Xiaojing Tang1, John C Lieske. 1. aDivision of Nephrology and Hypertension, Mayo Clinic bDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota, USA cDivision of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, China.
Abstract
PURPOSE OF REVIEW: Nephrolithiasis is a common systemic disease associated with both acute kidney injury (AKI) and chronic kidney disease (CKD). The purpose of this review is to discuss recent publications regarding nephrolithiasis-associated kidney damage, with an emphasis on AKI. RECENT FINDINGS: Nephrolithiasis is not a common cause of adult AKI (1-2% of cases), although it may be a more important factor in young children (up to 30%). The primary mechanism of nephrolithiasis-associated AKI is obstructive nephropathy, and factors on presentation with obstructive uropathy predict the likelihood of long-term renal recovery. Crystalline nephropathy is another potential pathway in certain circumstances that is often associated with a worse outcome. Recent studies have elucidated additional pathways whereby calcium oxalate crystals can cause acute injury, implicating innate immunity and intracellular inflammasome pathways. Several large cohort studies have demonstrated an independent association of nephrolithiasis with CKD and end-stage renal disease, although the effect size is modest. Urologic comorbidities, urinary infection, and shared underlying risk factors (e.g., diabetes, hypertension) all impact nephrolithiasis-associated CKD risk. SUMMARY: Obstructive nephropathy and crystalline nephropathy both contribute to nephrolithiasis-associated AKI, although the latter appears to have a worse prognosis. Nephrolithiasis is an independent, albeit small, risk factor for CKD. Further study is needed to clarify the incidence and mechanisms of nephrolithiasis-associated AKI, and the relationship between nephrolithiasis-associated AKI and CKD.
PURPOSE OF REVIEW: Nephrolithiasis is a common systemic disease associated with both acute kidney injury (AKI) and chronic kidney disease (CKD). The purpose of this review is to discuss recent publications regarding nephrolithiasis-associated kidney damage, with an emphasis on AKI. RECENT FINDINGS:Nephrolithiasis is not a common cause of adult AKI (1-2% of cases), although it may be a more important factor in young children (up to 30%). The primary mechanism of nephrolithiasis-associated AKI is obstructive nephropathy, and factors on presentation with obstructive uropathy predict the likelihood of long-term renal recovery. Crystalline nephropathy is another potential pathway in certain circumstances that is often associated with a worse outcome. Recent studies have elucidated additional pathways whereby calcium oxalate crystals can cause acute injury, implicating innate immunity and intracellular inflammasome pathways. Several large cohort studies have demonstrated an independent association of nephrolithiasis with CKD and end-stage renal disease, although the effect size is modest. Urologic comorbidities, urinary infection, and shared underlying risk factors (e.g., diabetes, hypertension) all impact nephrolithiasis-associated CKD risk. SUMMARY:Obstructive nephropathy and crystalline nephropathy both contribute to nephrolithiasis-associated AKI, although the latter appears to have a worse prognosis. Nephrolithiasis is an independent, albeit small, risk factor for CKD. Further study is needed to clarify the incidence and mechanisms of nephrolithiasis-associated AKI, and the relationship between nephrolithiasis-associated AKI and CKD.
Authors: Mitra de Cógáin; Amy E Krambeck; Andrew D Rule; Xujian Li; Eric J Bergstralh; Matthew T Gettman; John C Lieske Journal: Urology Date: 2011-11-16 Impact factor: 2.649
Authors: Amy E Krambeck; Matthew T Gettman; Audrey L Rohlinger; Christine M Lohse; David E Patterson; Joseph W Segura Journal: J Urol Date: 2006-05 Impact factor: 7.450
Authors: Ziad M El-Zoghby; John C Lieske; Robert N Foley; Eric J Bergstralh; Xujian Li; L Joseph Melton; Amy E Krambeck; Andrew D Rule Journal: Clin J Am Soc Nephrol Date: 2012-06-28 Impact factor: 8.237