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Urolithiasis
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Hypercalciuria: three mechanisms.AbsorptiveRenal-inducedResorptive hypercalciuria
Nutritional Disorders/Alternative Medicine
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Tolerance to vitamin D is variable. Hypervitaminosis D may cause hypercalciuria (increased calcium levels in the urine, -uria) or hypercalcemia (-emia, blood) with symptoms of weakness, anorexia, vomiting, diarrhea, excessive thirst (polydipsia), excessive urination (polyuria), mental changes and proteinuria. Because of vitamin D's roie in calcium utilization, deposits of calcium salts in soft tissue may result if the condition is prolonged. Chronic overdosage of vitamin D can lead to irreversible renal failure.
Beckwith–Wiedemann Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Jirat Chenbhanich, Sirisak Chanprasert, Wisit Cheungpasitporn
Genitourinary: Approximately 28%–61% of BWS patients have benign genitourinary anomalies including nephromegaly, collecting system abnormalities, cryptorchidism, inguinal hernia, cystic or dysplastic changes, nephrocalcinosis, and nephrolithiasis; some features may persist in adulthood [3,56,58,59]. Presence of nephromegaly or nephrogenic rests increases the risk of Wilms tumor. Children with ICR1 hypermethylation almost consistently have genitourinary anomalies, with nephromegaly being reported in all patients and collecting system abnormalities in half of them [58]. Approximately one-fifth develop urinary tract infections which may be complicated by severe sepsis [58]. Intrauterine vesicoureteral reflex with subsequent hydroureter can result in polyhydramnios [47]. Although hyper- or hypocalcemia do not characterize the syndrome, hypercalciuria was reported in 22% of the patients and can lead to its complications such as nephrocalcinosis and nephrolithiasis [59]. Cryptorchidism is commonly observed in children with BWS and is associated with abdominal wall defects. During adulthood, abnormal testicular functions such as impaired spermatogenesis and testicular atrophy, both of which potentially leading to infertility, have been reported [56].
Kidney stone proteomics: an update and perspectives
Published in Expert Review of Proteomics, 2021
Paleerath Peerapen, Visith Thongboonkerd
Hypercalciuria and hyperoxaluria are well recognized as the risk factors for CaOx kidney stone disease. The altered cellular proteome profile of MDCK cells due to high-calcium condition was investigated [82]. 2D-PAGE-based comparative proteomics study followed by MS/MS identification of cellular proteins revealed 20 significantly altered proteins induced by 20 mM CaCl2 treatment for 72 h [82]. These altered proteins participated in various biological processes, including calcium binding. Among these, the increase of annexin A1, a known calcium-binding protein, was related to the increased COM crystal-cell adhesion [82]. Similarly, 2D-PAGE of cellular proteins derived from MDCK cells incubated in 20 mM Na2C2O4-containing medium for 72 h revealed 14 differentially expressed proteins compared with the control [83]. Among these, the increment of α-enolase expression contributed to the increased COM crystal-cell adhesion. Additionally, these significantly altered proteins were associated with response to stress, energy production, and regulation of metabolism and transcription [83].
Occult urolithiasis in asymptomatic primary hyperparathyroidism
Published in Endocrine Research, 2018
Yu-Kwang Donovan Tay, Minghao Liu, Leonardo Bandeira, Mariana Bucovsky, James A. Lee, Shonni J. Silverberg, Marcella D. Walker
Applying both thresholds of >211 mg/24hr urinary calcium excretion and >91 pg/ml serum 1,25(OH)2D provided a sensitivity of 62.5% and specificity of 94.7%. A sensitivity of 100% was achieved with a urinary calcium value of 96 mg/day but with specificity of only 13%. Likewise, a sensitivity of 100% was achieved with a 1,25(OH)2D of 63 pg/ml with a specificity of 40%. The urinary calcium threshold used to define “hypercalciuria” in women (250mg/day) had a sensitivity of 63% and specificity of 67%. There was a moderate correlation between 24-hour urinary calcium excretion and 1,25(OH)2D (r = 0.58, p = 0.001; Figure 3). Limiting the ROC analysis to those who had both urine calcium and 1,25(OH)2D values (n = 23) available did not improve the discriminatory ability [AUC 0.697 (CI: 0.463–0.931), p = 0.11].
A pilot dynamic analysis of formative factors of nephrolithiasis related to metabolic syndrome: evidence in a rat model
Published in Renal Failure, 2022
Qiqi He, Yangguo Tang, Yuzhuo Li, Fei Wang, Junsheng Bao, Sanjay Gupta
Hypocalciuria was notably observed in the MS rats in our study, which is not consistent with the general risk factors theory of hypercalciuria in the regular stone pathogenic mechanism. To our knowledge, no literature has demonstrated and explained this manifestation and general mechanism. Only one clinical study has shown that urinary calcium has a very weak correlation with components of MS [22]. Due to limited literature, we hypothesize that the hypocalciuria in our study might be related to large amounts of ROS released in tissue. We also hypothesize that the long-term effects of excessive ROS would cause lipid peroxidation on the cell membrane and increase the permeability of the cell membrane and influx of calcium ions (Ca2+). All these circumstances induce continuous depolarization of mitochondria, inhibition of ATP production, and overload of intracellular Ca2+. Continuous Ca2+ influx might cause hypocalciuria, mitochondrial fragmentation, and inflammatory responses. Consistently, one recent study [23] indicated that mitochondrial dysfunction and fragmentation induced by excessive reactive oxygen species (ROS) in MS might promote calcium deposition on the surface of renal tubular epithelial cells and aggregation into crystals. Hypercalciuria is usually secondary to renal tubular acidosis and hyperparathyroidism. It leads to disturbances in calcium homeostasis and is recognized as a risk factor for nephrolithiasis. This finding might be more accurate and reliable with an increase in sample size. Due to ammonium chloride administration, lower urine pH levels were observed in both drug administration groups.