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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
If stone-forming substances in the urine, such as calcium phosphate, reach high enough concentrations to exceed their solubility, they come out of solution to form stones. Urinary stasis, infection and indwelling catheters all promote stone formation. Citrate, which is present in urine, inhibits stone formation by forming a soluble complex with calcium. Nephrocalcinosis describes diffuse renal calcium deposition, mainly in the medulla, and causes include hyperparathyroidism, distal renal tubular acidosis and medullary sponge kidney.
Renal calculi
Published in Mark Davenport, James D. Geiger, Nigel J. Hall, Steven S. Rothenberg, Operative Pediatric Surgery, 2020
Eleni Papageorgiou, Naima Smeulders
Creatinine, urea, potassium, sodium, chloride, bicarbonate, magnesium, calcium, phosphate, alkaline phosphatase, albumin, and urate tests are performed. The findings of nephrocalcinosis, bilateral calculi, or recurrent calculi suggest a metabolic abnormality. Nephrocalcinosis may be associated with renal tubular acidosis, hyperoxaluria, and hypercalcemia.
Vitamins
Published in Stanley R. Resor, Henn Kutt, The Medical Treatment of Epilepsy, 2020
Prophylactic treatment may be beneficial for patients who are inactive, lack sufficient vitamin D in the daily usual diet, and are deprived of sunlight. After 6 months on AEDs such as PHT, PB, or CBZ, determination of calcium, phosphorus, and alkaline phosphatase levels is helpful. If there is suspicion of vitamin D deficiency, then a vitamin D level can also be measured. The average patient with epilepsy who is otherwise well on a normal diet probably does not need prophylactic vitamin D supplements. The symptoms of hypercalcemia from hypervitaminosis D or excessive calcium intake include weakness, nausea, vomiting, diarrhea, and obtundation. Nephrocalcinosis, nephrolithiasis, and metastatic calcification can ensue (29). If vitamin D or calcium is prescribed, then monitoring of the calcium, phosphorus, alkaline phosphatase, and creatinine should be done after a month, then every 3 months. Vitamin D and circulating 25-hydroxyvitamin D levels should be checked 1 month after starting such therapy, and then every 6 months (30).
Impacts of ingested MWCNT-Embedded nanocomposites in Japanese medaka (Oryzias latipes)
Published in Nanotoxicology, 2021
Melissa Chernick, Alan Kennedy, Treye Thomas, Keana C. K. Scott, Christine Ogilvie Hendren, Mark R. Wiesner, David E. Hinton
Alterations in the kidney and thyroid were unexpected. Within head kidneys, altered tubular epithelial cells were observed in groups exposed to pristine MWCNTs and abraded nanocomposites. In teleosts, xenobiotic-induced kidney tubule damage occurs because of the high capacity for membrane transport and subsequent concentration of compounds in tubule lumens (Larsen and Perkins 2001). Calcifications were also observed in the trunk kidneys of some males exposed to MWCNTs. Nephrocalcinosis (or urolithiasis) is characterized by depositions of calcium and magnesium salts in the ureters of fish (Bruno 1996). These calcifications can distort kidney tubular epithelium and lead to blockages, with progression resulting in fibrosis of tubular tissue (Bruno 1996; Harrison and Richards 1979). Links to diet, particularly magnesium and selenium, have been made in aquaculture and ornamental fish, but the exact etiology of nephrocalcinosis remains uncertain (Bruno et al. 2013; Mousavi et al. 2016).
Severe hypercalcaemia and acute renal failure in an infant with subcutaneous fat necrosis
Published in Paediatrics and International Child Health, 2021
Tülay İnce Becerir, Ayça Altincik, Bayram Özhan, Selçuk Yüksel
Hypercalcaemia can lead to AKI in which diuresis is typically normal [13,14]. The pathophysiological mechanisms of AKI caused by hypercalcaemia are multifactorial and include hypovolaemia, vasoconstrictive mechanisms and intra-tubular calcification [13,14]. The decrease in glomerular filtration rate (GFR) is thought to be secondary to dehydration and arterial vasoconstriction caused by the hypercalcaemia. The attributed mechanism is that acute hypercalcaemia may cause vasoconstriction of the afferent renal arterioles, decreased extracellular fluid volume related to vomiting and decreased oral intake, resulting in a decrease in the GFR. Additionally, hypercalcaemia may also lead to activation of the calcium-sensing receptor which results in natriuresis and volume depletion [15,16]. However, in this case, the serum creatinine levels remained high after appropriate hydration. Although the acute renal failure did not improve with hydration, renal function normalised following recovery of hypercalcaemia owing to the pamidronate treatment. The AKI was most likely owing to tubular injury caused by prolonged hypercalcaemia and nephrocalcinosis. In the acute phase of nephrocalcinosis, deposition of calcium phosphate crystals within the renal tubules causes tubular injury. In the chronic phase, tubular atrophy and interstitial fibrosis are predominant [15,16].
From pathogenesis to novel therapies in primary hyperoxaluria
Published in Expert Opinion on Orphan Drugs, 2019
Gill Rumsby, Sally-Anne Hulton
Nephrocalcinosis, as observed under ultrasound, occurs following deposition of calcium salts in the tubules, or interstitial tissue of the kidney [30]. Oxalate crystals can also coalesce to form kidney stones and cause obstructive nephropathy leading to acute kidney injury (AKI). It has been estimated that obstructive nephropathy secondary to nephrolithiasis accounts for 1–2% of AKI events with higher percentage (30%) in children [31]. Removal of stones by open nephrolithotomy can contribute to chronic renal damage, and endoscopic ureterorenoscopy and lithoclast approaches are now favored as less invasive [32]. It is clear that the typical stones formed in PH contain a significant amount of calcium oxalate monohydrate that is more resistant to lithotripsy and in fact, this technique is not recommended for PH patients [33].