Disease relevance of Kidney Calculi

• X-linked recessive nephrolithiasis with renal failure [1].
• Of the patients, 98 had recurrent, "idiopathic" kidney stones, 8 had primary hyperparathyroidism, 7 had renal or urinary tract malformations, and 1 had primary hyperoxaluria [2].
• We measured calcium-magnesium-ATPase activity in erythrocytes from 38 patients (mean age [+/- SEM], 40 +/- 2.1 years) with idiopathic hypercalciuria (24-hour urinary calcium excretion greater than or equal to 0.1 mmol per kilogram of body weight) and a history of multiple calcium oxalate kidney stones [3].
• Primary hyperoxaluria is a rare congenital disorder characterized by large quantities of urinary oxalate with resultant nephrocalcinosis and nephrolithiasis and by deposits of calcium oxalate in other organs [4].
• Oxypurinol nephrolithiasis in regional enteritis secondary to allopurinol therapy [5].

Psychiatry related information on Kidney Calculi

• 'Bad dietary habits' and recurrent calcium oxalate nephrolithiasis [6].

High impact information on Kidney Calculi

• Disorders of distal nephron function, such as Gitelman's syndrome, nephrolithiasis, and adaptation to diuretic drug administration, emphasize the importance of this relatively short nephron segment to human physiology [7].
• A new study shows that Slc26a6-null mice manifest calcium-oxalate nephrolithiasis accompanied by enhanced net intestinal oxalate absorption [8].
• Calcium oxalate is the predominant component in 70-80% of kidney stones, and small changes in urinary oxalate concentration affect the risk of stone formation [9].
• A randomized double-blind study of acetohydroxamic acid in struvite nephrolithiasis [10].
• Three disorders of hypercalciuric nephrolithiasis (Dent's disease, X-linked recessive nephrolithiasis (XRN), and X-linked recessive hypophosphataemic rickets (XLRH)) have been mapped to Xp11.22 (refs 5-7) [11].

Chemical compound and disease context of Kidney Calculi

• An inheritable anomaly of red-cell oxalate transport in "primary" calcium nephrolithiasis correctable with diuretics [2].
• Triamterene-induced nephrolithiasis [12].
• Urine glycoprotein crystal growth inhibitors. Evidence for a molecular abnormality in calcium oxalate nephrolithiasis [13].
• The presence of protein-bound gamma-carboxyglutamic acid in calcium-containing renal calculi [14].
• These findings indicate that thy- mutants may develop in renal calculi during co-trimoxazole therapy [15].

Biological context of Kidney Calculi

• Calcium-oxalate nephrolithiasis is associated with a defect in erythrocyte oxalate self-exchange and an abnormal rate of erythrocyte membrane protein phosphorylation [16].
• Evidence is provided for linkage to nephrolithiasis with microsatellite marker D12S339 (near the VDR locus, P = 0.01), as well as with flanking markers (D12S1663: P = 0.03 and D12S368: P = 0.01) [17].
• The results confirm the previously proposed scheme that obesity may sometimes cause uric acid nephrolithiasis by producing excessively acid urine due to insulin resistance [18].
• Osteopontin is associated with cell proliferation/tumerogenesis and also inhibits kidney stone mineral crystal growth [1] [19].
• Proteus mirabilis, a common cause of urinary tract infections (UTI) in individuals with functional or structural abnormalities or with long-term catheterization, forms bladder and kidney stones as a consequence of urease-mediated urea hydrolysis [20].

Anatomical context of Kidney Calculi

• Since 1971 thymine-requiring (thy-) pathogens have been isolated from the urine of 8 patients with renal calculi, and from the sputum of 1 patient with chronic chest infection [15].
• Uric acid nephrolithiasis developed in a 75-year-old man who had received a large cumulative dose of streptozotocin for treatment of metastatic islet cell carcinoma of the pancreas [21].
• These results support the notion that surface-associated NRP could mediate attachment of CaOx to the renal tubule epithelium, thereby causing retention of crystals that might eventually become kidney stones [22].
• BACKGROUND: Oxalate, a common constituent of kidney stones, is cytotoxic for renal epithelial cells [23].
• We hypothesize that in Dent's disease, endocytic failure leads to an accumulation at the plasma membrane of crystal-binding molecules that include annexin A2 leading to retention of calcium crystals and ultimately nephrocalcinosis and nephrolithiasis [24].

Gene context of Kidney Calculi

• Concentrations and relative amounts of TFF1 in the urine of patients with idiopathic CaOx kidney stone were significantly less (2.5-fold for the concentrations and 5- to 22-fold for the relative amounts) than those found in controls [25].
• Characterisation of renal chloride channel, CLCN5, mutations in hypercalciuric nephrolithiasis (kidney stones) disorders [26].
• We find trpm7 expression in the mesonephric kidney and show that mutants develop kidney stones, indicating renal dysfunction [27].
• 5. The protein encoded by ORG has a similar pattern of expression and identical structural features to nephrocalcin, a calcium-binding protein partially purified from kidney that plays a role in calcium reabsorption and in prevention of nephrolithiasis [28].
• Mutations in the CLCN5 gene have been demonstrated in three disorders of hypercalciuric nephrolithiasis, i.e., Dent's disease, X-linked recessive nephrolithiasis, and X-linked recessive hypophosphatemic rickets [29].

Analytical, diagnostic and therapeutic context of Kidney Calculi

• Primary hyperparathyroidism must be considered in the differential diagnosis of hypercalcemia, nephrolithiasis, metabolic bone disease, and pancreatitis and peptic-ulcer disease [30].
• Calcium oxalate nephrolithiasis in rats, induced by single intraperitoneal injection of sodium oxalate, is associated with pathologic changes in the renal papillary tip [31].
• In the present study, epidemiologic studies with patients at high risk for calcium oxalate urolithiasis showed a direct correlation between the number of recurrent kidney stone episodes and the lack of O. formigenes colonization [32].
• A history of nephrolithiasis and hypercalcemia preceding the institution of drug therapy allowed this patient's underlying parathyroid disease to be defined as primary hyperparathyroidism, which had been obscured by anticonvulsant therapy [33].
• Hyperoxaluria and calcium oxalate nephrolithiasis after jejunoileal bypass [34].

References