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Idiopathic calcium oxalate (CaOx) stones often develop attached to Randall’s plaque present on kidney papillary surfaces. Similar to the plaques formed during vascular calcification, Randall’s plaques consist of calcium phosphate crystals mixed with an organic matrix that is rich in proteins, such as inter-α-trypsin inhibitor, as well as lipids, and includes membrane-bound vesicles or exosomes, collagen fibres and other components of the extracellular matrix. Kidney tissue surrounding Randall’s plaques is associated with the presence of classically activated, pro-inflammatory macrophages (also termed M1) and downregulation of alternatively activated, anti-inflammatory macrophages (also termed M2). In animal models, crystal deposition in the kidneys has been associated with the production of reactive oxygen species, inflammasome activation and increased expression of molecules implicated in the inflammatory cascade, including osteopontin, matrix Gla protein and fetuin A (also known as α2-HS-glycoprotein). Many of these molecules, including osteopontin and matrix Gla protein, are well known inhibitors of vascular calcification. We propose that conditions of urine supersaturation promote kidney damage by inducing the production of reactive oxygen species and oxidative stress, and that the ensuing inflammatory immune response promotes Randall’s plaque initiation and calcium stone formation.Calcium oxalate kidney stones are often found attached to Randall’s plaques in the kidney papilla. Here, the authors examine the mechanisms underlying the formation of Randall’s plaques, including the role of mineralization modulators, as well as inflammation and immune cells.

The incidence and prevalence of kidney stones have increased over the past four decades. However, the diagnosis of ‘kidney stone’ can range from an incidental asymptomatic finding of limited clinical significance to multiple painful episodes of ureteral obstruction with eventual kidney failure. Some general strategies may be useful to prevent the recurrence of kidney stones. In particular, greater attention to kidney stone classification, approaches to assessing the risk of recurrence and individualized prevention strategies may improve the clinical care of stone formers. Although there have been some advances in approaches to predicting the recurrence of kidney stones, notable challenges remain. Studies of kidney stone prevalence, incidence and recurrence have reported inconsistent findings, in part because of the lack of a standardized stone classification system. A kidney stone classification system based on practical and clinically useful measures of stone disease may help to improve both the study and clinical care of stone formers. Any future kidney stone classification system should be aimed at distinguishing asymptomatic from symptomatic stones, clinically diagnosed symptomatic stone episodes from self-reported symptomatic stone episodes, symptomatic stone episodes that are confirmed from those that are suspected, symptomatic recurrence from radiographic recurrence (that is, with radiographic evidence of a new stone, stone growth or stone disappearance from presumed passage) and determine stone composition based on mutually exclusive categories.Available data suggest that the prevalence and incidence of kidney stones is increasing; however, much of this variation might result from differences in approaches used to identify stone formers. This Review describes the need for a classification system to facilitate use of consistent terminology and enable meaningful comparisons of the burden of kidney stone disease across different populations.

The prevalence of kidney stone disease is increasing worldwide. The recurrence rate of urinary stones is estimated to be up to 50%. Nephrolithiasis is associated with increased risk of chronic and end stage kidney disease. Diet composition is considered to play a crucial role in urinary stone formation. There is strong evidence that an inadequate fluid intake is the major dietary risk factor for urolithiasis. While the benefit of high fluid intake has been confirmed, the effect of different beverages, such as tap water, mineral water, fruit juices, soft drinks, tea and coffee, are debated. Other nutritional factors, including dietary protein, carbohydrates, oxalate, calcium and sodium chloride can also modulate the urinary risk profile and contribute to the risk of kidney stone formation. The assessment of nutritional risk factors is an essential component in the specific dietary therapy of kidney stone patients. An appropriate dietary intervention can contribute to the effective prevention of recurrent stones and reduce the burden of invasive surgical procedures for the treatment of urinary stone disease. This narrative review has intended to provide a comprehensive and updated overview on the role of nutrition and diet in kidney stone disease.

Kidney stones are one of the oldest known and common diseases in the urinary tract system. Various human studies have suggested that diets with a higher intake of vegetables and fruits play a role in the prevention of kidney stones. In this review, we have provided an overview of these dietary plants, their main chemical constituents, and their possible mechanisms of action. Camellia sinensis (green tea), Rubus idaeus (raspberry), Rubia cordifolia (common madder), Petroselinum crispum (parsley), Punica granatum (pomegranate), Pistacia lentiscus (mastic), Solanum xanthocarpum (yellow-fruit nightshade), Urtica dioica (stinging nettle), Dolichos biflorus (horse gram), Ammi visnaga (khella), Nigella sativa (black-cumin), Hibiscus sabdariffa (roselle), and Origanum vulgare (oregano) have received considerable interest based on scientific evidence. Beside these dietary plants, phytochemicals—such as catechin, epicatechin, epigallocatechin-3-gallate, diosmin, rutin, quercetin, hyperoside, and curcumin—as antioxidant dietary phyto-phenols were found to be effective for the prevention of urolithiasis (the process of stone formation in the urinary tract). The main underlying mechanisms of these dietary plants and their isolated phytonutrients in the management of urolithiasis include diuretic, antispasmodic, and antioxidant activity, as well as an inhibitory effect on crystallization, nucleation, and aggregation of crystals. The results as presented in this review demonstrate the promising role of dietary plants and phytophenols in the prevention and management of kidney stones. Further investigations are required to confirm the safety and efficacy of these compounds.

Nephrolithiasis is a common medical condition influenced by multiple environmental factors, including diet. Since nutritional habits play a relevant role in the genesis and recurrence of kidney stones disease, dietary manipulation has become a fundamental tool for the medical management of nephrolithiasis. Dietary advice aims to reduce the majority of lithogenic risk factors, reducing the supersaturation of urine, mainly for calcium oxalate, calcium phosphate, and uric acid. For this purpose, current guidelines recommend increasing fluid intake, maintaining a balanced calcium intake, reducing dietary intake of sodium and animal proteins, and increasing intake of fruits and fibers. In this review, we analyzed the effects of each dietary factor on nephrolithiasis incidence and recurrence rate. Available scientific evidence agrees on the harmful effects of high meat/animal protein intake and low calcium diets, whereas high content of fruits and vegetables associated with a balanced intake of low-fat dairy products carries the lowest risk for incident kidney stones. Furthermore, a balanced vegetarian diet with dairy products seems to be the most protective diet for kidney stone patients. Since no study prospectively examined the effects of vegan diets on nephrolithiasis risk factors, more scientific work should be made to define the best diet for different kidney stone phenotypes.

Key Points Idiopathic calcium stones are always accompanied by mineral deposits: interstitial deposits of apatite in patients with calcium oxalate (CaOx) stones or calcium phosphate (CaP) plugs in those with CaP stones Overgrowth of CaOx stones on plaque depends on the formation of an initial CaP phase; urine saturations of CaP and CaOx might, therefore, be equally important Microliths form on the open ends of tubule plugs but proof that these microliths can grow into clinically relevant stones is lacking Patients with tubule plugs who form CaP stones show varying degrees of cortical fibrosis and nephron loss Trial data support the use of high fluid intake, potassium citrate, thiazide diuretic agents and a reduced sodium diet for prevention of recurrent calcium renal stones As idiopathic hypercalciuria arises from reduced renal tubule calcium reabsorption and is associated with negative calcium balance and bone disease, management with a low calcium diet is contraindicated The most common predisposing factor for the formation of idiopathic calcium stones is hypercalciuria. Here, the authors discuss the mechanisms of idiopathic calcium stone formation and hypercalciuria as well as potential therapeutic strategies to reduce the risk of stone formation. The most common presentation of nephrolithiasis is idiopathic calcium stones in patients without systemic disease. Most stones are primarily composed of calcium oxalate and form on a base of interstitial apatite deposits, known as Randall's plaque. By contrast some stones are composed largely of calcium phosphate, as either hydroxyapatite or brushite (calcium monohydrogen phosphate), and are usually accompanied by deposits of calcium phosphate in the Bellini ducts. These deposits result in local tissue damage and might serve as a site of mineral overgrowth. Stone formation is driven by supersaturation of urine with calcium oxalate and brushite. The level of supersaturation is related to fluid intake as well as to the levels of urinary citrate and calcium. Risk of stone formation is increased when urine citrate excretion is <400 mg per day, and treatment with potassium citrate has been used to prevent stones. Urine calcium levels >200 mg per day also increase stone risk and often result in negative calcium balance. Reduced renal calcium reabsorption has a role in idiopathic hypercalciuria. Low sodium diets and thiazide-type diuretics lower urine calcium levels and potentially reduce the risk of stone recurrence and bone disease.

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.Kidney stone disease is common and can be associated with alterations in urinary solute composition. Here, the authors outline general approaches for stone prevention, describe current understanding of the genetic influences underlying kidney stone formation and discuss the implications of a correct diagnosis for the clinical management of recurrent stone formers.

The data on the prevalence of kidney stones in mainland China are still lacking. We performed the present meta-analysis to assess the stone prevalence in mainland China from 1990 through 2016. A total of 18 articles were included. The pooled overall prevalence was 7.54% (95% CI, 5.94–9.15). The prevalence in age groups of <20 years, 20–29 years, 30–39 years, 40–49 years, 50–59 years, and 60 years and older was 0.27%, 3.15%, 5.96%, 8.18%, 9.14%, and 9.68%, respectively, showing that it increased with age. Moreover, the prevalence was 10.34% in males and 6.62% in females, with an odds ratio (OR) of 1.63 [95% CI: 1.51–1.76], indicating that males are more likely to suffer from this disease than females. However, urban areas (6.03%, 95% CI: 3.39–8.68) and rural areas (7.48%, 95% CI: 3.39–11.57) did not differ in the stone prevalence rate (OR = 0.84, 95% CI: 0.42–1.68). The prevalence in the year groups of 1991–2000, 2001–2010, and 2011 to date was 5.95%, 8.86%, and 10.63%, respectively, which indicated an increasing trend. Further high-quality surveys throughout mainland China are needed to confirm these findings.

The primary hyperoxalurias are a group of autosomal recessive disorders of endogenous oxalate overproduction. This review discusses the major biochemical, genetic, and therapeutic advances that have led to a better understanding of the disease. The primary hyperoxalurias are a group of autosomal recessive disorders involving the overproduction of oxalate. Although the initial recognition of the disease is attributed to Lepoutre, who reported it in 1925, 1 the elucidation of the underlying biochemical abnormalities occurred many years later. This review discusses the major biochemical, genetic, and therapeutic advances that have led to a better understanding of primary hyperoxaluria. Oxalate, a dicarboxylic acid (HOOC-COOH), is a highly insoluble end product of metabolism in humans. It is excreted almost entirely by the kidney, particularly in the form of its calcium salt, and has a tendency to crystallize in . . .

Diet and uric acid are closely linked to the formation of kidney stones. However, the specific dietary indices associated with kidney stone risk and the mediating role of uric acid remain unclear. This study investigates the association between four dietary indices and kidney stone risk while exploring the mediating role of uric acid. Data were obtained from the National Health and Nutrition Examination Survey (NHANES). Four dietary indices were calculated: the Mediterranean Diet (MED), Healthy Eating Index-2020 (HEI-2020), Alternate Healthy Eating Index (AHEI), and Dietary Approaches to Stop Hypertension (DASH). Univariate logistic regression analysis and restricted cubic splines (RCS) curve were used to analyze the single effect of dietary index and kidney stones. Weighted Quantile Sum (WQS) and Bayesian Kernel Machine Regression (BKMR) to visualize the mixed effects of multiple dietary indices and kidney stone risk. Finally, mediation analyses were employed to assess associations and mediation effects. Among 25,421 participants, 2,470 had a history of kidney stones. All four dietary indices showed a significant negative association with kidney stone risk, with MED and HEI-2020 showing the strongest effects. WQS regression results indicated that the mixed effects of the four dietary indices were negatively correlated with kidney stones, with the highest weight attributed to HEI2020 (49.2%), followed by DASH (26.4%), MED (21.8%), and AHEI (2.9%). BKMR analysis revealed a negative exposure-response trend for each dietary indices to the risk of kidney stones and HEI2020, DASH, MED, and AHEI are negative related with kidney stones at all three quantiles. Mediation analysis revealed that uric acid mediated the relationship between dietary indices and kidney stone risk, with mediation proportions of 25.56% (MED), 12.14% (AHEI), 5.88% (DASH), and 2.52% (HEI-2020). Healthy dietary patterns are associated with a reduced risk of kidney stones, partially mediated by uric acid levels.