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• W2068579384 abstract "To define the renal tissue changes in stone-forming patients with distal renal tubular acidosis (dRTA), we performed intra-operative papillary and cortical biopsies in five patients. The main abnormalities were plugging of inner medullary collecting ducts (IMCD) and Bellini ducts (BD) with deposits of calcium phosphate in the form of apatite; epithelial cell injury and loss was marked. Plugged ducts were surrounded by interstitial fibrosis, but the fibrosis was generalized, as well, and was a main feature of the histopathology even when plugging was not present. In contrast, common idiopathic calcium oxalate stone formers (SF) never manifest intra-tubule crystals or interstitial fibrosis. Patients with brushite (calcium monohydrogen phosphate) stones and those with cystine stones have many fewer IMCD and BD plugged with apatite (or cystine, in cystinuria), and interstitial fibrosis is limited to the regions around plugged ducts. Patients with dRTA often present a radiographic picture of nephrocalcinosis. Our direct surgical observations reveal that these may be surgically removable stones, especially in patients with well preserved renal function. In all, dRTA SF have a more diffuse papillary renal disease than other SF thus studied, and are also unusual for the degree of interstitial fibrosis. To define the renal tissue changes in stone-forming patients with distal renal tubular acidosis (dRTA), we performed intra-operative papillary and cortical biopsies in five patients. The main abnormalities were plugging of inner medullary collecting ducts (IMCD) and Bellini ducts (BD) with deposits of calcium phosphate in the form of apatite; epithelial cell injury and loss was marked. Plugged ducts were surrounded by interstitial fibrosis, but the fibrosis was generalized, as well, and was a main feature of the histopathology even when plugging was not present. In contrast, common idiopathic calcium oxalate stone formers (SF) never manifest intra-tubule crystals or interstitial fibrosis. Patients with brushite (calcium monohydrogen phosphate) stones and those with cystine stones have many fewer IMCD and BD plugged with apatite (or cystine, in cystinuria), and interstitial fibrosis is limited to the regions around plugged ducts. Patients with dRTA often present a radiographic picture of nephrocalcinosis. Our direct surgical observations reveal that these may be surgically removable stones, especially in patients with well preserved renal function. In all, dRTA SF have a more diffuse papillary renal disease than other SF thus studied, and are also unusual for the degree of interstitial fibrosis. Elsewhere1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar we have described medullary and cortical pathology in the kidneys of patients who form brushite (BR, calcium monohydrogen phosphate) stones. In brief, inner medullary collecting ducts (IMCD) and ducts of Bellini (BD) are frequently plugged with masses of apatite crystal; plugged ducts are greatly enlarged and their epithelial cells destroyed. Around them, the interstitium is inflamed and fibrotic. In the cortex, nephron loss is clearly evident in comparison with normal controls. This picture differs radically from that of patients with idiopathic calcium oxalate (CaOx) stone disease (ICSF), who lack any evidence of cortical abnormalities, and whose sole medullary abnormalities are interstitial deposits of apatite, so-called Randall's plaque.2.Evan A.P. Lingeman J.E. Coe F.L. et al.Randall's plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle.J Clin Invest. 2003; 111: 607-616Crossref PubMed Scopus (495) Google Scholar We have found that fewer than half of calcium phosphate stones contain BR, the majority being apatite,3.Parks J.H. Worcester E.M. Coe F.L. et al.Clinical implications of abundant calcium phosphate in routinely analyzed kidney stones.Kidney Int. 2004; 66: 777-785Abstract Full Text Full Text PDF PubMed Scopus (186) Google Scholar but little is known about the renal pathology of apatite stone formers (SF). Some have the syndrome of distal renal tubular acidosis (dRTA), consisting of a non-anion gap metabolic acidosis accompanied by an alkaline urine pH that does not fall normally during an exogenous acid challenge, and by hypokalemia due to renal potassium losses.4.Karet F.E. Inherited distal renal tubular acidosis.J Am Soc Nephrol. 2002; 13: 2178-2184Crossref PubMed Scopus (150) Google Scholar Here we focus on apatite SF with the syndrome of dRTA. One might imagine that dRTA, being a specific form of renal dysfunction, would manifest a unique pathology of its own, but present information is less than complete. Prior studies of the pathology of dRTA have used cortical biopsy tissue,5.Feest T.G. Lockwood C.M. Morley A.R. Uff J.S. Renal histology and immunopathology in distal renal tubular acidosis.Clin Nephrol. 1978; 10: 187-190PubMed Google Scholar,6.Dietrichson O. Jorgensen F. Thomsen A.C. A light and electron microscopy study of the kidney in renal tubular acidosis.Acta Pathol Microbiol Scand Suppl. 1970; : 212Google Scholar whereas our work has found considerable medullary pathology in BR SF and one might expect the medulla to be involved in SF with dRTA, especially because radiographs commonly demonstrate medullary and papillary nephrocalcinosis. Here we present the surgical anatomy of dRTA and findings from intra-operative papillary, medullary, and cortical biopsies in five patients. As well, we attempt to correlate radiographic findings with surgical observations in order to improve clinical interpretation of renal calcifications found in this disease. All five patients formed at least one stone composed predominantly of apatite and no stones that contained BR (Table 1) except for one of 10 stones, with 4% BR, in patient 2. The other component of stones with less than 100% apatite was CaOx (Table 1). All had overt nephrocalcinosis. One patient with dRTA had known Sjogren syndrome (Table 1), and two presented with dRTA, nephrocalcinosis, or polyuria in childhood, suggesting one of the hereditary forms of the disease. None had overt hearing loss or knew of affected relatives with dRTA, although relatives did form stones. The remaining two patients presented in adulthood and the cause of their dRTA is completely unclear. As expected, all five dRTA patients had a low serum CO2 content (Table 2), one (patient 4) despite alkali treatment at the time of study. Low urine citrate7.Brodwall E.K. Westlie L. Myhre E. The renal excretion and tubular reabsorption of citric acid in renal tubular acidosis.Acta Med Scand. 1972; 192: 137-139Crossref PubMed Scopus (3) Google Scholar and high urine pH values were present (Table 2) despite the low serum CO2 content. Urine calcium excretions and volumes were generally high in all patients as expected.8.Worcester E.M. Parks J.H. Evan A.P. Coe F.L. Renal function in patients with nephrolithiasis.J Urol. 2006; 176: 600-603Abstract Full Text Full Text PDF PubMed Scopus (96) Google Scholar,9.Buckalew Jr, V.M. Purvis M.L. Shulman M.G. et al.Hereditary renal tubular acidosis. Report of a 64 member kindred with variable clinical expression including idiopathic hypercalciuria.Medicine (Baltimore). 1974; 53: 229-254Crossref PubMed Scopus (80) Google Scholar Stone culture revealed bacterial colonization in three patients (Table 2); urine culture was negative in two of the three (Table 1) and in patient 5 revealed only non-pathogenic Streptococci. In other words, stone cultures and urine cultures diverged markedly.Table 1Clinical characteristics of biopsied patientsCaseSexAge at first stoneSymptomatic stonesESWLPNLProceduresAge at biopsy% Apatite in stonesUTI1F43102/12/14398/100No2aSjogren's syndrome.F68>104/33/29/671100/92No3bBilateral biopsies.F4851/16/613/1350100/100No4cdRTA diagnosed at 6 weeks of age.M1933/28/417/1025100No5dPolyuria, polydipsia in infancy, nephrocalcinosis noted at age 8; urine at time of biopsy grew Enterococcus and Candida glabrata.F23204/26/24640/76YesESWL, extracorporeal shock wave lithotripsy before Bx (total/Bx side); F, female; M, male; PNL, percutaneous nephrolithotomy before Bx (total/Bx side); Procedures, total of all procedures before Bx (includes ESWL, PNL, ureteroscopy, open surgery, cystolithopaxy) (total/Bx side); % apatite, % apatite in first available analysis/% apatite in most recent analysis; Symptomatic stones, number of stones before biopsy (Bx); UTI, urinary tract infection with positive urine culture before biopsy.a Sjogren's syndrome.b Bilateral biopsies.c dRTA diagnosed at 6 weeks of age.d Polyuria, polydipsia in infancy, nephrocalcinosis noted at age 8; urine at time of biopsy grew Enterococcus and Candida glabrata. Open table in a new tab Table 2Selected laboratory data for biopsied patientsCaseSexSerum chemistries24-h urine chemistriesStone cultureCreat (mg/dl)Cl (mEq/l)CO2 mmol/lK (mEq/l)pHVolume (l/day)Citrate (mg/day)Ca/creat (mg/g)SSCaP1F1.0113203.86.842.40722911.4GpD Entercoccus2F1.8118184.16.743.301652950.9No growth3F1.9112193.86.301.6349810.4No growth4aCollected on potassium chloride supplement. Normal ranges for serum chemistries: chloride 90–105; total CO2 24–28.M0.9111233.56.974.462851521.1GpD Enterococcus5aCollected on potassium chloride supplement. Normal ranges for serum chemistries: chloride 90–105; total CO2 24–28.F1.9103223.56.694.652622300.9GpD Enterococcus Candida glabrataCreat, creatinine; F, female; M, male; SSCaP, supersaturation with respect to brushite.a Collected on potassium chloride supplement. Normal ranges for serum chemistries: chloride 90–105; total CO2 24–28. Open table in a new tab ESWL, extracorporeal shock wave lithotripsy before Bx (total/Bx side); F, female; M, male; PNL, percutaneous nephrolithotomy before Bx (total/Bx side); Procedures, total of all procedures before Bx (includes ESWL, PNL, ureteroscopy, open surgery, cystolithopaxy) (total/Bx side); % apatite, % apatite in first available analysis/% apatite in most recent analysis; Symptomatic stones, number of stones before biopsy (Bx); UTI, urinary tract infection with positive urine culture before biopsy. Creat, creatinine; F, female; M, male; SSCaP, supersaturation with respect to brushite. The radiographic renal calcifications seen in patient 4 (Figure 1a) are similar to those typically described in patients with dRTA: bilateral, extensive, nodular, and overlying all the regions of the renal medulla and papillae. Viewed directly (Figure 1c), these calcifications were mainly non-attached intra-calyceal stones amenable to surgical removal. Postoperative radiographs reveal only scattered, fine calcifications (Figure 1b). At second look nephroscopy (Figure 1d) these residual calcifications were not stones but were, rather, within the renal tissue. More detailed analysis of biopsied tissue using micro computed tomography (CT) (Figure 1e) reveals that the tissue calcifications were intra-luminal. Light microscopy (Figure 1f) of these tissues confirms that deposits are indeed within IMCD and BD, as we have found in BR nephropathy.1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar By contrast, in a radiograph taken after removal of all surgically accessible stones from patient 3 (Figure 2a) extensive and bilateral renal calcifications remain. At second-look nephroscopy, the calcifications are very extensive and appear mainly within renal tissue (Figure 2b), an impression confirmed by micro-CT analysis (Figure 2c) and light microscopy (Figure 2d). The papillae themselves are uniformly retracted; their surfaces are marked by large pits. No recognizable anatomical landmarks or features remain. The right upper pole stones could not be accessed surgically. The surgical pathology varied from minimal disease (Figure 3a and b) in patient 1 (Tables 1 and 2) to extreme damage (Figures 2b and 3d, patient 3), with intervening levels of disease (Figure 3c, patient 4). At worst (Figures 2b and 3d), the papilla is retracted; its surface is pitted and has a whitish thickened membrane appearance. Some pitted areas represent dilated BD, frequently with mineral plugs protruding from their mouths. In patient 1 (Figure 3a and b), the protruding mineral deposit is particularly clear because the remainder of the papilla is relatively normal. Yellow plaque, which we1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar have shown is plugs of mineral in IMCD and BD, was abundant (Figure 3c) in all but patient 1. Of interest, white plaque, which represents interstitial apatite crystal deposition,10.Evan A. Lingeman J. Coe F.L. Worcester E. Randall's plaque: pathogenesis and role in calcium oxalate nephrolithiasis.Kidney Int. 2006; 69: 1313-1318Abstract Full Text Full Text PDF PubMed Scopus (152) Google Scholar was almost never encountered. Often, we encountered sub-surface densities and upon incising the overlying tissue with a laser discovered tiny (1–2 mm) irregularly shaped stones lying in a cavity and easily dislodged (Figure 4a). A biopsy through one of these areas, viewed by micro-CT (Figure 4b), shows the stone isolated in tissue and surrounded by tiny foci of mineral that are presumably in tubules. In our patient (patient 1) with the most minimal gross morphological changes, biopsy and micro-CT revealed mineral deposits (Figure 5a with insert) in a few scattered IMCD lumens; by fourier transform infrared (FTIR) the mineral was apatite. A higher magnification of one of the sites of IMCD mineral deposition reveals extensive interstitial fibrosis and loss of epithelial cells in the plugged IMCD (Figure 5b). The fibrosis extends beyond the immediate vicinity of the plugged IMCD and surrounds tubules without deposits. Many of these tubules show cell atrophy even though they contain no crystals. In a patient with more advanced gross morphological abnormalities (patient 4), the tissue is diffusely involved with IMCD and BD plugging (Figure 5c with insert); plugged tubules have lost their cells and are surrounded by severe interstitial fibrosis (Figure 5d). It is difficult to find normal tubular profiles, so extensive is the damage (Figure 5e and f). Not shown here, the tissue was so difficult to section because of the massive nature of the mineral deposits that the most involved tissues could not be studied microscopically. In patient 5 we found adjacent tubules filled with mixed birefringent and non-birefringent mineral suggesting a mixture of calcium phosphate and CaOx (Figure 6a and b). By FTIR we documented apatite as the primary mineral, with a trace of CaOx (<5%). This is the only instance of a mixed crystal plug in the present series and the only instance we have thus far observed in human tissue. This is the one patient with dRTA who formed mixed apatite and CaOx stones. In the five dRTA patients (Table 3) cortical findings varied from mild to advanced glomerular disease; interstitial changes were mild in all cases. Regions of chronic inflammation were noted with lymphoid infiltrate. The apatite SF with the most severe papillary disease had mild glomerular and interstitial changes.Table 3Papillary and cortical pathology in dRTA stone formersCasePapillary pathologyGlomeruli numberGlomerular pathologyTubular atrophyInterstitial fibrosisGrossDepositsFibrosisMildModerateGlobal111212220222322300311333380131142229032115333940211dRTA, distal renal tubular acidosis.Numbers show grading from 0–3 (detailed in Materials and Methods). Open table in a new tab dRTA, distal renal tubular acidosis. Numbers show grading from 0–3 (detailed in Materials and Methods). In a crude sense, serum creatinine reflects the degree of renal pathology in that it was elevated in patients 2, 3, and 5 (Table 2) who had the most damaged kidneys (Table 3). On the other hand, patient 4 had a normal serum creatinine and more normal gross papillary morphology than 2, 3, and 5, but histopathology revealed significant IMCD and BD damage with crystal deposits. It was apparent to us in doing percutaneous nephrolithotomy (PNL) in these dRTA patients that most of the calcifications visible on radiographs represent surgically removable stones (nephroliths) rather than calcifications within renal tissue itself (nephrocalcinosis). Given our findings, one may expect PNL to reduce stone burden most in dRTA patients with normal renal function and progressively less in those with significant reduction of renal function. On the other hand, because these patients have been subjected to many surgical procedures and the stone material they harbor is frequently infected, PNL may well be indicated to remove infected material as completely as possible. Urine culture was a poor predictor of stone culture in our patients. A long-term outcome study of surgical procedures in dRTA patients is much needed. As in BR SF, these five dRTA SF had variable plugging of IMCD and BD with surrounding interstitial fibrosis and inflammation and accompanying modest cortical changes. Compared with dRTA, BR SF had fewer plugged IMCD, but plugged IMCD and BD were much more grossly dilated. On the other hand, the papillary renal tissue in dRTA is diffusely involved with fibrosis, whereas BR SF have a more focal renal papillary disease. In BR SF we find fibrosis only around IMCD and BD filled with crystal. In dRTA we find fibrosis around otherwise normal IMCD and BD. Despite this distinction concerning the renal papillum, cortical involvement in the two diseases is not very different, being moderate and involving some nephron loss. The reason for this dissociation between papillary and cortical interstitial fibrosis in dRTA vs BR SF is unclear. In passing, we note that white plaque (interstitial deposits of apatite) was extremely sparse in dRTA, whereas it was abundant in BR SF. Possibly the polyuria of dRTA reduced white plaque production.11.Kuo R.L. Lingeman J.E. Evan A.P. et al.Urine calcium and volume predict coverage of renal papilla by Randall's plaque.Kidney Int. 2003; 64: 2150-2154Abstract Full Text Full Text PDF PubMed Scopus (144) Google Scholar In hereditary forms of dRTA the initial lesion is by definition diffuse, acidification is abnormal in all nephrons, systemic acidosis occurs early, and apatite deposits can form in all tubules because of an abnormally high tubule fluid pH.4.Karet F.E. Inherited distal renal tubular acidosis.J Am Soc Nephrol. 2002; 13: 2178-2184Crossref PubMed Scopus (150) Google Scholar This would give the diffuse picture we find. In diseases like Sjogren syndrome12.Aasarod K. Haga H.J. Berg K.J. et al.Renal involvement in primary Sjogren's syndrome.Q J Med. 2000; 93: 297-304Crossref Scopus (71) Google Scholar,13.Cohen E.P. Bastani B. Cohen M.R. et al.Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosis.J Am Soc Nephrol. 1992; 3: 264-271PubMed Google Scholar and systemic lupus erythematosus,14.Caruana R.J. Barish C.F. Buckalew Jr, V.M. Complete distal renal tubular acidosis in systemic lupus: clinical and laboratory findings.Am J Kidney Dis. 1985; 6: 59-63Abstract Full Text PDF PubMed Scopus (14) Google Scholar immune-mediated loss of proton regulation would also lead to diffuse disease. In other patients (patients 1 and 3), marked hypercalciuria could have caused widespread crystallizations in tubules, and lead to so diffuse an involvement that dRTA occurred;9.Buckalew Jr, V.M. Purvis M.L. Shulman M.G. et al.Hereditary renal tubular acidosis. Report of a 64 member kindred with variable clinical expression including idiopathic hypercalciuria.Medicine (Baltimore). 1974; 53: 229-254Crossref PubMed Scopus (80) Google Scholar this speculation requires further study. Possibly these two patients may have an immune or inherited cause for their dRTA that is not yet apparent; Sjogren syndrome may follow onset of dRTA by years15.Eriksson P. Denneberg T. Enestrom S. et al.Urolithiasis and distal renal tubular acidosis preceding primary Sjogren's syndrome: a retrospective study 5–53 years after the presentation of urolithiasis.J Intern Med. 1996; 239: 483-488Crossref PubMed Scopus (34) Google Scholar and autosomal dominant dRTA may present in later life.4.Karet F.E. Inherited distal renal tubular acidosis.J Am Soc Nephrol. 2002; 13: 2178-2184Crossref PubMed Scopus (150) Google Scholar We are not the first to study the renal tissues of patients with dRTA, but all prior studies used cortical tissue. In two patients with apparent late onset of dRTA (ages 49 and 62) Dietrichson et al.6.Dietrichson O. Jorgensen F. Thomsen A.C. A light and electron microscopy study of the kidney in renal tubular acidosis.Acta Pathol Microbiol Scand Suppl. 1970; : 212Google Scholar found no changes in one (49 years old) and in the other minimal changes, including tubular atrophy and calcification, plasma cell interstitial infiltrate, and glomerular obsolescence. This patient had an increased blood gamma globulin level and may have had an immune disorder. In cortical biopsies from 10 patients with dRTA Feest et al.5.Feest T.G. Lockwood C.M. Morley A.R. Uff J.S. Renal histology and immunopathology in distal renal tubular acidosis.Clin Nephrol. 1978; 10: 187-190PubMed Google Scholar found seven with immune disease, and three without. Among the former, glomerular sclerosis and tubular atrophy were prominent; in five who had nephrocalcinosis, interstitial fibrosis was prominent. Among the other three, biopsies described tubular atrophy and glomerular loss, along with lymphoid infiltration. Pasternack and Linder16.Pasternack A. Linder E. Renal tubular acidosis: an immunopathological study on four patients.Clin Exp Immunol. 1970; 7: 115-123PubMed Google Scholar looking at four patients found mononuclear interstitial infiltrates around distal tubules. One of the patients showed many hyalinized glomeruli with tubular atrophy and interstitial fibrosis, and modest intra-tubular calcium deposits. One large study17.Orfila C. Rakotoarivony J. Durand D. Suc J.M. A correlative study of immunofluorescence, electron, and light microscopy in immunologically mediated renal tubular disease in man.Nephron. 1979; 23: 14-22Crossref PubMed Scopus (15) Google Scholar of 49 patients with immunologically mediated renal diseases describes renal ultrastructural changes, but does not specifically mention dRTA. Several studies of dRTA from Sjogren syndrome have documented complete loss of intercalated cell staining for the proton ATPase.13.Cohen E.P. Bastani B. Cohen M.R. et al.Absence of H(+)-ATPase in cortical collecting tubules of a patient with Sjogren's syndrome and distal renal tubular acidosis.J Am Soc Nephrol. 1992; 3: 264-271PubMed Google Scholar, 18.Bastani B. Haragsim L. Gluck S. Siamopoulos K.C. Lack of H-ATPase in distal nephron causing hypokalaemic distal RTA in a patient with Sjogren's syndrome.Nephrol Dial Transplant. 1995; 10: 908-909PubMed Google Scholar, 19.DeFranco P.E. Haragsim L. Schmitz P.G. Bastani B. Absence of vacuolar H(+)-ATPase pump in the collecting duct of a patient with hypokalemic distal renal tubular acidosis and Sjogren's syndrome.J Am Soc Nephrol. 1995; 6: 295-301PubMed Google Scholar Absence of staining was also shown in a single patient with Sjogren syndrome but also in another with dRTA of unspecified cause.20.Joo K.W. Jeon U.S. Han J.S. et al.Absence of H(+)-ATPase in the intercalated cells of renal tissues in classic distal renal tubular acidosis.Clin Nephrol. 1998; 49: 226-231PubMed Google Scholar Among five biopsied patients with stones and dRTA who eventually went on to manifest Sjogren syndrome, interstitial fibrosis was the most prominent feature.15.Eriksson P. Denneberg T. Enestrom S. et al.Urolithiasis and distal renal tubular acidosis preceding primary Sjogren's syndrome: a retrospective study 5–53 years after the presentation of urolithiasis.J Intern Med. 1996; 239: 483-488Crossref PubMed Scopus (34) Google Scholar All five had positive anti-Sjogrew's Syndrome-A (SS-A) antibodies at the time of biopsy. As expected, the intercalated cells of one patient with autosomal dominant dRTA due to loss of chloride-bicarbonate anion exchanger (AE1) did not contain detectable AE121.Shayakul C. Jarolim P. Zachlederova M. et al.Characterization of a highly polymorphic marker adjacent to the SLC4A1 gene and of kidney immunostaining in a family with distal renal tubular acidosis.Nephrol Dial Transplant. 2004; 19: 371-379Crossref PubMed Scopus (25) Google Scholar upon immunostaining. We must emphasize that our present work is not directly comparable with these past studies, because we present biopsies from the inner medulla and papillum. As well, we have made no attempt in our one Sjogren case to document the well-established loss of the proton ATPase. We do not know the genetic basis for dRTA in any of our cases, and have made no attempt to study possible transporter defects directly. Our main goal was to study the calcifications and cell injuries in this condition and contrast them with other SF. In this, we have found, as noted, a rather different picture from that of BR nephropathy, which, at least for the present, we consider specific to dRTA. We studied all five patients who formed apatite stones (>50% apatite), had dRTA, and required PNL at this institution during the past 6 years and who consented to participate in the study (Table 1). Patients were not otherwise selected. Clinical history was obtained directly, along with reviews of old records. Radiographs were evaluated by us. Two 24-h urine collections were obtained from each patient and blood was drawn for routine measurements. Measurements were as described elsewhere.1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar Renal papillae were imaged and biopsied during PNL as detailed elsewhere.1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar Unlike some past studies, we did not attempt to quantify surface coverage with plaque. We graded the degree of gross papillary changes from 0 to 3: 0, no abnormalities; 1, minimal yellow plaque and dilated BD openings; 2, diffuse yellow plaque, dilated BD openings, and retraction; 3, diffuse yellow plaque, dilated BD openings, retraction, pitting, and erosion of urothelium. Twenty-six papillary and five cortical biopsies were studied using light and transmission microscopy. Tissue was prepared and studied as described elsewhere.1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar, 2.Evan A.P. Lingeman J.E. Coe F.L. et al.Randall's plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle.J Clin Invest. 2003; 111: 607-616Crossref PubMed Scopus (495) Google Scholar, 22.Evan A.P. Coe F.L. Lingeman J.E. et al.Renal crystal deposits and histopathology in patients with cystine stones.Kidney Int. 2006; 69: 2227-2235Abstract Full Text Full Text PDF PubMed Scopus (104) Google Scholar Cortical biopsies were graded for pathology as in past studies.1.Evan A.P. Lingeman J.E. Coe F.L. et al.Crystal-associated nephropathy in patients with brushite nephrolithiasis.Kidney Int. 2005; 67: 576-591Abstract Full Text Full Text PDF PubMed Scopus (149) Google Scholar,22.Evan A.P. Coe F.L. Lingeman J.E. et al.Renal crystal deposits and histopathology in patients with cystine stones.Kidney Int. 2006; 69: 2227-2235Abstract Full Text Full Text PDF PubMed Scopus (104) Google Scholar Glomerular sclerosis was defined as increased mesangial matrix with or without wrinkling, thickening or collapse of glomerular basement membranes. Sclerosis of individual glomerulae was scored as segmental (<25%, mild; 25–75%, moderate) or global (>75%, severe or total obsolescence). Micro-CT studies were accomplished as we have described for cystine stone disease.22.Evan A.P. Coe F.L. Lingeman J.E. et al.Renal crystal deposits and histopathology in patients with cystine stones.Kidney Int. 2006; 69: 2227-2235Abstract Full Text Full Text PDF PubMed Scopus (104) Google Scholar We graded papillary histopathological changes from 0 to 3 in relation to deposits and fibrosis. For deposits: 0, none; 1, scattered small IMCD and BD deposits; 2, half of tubules involved; 3, over half of tubules involved. For fibrosis: 0, none; 1, limited to immediate vicinity of IMCD with deposit; 2, fibrosis surrounds IMCD lacking deposits; 3, diffuse, involves all tubules." @default.
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• W2068579384 title "Renal histopathology of stone-forming patients with distal renal tubular acidosis" @default.
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