in which 23 patients (41.8%) had a metabolic abnormality.The common abnormality found in this geographical area was hyperuricosuria (29.1%) followed by hypercalciuria (7.3%). Hypercalciuria was notstatistically significant, but hyperuricosuria and acidic urine pH were significant factors that contribute to stone formation.Conclusion: Metabolic evaluation is a must for renal stone patients which greatly help reduce the risk of stone recurrence. Hyperuricemia wasobserved to be the major abnormality followed by hypercalciuria. Acidic urine pH and low urine volume were other significant risk factors.Keywords: Nephrolithiasis, Metabolic evaluation, Hyperuricosuria, Hypercalciuria.


2002 ◽  
Vol 282 (6) ◽  
pp. F1049-F1055 ◽  
Author(s):  
Surinder Cheema-Dhadli ◽  
Shih-Hua Lin ◽  
Mitchell L. Halperin

Our objective was to describe the process of alkali disposal in rats. Balance studies were performed while incremental loads of alkali were given to rats fed a low-alkali diet or their usual alkaline ash diet. Control groups received equimolar NaCl or KCl. Virtually all of the alkali was eliminated within 24 h when the dose exceeded 750 μmol. The most sensitive response to alkali input was a decline in the excretion of NH[Formula: see text]. The next level of response was to increase the excretion of unmeasured anions; this rise was quantitatively the most important process in eliminating alkali. The maximum excretion of citrate was ∼70% of its filtered load. An even higher alkali load augmented the excretion of 2-oxoglutarate to >400% of its filtered load. Only with the largest alkali load did bicarbonaturia become quantitatively important. We conclude that renal mechanisms eliminate alkali while minimizing bicarbonaturia. This provides a way of limiting changes in urine pH without sacrificing acid-base balance, a process that might lessen the risk of kidney stone formation.


2013 ◽  
Vol 2013 ◽  
pp. 1-21 ◽  
Author(s):  
Kanu Priya Aggarwal ◽  
Shifa Narula ◽  
Monica Kakkar ◽  
Chanderdeep Tandon

Urinary stone disease is an ailment that has afflicted human kind for many centuries. Nephrolithiasis is a significant clinical problem in everyday practice with a subsequent burden for the health system. Nephrolithiasis remains a chronic disease and our fundamental understanding of the pathogenesis of stones as well as their prevention and cure still remains rudimentary. Regardless of the fact that supersaturation of stone-forming salts in urine is essential, abundance of these salts by itself will not always result in stone formation. The pathogenesis of calcium oxalate stone formation is a multistep process and essentially includes nucleation, crystal growth, crystal aggregation, and crystal retention. Various substances in the body have an effect on one or more of the above stone-forming processes, thereby influencing a person’s ability to promote or prevent stone formation. Promoters facilitate the stone formation while inhibitors prevent it. Besides low urine volume and low urine pH, high calcium, sodium, oxalate and urate are also known to promote calcium oxalate stone formation. Many inorganic (citrate, magnesium) and organic substances (nephrocalcin, urinary prothrombin fragment-1, osteopontin) are known to inhibit stone formation. This review presents a comprehensive account of the mechanism of renal stone formation and the role of inhibitors/promoters in calcium oxalate crystallisation.


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