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NDT Advance Access originally published online on December 2, 2005
Nephrology Dialysis Transplantation 2006 21(3):701-706; doi:10.1093/ndt/gfi302
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© The Author [2005]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Original Articles: Clinical Nephrology

Evidence against a contribution of conventional urine risk factors to de novo ESRD renal stones

Nicole Stankus, Elaine Worcester, Mary Hammes and Fredric L. Coe

Section of Nephrology, Department of Medicine, University of Chicago, 5841 South Maryland Avenue MC 5100, Chicago, IL 60637, USA

Correspondence and offprint requests to: Nicole Stankus, Section of Nephrology, Department of Medicine, University of Chicago, 5841 South Maryland Avenue MC 5100, Chicago, IL 60637, USA. Email: nstankus{at}medicine.bsd.uchicago.edu



   Abstract
Top
 Abstract
Introduction
 Materials and methods
 Results
 Discussion
 Summary
 References
 
Background. The authors measured urine and blood stone risk factors in African-American (AA) haemodialysis (HD) patients with new onset of stones during dialysis.

Methods. Patients with nephrolithiasis (NL) newly manifested during dialysis were matched by age, sex and urine output and dialysis duration to AA HD patients without history or symptoms of stones. Two 24 h urine and serum samples were collected and analysed for conventional stone risk factors.

Results. Three percent of the patients formed new stones while on HD; none had formed stones prior to end-stage renal disease. Newly onset NL patients had higher urine citrate and lower serum potassium levels than HD patients without stones.

Conclusion. Usual stone risk factors did not correlate with new stones during dialysis.

Keywords: African-Americans; haemodialysis; kidney calculi; kidney failure



   Introduction
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 Abstract
 Introduction
Materials and methods
 Results
 Discussion
 Summary
 References
 
Symptomatic renal calculi occur in 5–13% of all patients with end-stage renal disease (ESRD) [1] and cause morbidity and healthcare expense. Radiological evidence of calcifications in kidneys of patients with ESRD is extremely common – from 51% [2] to as high as 71% in patients with secondarily acquired renal cysts [3]. Some patients become stone formers (SF) while on renal replacement therapies, without having prior history of kidney stones, and they are the object of the present work that aims to identify urine or blood abnormalities that might cause new onset of stones. The usual mineral phase is calcium oxalate (CaOx) [4]; however, many stones are primarily composed of a mixture of proteins, known as matrix calculi, which may be partially mineralized [5]. Patients whose stones antedate ESRD may harbour stone risks apart from those arising from ESRD treatment; we exclude them here. Our specific question here is whether commonly used urine and blood stone risk factors differentiate ESRD patients with and without de novo stones during years of haemodialysis (HD) treatment.



   Materials and methods
Top
 Abstract
 Introduction
 Materials and methods
Results
 Discussion
 Summary
 References
 
Dialysis population
The ESRD patients in the three geographically separate HD facilities of the University of Chicago arise from our emergency room and clinic populations, and are 95% AA. The units provide care for patients in the surrounding communities, and are not targets of specific referral per se. Our dialysis units contained a total of 303 AA patients. Of these, 300 (160 females) were eligible to participate (three were demented).

Interview protocol
All prevalent AA chronic patients aged 18 and older at the University of Chicago outpatient HD units, except for those with advanced dementia, were eligible to participate. A face-to-face screening questionnaire was administered by the medical director of each facility to determine presence or absence of history and symptoms consistent with stones. This was done once in each unit over several months during 2002. Specifically, patients were asked: ‘Have you ever had a kidney stone? Has a doctor ever told you that you had a kidney stone?’ Affirmative answer to either of these questions was taken to indicate a history of kidney stones. Twenty-five patients had stones prior to ESRD and are not considered here; none of these patients formed stones while on renal replacement therapy.

Subjects
Nine patients (six females) with symptomatic stones while on but not prior to starting HD were classified as ESRD stone formers (ESRD SF). Two ESRD patients with no prior history of kidney stones or symptoms suggestive for kidney stones by the administered questionnaire were matched as controls (C) to each ESRD SF by age, sex and dialysis duration. All of the ESRD SF produced urine; therefore we selected our controls from the group of ESRD patients who reported still producing urine.

Urine studies
ESRD SF and C each collected two 24 h urine samples following detailed written instructions. Patients who dialyse on a Monday, Wednesday, Friday schedule collected their urine on Sundays; patients who dialyse on a Tuesday, Thursday, Saturday schedule collected their urine on Mondays. Urine samples were delivered to the dialysis unit by the patient on Monday and Tuesday, respectively. Blood samples for biochemical analysis were collected at the start of the first HD session of the same week. Urine was analysed for volume, sodium, potassium, pH, citrate, uric acid, oxalate, calcium, magnesium, phosphorus, creatinine, ammonia, sulphate and chloride using methods previously described [6,7]. Urine supersaturation (SS) with respect to CaOx was calculated using EQUIL2 [8].

Serum studies
Serum levels of sodium, potassium, uric acid, calcium, magnesium, phosphorus, creatinine, chloride and bicarbonate were measured using previously reported methods [6,9]. Serum calcium was corrected for serum albumin: Ca (corrected) = Ca (measured) + 0.8*(4-albumin), if serum albumin level was below 4.0. Serum intact parathyroid harmone (PTH) was measured using an electrochemiluminiscence immunoassay (RocheTM) and albumin levels were measured using bromcresol green spectrophotometry (RocheTM).

Imaging studies
Non-contrast computed tomography (CT) scans using 5 mm cuts were performed on most ESRD SF with clinical symptoms as a part of standard medical care. Some patients required urological interventions, such as cystoscopies and ureteral stent placements. CT scans were reviewed and the density of the kidney stone was measured in Hounsfield units (HU) using iSite Enterprise, version 3.3.0 (by Stentor, Inc, CA, USA) radiology software programme. Measurement of the density of kidney stones on CT scan has been correlated with stone composition in several studies [10–13].

Statistical analyses
Blood and urine stone risk factors were analysed using standard t-tests, discriminant analysis for continuous outcomes and logistic regression for dichotomous outcomes. Specifically, a model of discriminant function analysis was built step-by-step by reviewing all variables at each step and determining which one will contribute most to the discrimination between groups. That variable was then included in the model. The stepwise procedure was controlled by the respective F to enter value. The F value for a variable indicates its statistical significance in the discrimination between groups, that is, it is a measure of the extent to which a variable makes a unique contribution to the prediction of group membership. Those variables with the largest (standardized) regression coefficients were the ones contributing most to the prediction of group membership (Table 2). A P-value of <0.05 was considered statistically significant. Multivariate linear modelling was performed to analyse correlates of CaOx SS. All statistical analyses were performed using standard software (SYSTAT, Systat Software Inc. Richmond, Ca). The study protocol and the informed consent were approved by the University of Chicago Institutional Review Board.


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  		Table 2. Linear discriminant analysis and logistic regression

 


   Results
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 Abstract
 Introduction
 Materials and methods
 Results
Discussion
 Summary
 References
 
Clinical characteristics of ESRD SF and C
Mean age (±SD) of the patients at the time of stone episode was 54±19 (females) and 50±5 (males). Time on dialysis of the ESRD SF (grey circles) and C (black circles) is shown in Figure 1, middle panel. Symptoms of nephrolithiasis (NL) started more than 2 years after initiation of HD in six patients and recurrent episodes occurred in three patients. Shortest time from the start of HD to the onset of renal colic was 12 months, longest was 9 years.


Figure 1
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  		Fig. 1. Urine measurements that discriminate between ESF (grey circles and grey triangles) and Control (black circles and black triangles) patients. Urine citrate is higher and serum potassium lower in ESF vs C. Although time on dialysis did not differ between the two groups, it entered as a significant differentiating variable during discriminant analysis. A multivariable score using all three measurements separates the two groups with 85% overall accuracy (lower panel of figure).

 
In ESRD SF, evidence of existing calculi was found in six patients. One of them had stone fragments and proteinaceous debris documented during cystoscopy. In five other patients, CT scans documented stones in the kidney. The HU density of these stones was between 95 and 400 (median 222 HU). This suggests that these stones are either uric acid calculi or, more likely, calculi composed of a high percentage of protein matrix which has been variably calcified, as has been reported previously in dialysis patients [1,5,14–16]. Hydronephrosis, consistent with a recently passed calculus, was demonstrated in the remaining three ESRD SF.

Average dose of intravenous paricalcitol in our patients was 1.9 times higher in the C compared to SF. More C (50%) were treated with calcium acetate (average dose 2.9 tablets per meal) compared to 30% of SF (one tablet per meal). Average dose of calcium carbonate was 1.3 tablets and 1.7 tablets per meal in C and cases (17% and 30% of patients, respectively). In both groups 22% of patients were on sevelamer and 11% were not taking any phosphate binders. Causes of ESRD in SF and C were similar, and distributed as follows: diabetic nephropathy in 44% vs 50%, HTN in 22% vs 17%, systemic lupus erythrematosis in 22% vs none, primary glomerular nephritis in none vs 22%, interstitial nephritis in none vs 11% and HIV nephropathy in 11% vs none. Thus, proteinuric renal disease was found about equally in both SF and C.

Measurements that discriminate ESRD SF and C
Blood and urine studies were performed on nine ESRD SF and compared to the 18 C subjects. Serum potassium was lower and urine citrate higher in ESRD SF vs C (Table 1). These differences reflect a general displacement of population values between the two groups (Figure 1, upper left and right panels). There were no differences between the groups in dialysis duration (Figure 1, middle panel) as expected from our matching protocol. Using linear discriminant analysis with stepping, serum potassium, urine citrate and duration of ESRD treatment were all entered as significant and independent variables (Table 2) with an overall correct classification of 85%; a score derived from the analysis separated the two groups (Figure 1, lower panel). Using logistic regression, urine citrate and serum potassium entered as significant (Table 2), confirming the significance of the univariate comparisons and the linear discriminant analysis.


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  		Table 1. Laboratory findings related to stone formation

 
Determinants of urine SS CaOx
Our data are consistent with the observation that CaOx is the usual mineral phase in ESRD stones, because only SS CaOx is above one (Table 1). Nonetheless, urine calcium and oxalate concentrations did not differ between SF and ESRD C (Table 1), and likewise, SS CaOx did not differ between these two groups. However, while urine calcium concentration (and daily excretion) of both ESRD groups is below that of normals, urine oxalate concentration is high compared to normal values (Table 1); this reflects a surprisingly well-preserved oxalate excretion rate coupled with the usual low urine volumes found in ESRD patients. It is the well-known very low calcium excretion and concentration values in ESRD that prevent extremely high urine SS CaOx.

In a linear multivariate model with SS CaOx as dependent and urine concentrations of calcium, oxalate, citrate, sodium, and phosphate, and stone formation as predictor variables, urine calcium and oxalate concentrations, and stone formation entered (all three P values <0.02). Adjusted means differed (2.82±0.2 vs 3.46±0.1, P = 0.014, C vs SF, respectively) whereas unadjusted values (Table 1) did not differ; this presumably reflects allowance for the higher calcium concentration of the ESRD SF vs C.



   Discussion
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 Abstract
 Introduction
 Materials and methods
 Results
 Discussion
Summary
 References
 
ESRD stones can contain CaOx
Prior studies have described ESRD stones as predominantly containing calcium oxalate as their mineral phase [4] [17,18]; however, these stones often contain a large amount of protein matrix as well. Oxaloprotein stones (containing more than 30% of calcium oxalate) were found in 50% of the cases by Daudon; another 30% were composed largely of protein that was more sparingly mineralized with CaOx [19]. Likewise, Cheng found a spectrum of composition with varying amounts of protein and CaOx in such stones [20]. In the study by Oren et al. [21] the ultra structural composition of five out of seven analysed stones in ESRD patients was that of CaOx. In our study, the density of the stones seen on CT scan is consistent with the presence of larger amounts of protein matrix with a variable amount of mineralization; all the stones had a lower density than that reported for the usual CaOx or phosphate stones seen in ordinary SF (26). Although the density could also be consistent with uric acid stones, these seem much less likely in view of the undersaturation of the patient's urine with respect to this mineral. Our study addresses the mineralization process for patients such as these. No prior study has reported urine stone risk factors in a group of SF on HD, compared with a group of non-SF ESRD patients.

Increased SS CaOx is not an explanation for ESRD stones in our patients
Conventional urinary stone risk factors do not predict ESRD stone formation. SS values for CaP and UA are below one. For CaOx SS, mean values are not high compared to normal subjects (Table 1). However, mean urine oxalate concentration is above normal; in fact, if urine calcium levels were in the normal range, CaOx SS would be quite high. The high urine oxalate concentration reflects the approximate 10:1 urine to serum creatinine ratio (12 and 10, ESRD SF vs C, P, NS), the fact that oxalate is not reabsorbed by renal tubules and may be secreted, and the usual serum oxalate levels in ESRD that approximate 30–50 µM/l [22]. Although high urine oxalate concentration could well play a role in stone production, it was not higher in the ESRD SF vs C, and therefore cannot explain stones in our patients.

Higher urine calcium may be a factor in ESRD stone formation
In the only other study of urine stone risk factors in ESRD patients (who were on CAPD) [21], ESRD CaOx SF had higher urine ionic-oxalate molarities than normal subjects, but their CaOx activity product correlated with the ionic-calcium not the ionic-oxalate concentration. We did not measure oxalate ion specifically, but our data are compatible with their result in that it was urine calcium that was higher, though not to a statistically significant degree among the ESRD SF vs our ESRD C. Taking the two studies together, it is indeed possible that urine calcium may control whether CaOx mineral phases form in the kidneys. This should be tested in other populations to confirm the matter, as it could have an influence on calcium and vitamin D dosing in ESRD. Nonetheless, our SF did not receive more calcium-containing binders or more vitamin D than the non-SF ESRD C.

Urine citrate and serum potassium define ESRD SF vs C but do not explain stones
Our ESRD SF had higher urine citrate and lower serum potassium levels than C. We cannot easily link these differences to stone formation. A natural hypothesis is that ESRD SF have higher residual values for glomerular filtration. However, 24 h creatinine clearances (l/d) were 5.3 for both groups. Certainly the higher urine citrate was not a cause of stones, in that citrate is actually felt to be an inhibitor of calcium stone formation [23]. We cannot presently explain the association.

The role of matrix may be important, and was not considered here
Some believe that the organic matrix component plays a major role in ESRD stone formation [19]. Protein stones may be difficult to detect by radiographic methods and they may present as recurrent episodes of hydronephrosis [24]. Various protein structures have been detected in HD stone formers, microfibrillary [5,24], amyloidal [14] among them. Japanese investigators [15] compared protein composition of these stones to the protein matrix composition of CaOx stones in non-dialysis patients and found the structural patterns to be different: in chronic HD patients (ß2 microglobulin>lysozyme>albumin, serum amyloid P component (SAP), Tamm-Horsfall protein (THP) vs non-dialysis patients (albumin>lysozyme>SAP, THP). However, Watanabe et al. [16] did not detect any significant differences in urinary or serum levels of ß2 microglobulin in patients with amyloid protein calculi versus patients without urinary calculi. Our work does not address the matter of matrix, however, if CaOx mineral is to be deposited in the matrix, the driving forces are the ones we have explored here.

Our work has obvious limitations
Our analysis would have been strengthened if stone analysis was available on our patients. This work may not have been able to fully discern the causes of NL, but it does suggest that standard NL preventive measures would not be effective in an ESRD population.

Although we cannot distinguish pure or nearly pure protein—SF from ones who form CaOx stones with a variable protein content—our results suggest that CaOx containing stones do not form quite the same way in patients with renal failure as they do in patients with normal renal function, thus favouring proteinaceous matrix stone formation theory. It is also supported by the low density (under 400 HU) of CT documented stones. Use of non-contrast helical CT for assessing the chemical composition of urinary tract stones has been tested in both in vitro and in vivo settings [25,26]. CaOx stones are among the most dense, usually measuring about 650 HU or more [10].

Stone formation risk factors were originally determined in non ESRD populations [27]. The level of SS with respect to CaOx in our ESRD patients, both C and SF, is below that of normals. The ability of normal subjects to tolerate a level of SS above the thermodynamic solubility product implies the presence of inhibitors of crystallization [28,29], and these may well be lacking in ESRD. The level of SS at which mineral begins to precipitate in urine, referred to as the upper limit of metastability (ULM), is known to be lower in ordinary SF compared with normal C [30]. The ULM for CaOx was not tested in our patients, but could in fact be lower than in subjects with normal renal function, accounting for stone formation at lower levels of SS. In addition, increased urinary protein, which is often seen in chronic kidney disease, may influence the precipitation threshold, probably by lowering it, as protein debris could serve as a nidus and a matrix. We did not measure urine protein in our SF and C but a similar proportion of patients in both groups had proteinuric renal disease prior to initiation of HD.

The time of occurrence of the first stone is important in that the closer symptoms of NL are to the initiation of HD, the more likely the stone was already pre-formed. We had three patients who manifested stones between 1 and 2 years after the start of HD. Two of them had recurrent episodes of pain and hydronephrosis without radiological evidence of a stone, which would be consistent with protein stones. They underwent cystoscopies and proteinaceous debris was documented. The third patient had a kidney ultrasound 1 year prior to the renal colic episode, which did not demonstrate NL. He manifested symptoms 1 year after the start of HD. CT scan documented a stone that was very small and of a very low density – only 95 HU, which would also point to a protein matrix stone. Though we cannot totally exclude the pre-existence of stones prior to ESRD, we thought it to be rather less likely.

It would be interesting to compare our findings in African-American patients to other ethnic groups. It is possible that mechanisms which play a protective role in kidney stone formation in the African-American population are somehow disabled in patients on HD. Or, as our data would suggest, traditional mechanisms of stone formation do not apply to HD patients, and currently available preventive strategies therefore would not be effective.



   Summary
Top
 Abstract
 Introduction
 Materials and methods
 Results
 Discussion
 Summary
References
 
Our studies of patients with first onset of stones during ESRD are new in that we are the first to make comprehensive stone risk measurements of such patients compared to reasonably well-chosen parallel C. Observed findings, however, are not easy to interpret. Higher urine citrate and lower serum potassium might reflect higher residual renal function that permitted stones to form. This is mere conjecture. Of importance, conventional stone risk measurements do not appear useful, and therefore are not promising in stone management of this particular population.

Conflict of interest statement. None of the authors had involvements that might raise the question of bias in the work reported or in the conclusions, implications or opinions stated.



   References
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 Abstract
 Introduction
 Materials and methods
 Results
 Discussion
 Summary
 References
 

  1. Viterbo R, Mydlo JH. Incidence and management of dialysis patients with renal calculi. Urol Int 2002; 69: 306–308[Medline]
  2. Koga N, Nomura G, Yamagata Y, Koga T. Ureteric pain in patients with chronic renal failure on hemodialysis. Diagnostic approach with ultrasonography and computer tomography. Nephron 1982; 31: 55–58[Medline]
  3. Bahner ML, Bommer J, Sommerer C, van Kaick G. Radiologic diagnosis of the kidneys in dialysis patients. Radiologe 1999; 39: 398–403[Medline]
  4. Oreopoulos DG, Silverberg S. Calcium oxalate urinary-tract stones in patient's on maintenance dialysis. N Engl J Med 1974; 290: 1438–1439 (letter)[Medline]
  5. Bommer J, Ritz E, Tschope W, Waldherr R, Gebhardt M. Urinary matrix calculi consisting of microfibrillar protein in patients on maintenance hemodialysis. Kidney Int 1979; 16: 722–728[Medline]
  6. Weber DV, Coe FL, Parks JH, Dunn MS, Tembe V. Urinary saturation measurements in calcium nephrolithiasis. Ann Intern Med 1979; 90: 180–184[Medline]
  7. Parks JH, Coward M, Coe FL. Correspondence between stone composition and urine supersaturation in nephrolithiasis. Kidney Int 1997; 51: 894–900[ISI][Medline]
  8. Werness PG, Brown CM, Smith LH, Finlayson B. EQUIL2: a BASIC computer program for the calculation of urinary saturation. J Urol 1985; 134: 1242–1244[ISI][Medline]
  9. Coe FL, Strauss AL, Tembe V, Le Dun S. Uric acid saturation in calcium nephrolithiasis. Kidney Int 1980; 17: 662–668[ISI][Medline]
  10. Nakada SY, Hoff DG, Attai S, Heisey D, Blankenbaker D, Pozniak M. Determination of stone composition by noncontrast spiral computed tomography in the clinical setting. Urology 2000; 55: 816–819[Medline]
  11. Gupta NP, Ansari MS, Kesarvani P, Kapoor A, Mukhopadhyay S. Role of computed tomography with no contrast medium enhancement in predicting the outcome of extracorporeal shock wave lithotripsy for urinary calculi. BJU Int 2005; 95: 1285–1288[Medline]
  12. Joseph P, Mandal AK, Singh SK, Mandal P, Sankhwar SN, Sharma SK. Computerized tomography attenuation value of renal calculus: can it predict successful fragmentation of the calculus by extracorporeal shock wave lithotripsy? A preliminary study. J Urol 2002; 167: 1968–1971[Medline]
  13. Liu CC, Li CC, Shih MC, Chou YH, Huang CH. Matrix stone. J Comput Assist Tomogr 2003; 27: 810–813[CrossRef][Medline]
  14. Linke RP, Bommer J, Ritz E, Waldherr R, Eulitz M. Amyloid kidney stones of uremic patients consist of beta 2-microglobulin fragments. Biochem Biophys Res Commun 1986; 136: 665–671[CrossRef][Medline]
  15. Ozasa H, Suzuki T, Takahashi K, Ota K. Protein components of amyloid-like kidney stones of chronic hemodialysis patients. Nephron 1989; 53: 257–260[Medline]
  16. Watanabe K, Nakamura R, Kano S, Ohtake T, Hosoda Y, Saruta T. Amyloid urinary-tract calculi in patients on chronic dialysis. Nephron 1989; 52: 334–337[Medline]
  17. Caralps A, Lloveras J, Andreu J et al. Urinary calculi in chronic dialysis patients. Lancet 1979; 2: 1024–1025[Medline]
  18. Caralps A, Lloveras J, Masramon J, Andreu J, Brulles A, Gil-Vernet JM. Urinary calculi after renal transplantation. Lancet 1977; 1: 544[Medline]
  19. Daudon M, Lacour B, Jungers P et al. Urolithiasis in patients with end stage renal failure. J Urol 1992; 147: 977–980[Medline]
  20. Cheng PT, Reid A, Millard J, Pritzker KP, Khanna R, Oreopoulos DG. Ultrastructural studies of renal stones from patients on continuous ambulatory peritoneal dialysis. Scan Electron Microsc 1983; 4: 1939–1946
  21. Oren A, Husdan H, Cheng PT et al. Calcium oxalate kidney stones in patients on continuous ambulatory peritoneal dialysis. Kidney Int 1984; 25: 534–538[Medline]
  22. McConnell KN, Rolton HA, Modi KS, Macdougall AI. Plasma oxalate in patients with chronic renal failure receiving continuous ambulatory peritoneal dialysis or hemodialysis. Am J Kidney Dis 1991; 18: 441–445[Medline]
  23. Kok DJ, Papapoulos SE, Bijvoet OL. Excessive crystal agglomeration with low citrate excretion in recurrent stone-formers. Lancet 1986; 1: 1056–1058[CrossRef][Medline]
  24. Bommer J, Ritz E, van Kaick G. Acute flank pain in dialysed patients. Demonstration of hydronephrosis by computer tomography. J Dial 1980; 4: 109–114[Medline]
  25. Bellin MF, Renard-Penna R, Conort P et al. Helical CT evaluation of the chemical composition of urinary tract calculi with a discriminant analysis of CT-attenuation values and density. Eur Radiol 2004; 14: 2134–2140[CrossRef][Medline]
  26. Deveci S, Coskun M, Tekin MI, Peskircioglu L, Tarhan NC, Ozkardes H. Spiral computed tomography: role in determination of chemical compositions of pure and mixed urinary stones–an in vitro study. Urology 2004; 64: 237–240[CrossRef][Medline]
  27. Parmar MS. Kidney stones. Bmj 2004; 328: 1420–1424[Free Full Text]
  28. Kumar V, Yu S, Farell G, Toback FG, Lieske JC. Renal epithelial cells constitutively produce a protein that blocks adhesion of crystals to their surface. Am J Physiol Renal Physiol 2004; 287: F373–F383[Abstract/Free Full Text]
  29. Marangella M, Bagnis C, Bruno M, Vitale C, Petrarulo M, Ramello A. Crystallization inhibitors in the pathophysiology and treatment of nephrolithiasis. Urol Int 2004; 72 [Suppl 1]: 6–10
  30. Asplin JR, Parks JH, Chen MS et al. Reduced crystallization inhibition by urine from men with nephrolithiasis. Kidney Int 1999; 56: 1505–1516[CrossRef][ISI][Medline]
Received for publication: 29. 6.05
Accepted in revised form: 8.11.05


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