Uric acid stones, clinical manifestations and therapeutic considerations

Ma, Qin; Li, Fang; Su, Rui; Ma, Liang; Xie, Gary; Cheng, Yufeng

doi:10.1136/postgradmedj-2017-135332

Cited by 23 publications

(18 citation statements)

References 49 publications

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“…Stones that form in the kidney (FIG. 1) most commonly comprise calcium oxalate (65%) but can also contain calcium phosphate (10%), uric acid (15%), magnesium ammonium phosphate (10%), cystine (1%), 2,8-dihydroxyadenine (<1%), xanthine (<1%), or excreted drugs such as indinavir (<1%) [6][7][8][9][10] . The composition of kidney stones shows worldwide geographical variation and although the proportion of calcium oxalate stones has been reported to be relatively consistent between countries, magnesium ammonium phosphate stones, which are associated with infection, are more frequent in Sub-Saharan Africa than in more developed regions 11 Unsurprisingly, therefore, nephrolithiasis is often associated with metabolic abnormalities of urinary solute concentration or decreased urinary solubility; these abnormalities include hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria, cystinuria, low urinary volume and defects in urinary acidification 8,12 .…”

Section: [H1] Introductionmentioning

confidence: 99%

Genetics of kidney stone disease

2020

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Kidney stone disease (nephrolithiasis) is a common problem that can be associated with alterations in urinary solute composition including hypercalciuria. Studies suggest that the prevalence of monogenic kidney stone disorders, including renal tubular acidosis with deafness, Bartter syndrome, primary hyperoxaluria, and cystinuria, in patients attending kidney stone clinics is 15%. However, for the majority of individuals, nephrolithiasis has a multifactorial aetiology involving genetic and environmental factors. Nonetheless, the genetic influence on stone formation in these idiopathic stone formers remains considerable and twin studies estimate a heritability of >45% for nephrolithiasis and >50% for hypercalciuria. The contribution of polygenic influences from multiple loci have been investigated by genome-wide association and candidate gene studies, which indicate that a number of genes and molecular pathways contribute to the risk of stone formation. Genetic approaches, studying both monogenic and polygenic factors in nephrolithiasis, have revealed that the following have important roles in the aetiology of kidney stones: transporters and channels; ions, protons and amino acids; the calcium-sensing receptor (a G-protein-coupled receptor) signalling pathway; and the metabolic pathways for vitamin D, oxalate, cysteine, purines and uric acid. These advances, which have increased our understanding of the pathogenesis of nephrolithiasis, will hopefully facilitate the future development of targeted therapies for precision medicine approaches in patients with nephrolithiasis.

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Section: [H1] Introductionmentioning

confidence: 99%

Genetics of kidney stone disease

2020

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“…Increased levels of monosodium urate in the urine, acting as a stone core / nidus for the formation of calcium oxalate through heterogeneous nucleation or epitaxial crystal growth. The most common cause of uric acid in the urine comes from foods that contain lots of purines and from endogenous metabolism [20].…”

Section: Hyperuricosuriamentioning

confidence: 99%

Risk Factor and Pathophysiology of Nephrolithiasis: A Review Article

Gofur¹

2021

JCSR

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Introduction: Nephrolithiasis is a urinary tract stone disease that can be found in the kidneys, ureters, bladder, and urethra. This disease is the three most common diseases in the field of urology besides urinary tract infections and benign prostate enlargement. Kidney stones are the most common, with an estimated lifetime prevalence as high as 15%. Bladder stones have significant morbidity but occur much less frequently than kidney stones. Many factors cause reduced urine flow and cause obstruction, one of which is urine static and decreased urine volume due to dehydration and inadequate fluid intake, this can increase the risk of nephrolithiasis. Low urine flow is a common abnormal symptom. In addition, various conditions that trigger nephrolithiasis such as the composition of various stones are the main factors in identifying the cause of nephrolithiasis. Aims of this article is to review risk factors and pathophysiology of nephrolithiasis. Discussion: Symptoms associated with urinary tract stones depend on the location of the stone, the size of the stone, and any complications that have occurred. Usually, stones in the kidney calyx are asymptomatic. When the stone falls off and descends into the narrow ureter, it becomes symptomatic. Stones generally get stuck in the narrowest part of the ureter, such as the uretero-pelvic junction, when the ureter crosses the iliac vasa, and the uretero-vesical junction. The main symptom of ureteric stones is often an acute onset of pain in the back. This pain can be colicky or not. Colic pain occurs because the peristaltic activity of the smooth muscle of the calical system or ureter increases in an attempt to remove stones from the urinary tract. The increase in peristalsis causes the intraluminal pressure to increase so that there is stretching of the nerve terminals that provide a sensation of pain. The pain can radiate from the pelvis and to the ipsilateral groin. Other symptoms include nausea, vomiting and hematuria. Hematuria can occur macros or microscopy from urinalysis. Hematuria occurs as a result of trauma to the urinary tract mucosa caused by stones. Conclusion: Nephrolithiasis is rock-forming salt reaches a urine concentration that exceeds the equilibrium point between the dissolved component and crystallization occurs. There are several risk factors that nephrolithiasis occurs due to various causes. Therapy and lifestyle changes are interventions that can change risk factors, but there are also risk factors that cannot be changed.

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“…The history of diabetes and obesity increase the risk of stone formation. 2 Gentle et al 3 reported uric acid stone prevalence of 11% in a geriatric population.…”

Section: Prevalencementioning

confidence: 99%

Revisit percutaneous dissolution of uric acid stones: A case report with review

Sandhu¹,

Servilla²,

Kapsner³

et al. 2018

UNOAJ

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Two main risk factors for uric acid stones formation are low urinary pH and hyperuricosuria. Of these two major risk factors, acidic (low, <5.5) urinary pH is most common and it is usually caused by tubular disorders, low urinary volume, chronic diarrhea, or severe dehydration. Hyperuricuria (>800mg of urinary uric acid/24hrs) can be associated with hyperuricemia, such as in primary gout or myeloproliferative disorder, or may manifest as an isolated cause due to diet or uricosuric drugs. 7 The monogenic metabolic conditions such as Lesch-Nyhan also predisposes to uric acid nephrolithiasis. A gene ZNF365 located on chromosome 10q21-q22 linked to uric acid calculus formation is detected but its purpose is not well defined yet. 8 Recent analysis from multiple retrospective studies by Daudon et al. 9 has concluded that within frequent stones formers, uric acids stones are most common in patients who have diabetes, obesity, or metabolic syndrome. 9

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Uric acid stones, clinical manifestations and therapeutic considerations

Cited by 23 publications

References 49 publications

Genetics of kidney stone disease

Genetics of kidney stone disease

Risk Factor and Pathophysiology of Nephrolithiasis: A Review Article

Revisit percutaneous dissolution of uric acid stones: A case report with review

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