Relationship Between Glomerular Filtration Rate and 24-Hour Urine Composition in Patients With Nephrolithiasis

Gershman, Boris; Sheth, Sonali; Dretler, Stephen P.; Herrick, Benjamin; Lang, Katherine; Pais, Vernon M.; Eisner, Brian H.

doi:10.1016/j.urology.2011.12.019

Cited by 21 publications

(23 citation statements)

References 12 publications

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“…As GFR declines, renal oxalate clearance is decreasing, which leads to increased plasma oxalate as depicted in Figure 1C [59, 119, 120, 121, 122, 123, 124, 125]. Mean plasma oxalate levels reported for different kinds of chronic renal disease are above normal limits and inversely correlate with GFR [123, 126].…”

Section: Oxalate and Ckdmentioning

confidence: 99%

Oxalate, inflammasome, and progression of kidney disease

Ermer

Eckardt²,

Aronson³

et al. 2016

Current Opinion in Nephrology and Hypertension

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Purpose of review Oxalate is an end product of metabolism excreted via the kidney. Excess urinary oxalate, whether from primary or enteric hyperoxaluria, can lead to oxalate deposition in the kidney. Oxalate crystals are associated with renal inflammation, fibrosis and progressive renal failure. It has long been known that as glomerular filtration rate (GFR) becomes reduced in chronic kidney disease (CKD), there is striking elevation of plasma oxalate. Taken together, these findings raise the possibility that elevation of plasma oxalate in CKD may promote renal inflammation and more rapid progression of CKD independent of primary etiology. Recent findings The inflammasome has recently been identified to play a critical role in oxalate-induced renal inflammation. Oxalate crystals have been shown to activate the nucleotide-binding domain, leucine-rich repeat inflammasome 3 (also known as NALP3, NLRP3 or cryopyrin), resulting in release of Interleukin-1β and macrophage infiltration. Deletion of inflammasome proteins in mice protects from oxalate-induced renal inflammation and progressive renal failure. Summary The findings reviewed in this article expand our understanding of the relevance of elevated plasma oxalate levels leading to inflammasome activation. We propose that inhibiting oxalate-induced inflammasome activation, or lowering plasma oxalate, may prevent or mitigate progressive renal damage in CKD, and warrants clinical trials.

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Section: Oxalate and Ckdmentioning

confidence: 99%

Oxalate, inflammasome, and progression of kidney disease

Ermer

Eckardt²,

Aronson³

et al. 2016

Current Opinion in Nephrology and Hypertension

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“…Second, details of the stone disease in terms of urine metabolic abnormalities, frequency of stone events, symptomatic vs. asymptomatic stones, and stone composition are often not available in reported investigations. Third, evidence would suggest that reduction in GFR may in fact be protective against nephrolithiasis because low GFR is associated with decreased urine calcium and decreased supersaturation for calcium oxalate and calcium phosphate crystals [13 ▪ ]. Finally, most studies have been retrospective and the overlapping diagnostic evaluation of nephrolithiasis and CKD can inflate the strength of association [14 ▪▪ ].…”

Section: Risk Of Chronic Kidney Disease Due To Nephrolithiasismentioning

confidence: 99%

Nephrolithiasis and loss of kidney function

Keddis

Rule

2013

Current Opinion in Nephrology &Amp; Hypertension

116

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Purpose of review The prevalence of nephrolithiasis has been on the rise over recent decades. There have also been extensive efforts to identify risk factors for chronic kidney disease (CKD). The purpose of this review is to highlight recent evidence on the association of nephrolithiasis with the development of CKD and end-stage renal disease (ESRD). Recent findings Several epidemiologic studies over the past decade assessed the relationship between history of nephrolithiasis and CKD. Across several studies, patients with nephrolithiasis had about a two-fold higher risk for decreased renal function or need for renal replacement therapy. This risk appears to be independent of risk factors for CKD that are common in stone formers such as hypertension and diabetes mellitus. Specific risk factors for CKD in stone formers include recurrent urinary tract infections, struvite and possibly uric acid stone composition, symptomatic stones, solitary kidney, ileal conduit, neurogenic bladder, and hydronephrosis. Summary Recent evidence has shown a consistent relationship between nephrolithiasis history and an increased risk of CKD and ESRD. Understanding the characteristics that predispose to CKD may better inform how to optimally manage patients with nephrolithiasis and prevent this complication.

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“… 1 , 2 With declining kidney function, renal oxalate clearance decreases and oxalate accumulates. 3 , 4 , 5 , 6 , 7 In patients with end-stage renal disease (ESRD), plasma oxalate (P Ox ) concentrations frequently exceed the oxalosis cutoff of 30 μmol/l. 8 , 9 , 10 Elevated P Ox can lead to oxalate deposition in various tissues and can cause organ damage.…”

mentioning

confidence: 99%

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

Ermer

Kopp

Asplin

et al. 2017

Kidney International Reports

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IntroductionCalcium oxalate supersaturation is regularly exceeded in the plasma of patients with end-stage renal disease (ESRD). Previous reports have indicated that hemodialfiltration (HDF) lowers elevated plasma oxalate (POx) concentrations more effectively compared with hemodialysis (HD). We reevaluate the therapeutic strategy for optimized POx reduction with advanced dialysis equipment and provide data on the effect of extended treatment time on dialytic oxalate kinetics.MethodsFourteen patients with ESRD who underwent HDF 3 times a week for 4 to 4.5 hours (regular HDF; n = 8) or 7 to 7.5 hours (extended HDF; n = 6) were changed to HD for 2 weeks and then back to HDF for another 2 weeks. POx was measured at baseline, pre-, mid-, and postdialysis, and 2 hours after completion of the treatment session.ResultsBaseline POx for all patients averaged 28.0 ± 7.0 μmol/l. Intradialytic POx reduction was approximately 90% and was not significantly different between groups or treatment modes [F(1) = 0.63; P = 0.44]. Mean postdialysis POx concentrations were 3.3 ± 1.8 μmol/l. A rebound of 2.1 ± 1.9 μmol/l was observed within 2 hours after dialysis. After receiving 2 weeks of the respective treatment, predialysis POx concentrations on HD did not differ significantly from those on HDF [F(1) = 0.21; P = 0.66]. Extended treatment time did not provide any added benefit [F(1) = 0.76; P = 0.40].DiscussionIn contrast to earlier observations, our data did not support a benefit of HDF over HD for POx reduction. With new technologies evolving, our results emphasized the need to carefully reevaluate and update traditional therapeutic regimens for optimized uremic toxin removal, including those used for oxalate.

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Relationship Between Glomerular Filtration Rate and 24-Hour Urine Composition in Patients With Nephrolithiasis

Cited by 21 publications

References 12 publications

Oxalate, inflammasome, and progression of kidney disease

Oxalate, inflammasome, and progression of kidney disease

Nephrolithiasis and loss of kidney function

Impact of Regular or Extended Hemodialysis and Hemodialfiltration on Plasma Oxalate Concentrations in Patients With End-Stage Renal Disease

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