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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE  
Year : 2013  |  Volume : 24  |  Issue : 5  |  Page : 942-949
Peritubular capillaries and renal function in pediatric idiopathic nephrotic syndrome


Department of Pathology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, India

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Date of Web Publication12-Sep-2013
 

   Abstract 

Nephrotic syndrome (NS) is a common renal disorder with significant tubulo-interstitial damage due to the combined effects of proteinuria and obstruction of efferent blood flow. Peritubular capillary (PTC) loss has also been correlated with interstitial fibrosis. This study included 30 pediatric cases of idiopathic NS. Clinical details, including biochemical parameters, were recorded and renal biopsy slides were reviewed for histological features. PTCs were highlighted using anti-CD34 antibody and quantified with the help of image analysis software. Postmortem kidney biopsies from seven children were taken as controls for quantification of PTCs and interstitial fibrosis. Wherever possible, as ultrastructural examination of the renal biopsy was performed. Appropriate statistical methods were applied. Patients with minimal change disease (MCD) had lower serum creatinine as compared with those with focal and segmental glomerulosclerosis (FSGS). Similarly, tubular atrophy and interstitial fibrosis were significantly lower in MCD than in FSGS. PTC density was lower in all groups of NS as compared with the controls. Biopsies with FSGS had a lower PTC density compared with both MCD and mesangioproliferative glomerulonephritis. PTC density showed a negative correlation with serum creatinine and degree of proteinuria. PTC loss appears to play an important role in the development of renal biopsy changes in pediatric NS. This aspect of the renal vasculature requires further study in idiopathic NS.

How to cite this article:
Singh K, Ray R, Sharma A, Gupta R, Bagga A, Dinda AK. Peritubular capillaries and renal function in pediatric idiopathic nephrotic syndrome. Saudi J Kidney Dis Transpl 2013;24:942-9

How to cite this URL:
Singh K, Ray R, Sharma A, Gupta R, Bagga A, Dinda AK. Peritubular capillaries and renal function in pediatric idiopathic nephrotic syndrome. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2019 Nov 14];24:942-9. Available from: http://www.sjkdt.org/text.asp?2013/24/5/942/118091

   Introduction Top


Nephrotic syndrome (NS) is a common and extremely important renal disease affecting both pediatric and adult patients. Among the primary glomerular diseases, minimal change disease (MCD) has been shown to be the most common in children aged below eight years, while focal and segmental glomerulosclerosis (FSGS) is frequent beyond eight years of age. [1] The prognosis of NS is determined by clinical as well as pathological features. Among the latter, tubulo-interstitial changes are the prime prognostic factors. [2] Tubulo-interstitial fibrosis develops due to the effects of proteinuria as well as global glomerulosclerosis. [3] Loss of peritubular capillaries (PTCs) has been shown to be related to tubulo-interstitial hypoxia, leading to fibrosis and tubular atrophy. [4] Previous studies have demonstrated normal PTC flow in MCD with intact tubulo-interstitium, while FSGS showed severe reduction in PTC flow. [5]

Ultrastructural analysis of PTCs exclusively in children with NS has not been reported in the available literature. One study evaluated the PTC structure in renal allograft biopsies and native kidney biopsies. This study demonstrated PTC reduplication in one case of MCD while no ultrastructural changes in PTC were seen in FSGS. [6]

This prospective clinico-pathologic study evaluated the loss of PTCs in pediatric idiopathic NS along with an analysis of the ultrastructural changes in these capillaries.


   Materials and Methods Top


This was a prospective, clinico-pathological study carried out over a period of 1.5 years.

Patient selection

A total of 52 pediatric cases with idiopathic NS according to the International Study of Kidney Diseases in Children (ISKDC) criteria [7] who underwent percutaneous renal biopsy were included in the study. Children with secondary causes of nephritic-range proteinuria were excluded. Of the 52 patients selected, 22 patients had to be excluded due to limited tissue in renal biopsy. Hence, a total of 30 cases were finally selected and included in the study.

Clinico-laboratory data

Detailed clinical information was recorded, including age at onset of idiopathic NS, duration of illness till presentation, gender, anthropometry (height and weight) and presenting complaints like edema, hypertension, urinary output and hematuria. Biochemical parameters, including serum investigations (proteins, albumin, albumin/globulin ratio, creatinine, cholesterol) and degree of 24-h urinary protein excretion were noted. Glomerular filtration rate (GFR) was calculated using the Schwartz' formula, where GFR = 0.55 × height in centimeter × (serum creatinine in mg/dL) -[1] . The correction factor was changed for infants to 0.45, and was 0.7 for adolescent males.

Renal biopsy

All 30 patients underwent percutaneous renal biopsy after informed written consent. The biopsy samples were processed using standard protocols for light microscopy, immunofluorescence and electron microscopic examinations. For light microscopy, hematoxylin and eosin (H&E), periodic acid Schiff (PAS), silver methenamine (SM) and Masson's trichrome (MT) stains were performed. Immunofluorescence was performed for IgA, IgG, IgM and C3 on frozen sections. Renal biopsies with at least five glomeruli in the light microscopic section were considered as adequate. The histological diagnosis was made according to the standard definitions. [8] The degree of tubular atrophy was evaluated as proposed by Pirani et al. [9] The histological findings were evaluated by three pathologists (KS, RR, AKD) in a blinded fashion with no prior knowledge of the clinical and biochemical features.

Morphometric evaluation

Immunohistochemistry for CD34 (Dako Cytomation, Denmark) was performed on paraffinembedded renal biopsy sections using the streptavidin-biotin-peroxidase method with 3',3'-diaminobenzidine as the chromogen. The CD34-stained sections were examined for identification of PTCs. Digital images of renal cortical area in the entire biopsy were captured at 20× magnification using a research microscope (BX-50, Olympus, Japan) fitted with a digital camera (CoolSnap, Photometrics, Tuscon, AZ, USA). Image ProPlus software (Media Cybernetics, Rockville, MD, USA) was used to count the cortical PTCs as per the published guidelines in previous studies. [10] The total number of PTCs and the number of fields were counted in a blinded manner with no prior information about the histological findings [Figure 1]a. The number of PTCs in each field was calculated by dividing the total number of PTC with the number of fields captured. PTC density was then calculated by multiplying the number of PTCs with 0.7758 mm 2 (area of field captured under 20× objective and 10× objective).
Figure 1: A panel of photomicrographs demonstrating the methodology of PTC quantification by image analysis software (a). CD34-stained capillary cross-sections in a control case (b, ×100), a patient with minimal change disease (c, ×100) and focal segmental glomerulosclerosis (d, ×100).

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Interstitial fibrosis was quantitated using the MT-stained section of renal biopsy. The entire kidney biopsy section was digitally captured using the same technique as for PTCs. Interstitial fibrosis was selected using the Image ProPlus software. The total area of the field was calculated and the percentage of interstitial fibrosis computed by dividing the area of fibrosis with the total area of the field.

For comparison of PTC density and interstitial fibrosis quantification, renal biopsy taken at the postmortem examination of seven children with an age range of 5-18 years was taken. The cause of death in all these seven cases was trauma. The renal tissue was obtained and fixed within 2-5 h after death.

Ultrastructural examination

Ultrathin sections of glutaraldehyde-fixed renal biopsy tissues were stained with uranyl acetate- lead citrate and examined using an electron microscope. The following features of PTCs were assessed: Number and contour, endothelial cell characteristics and basement membrane changes of the capillaries (thinning and splitting).


   Statistical Analysis Top


Data were expressed as mean with standard deviation, median with range and percentage. Non-parametric tests: Kruskal-Wallis test, Mann-Whitney test and Spearman corelation employed as parametric assumptions were not met. P <0.05 was considered significant. SPSS statistical software was used for the statistical analysis.


   Results Top


The 30 cases included in the study comprised 13 patients with MCD, ten patients with FSGS and seven patients with mesangioproliferative glomerulonephritis (mesPGN, non-IgA).

Clinical features

There was a male predominance (19 males, 11 females; M:F 1.7:1). The M:F ratio was highest in FSGS (9:1) compared with that in mesPGN (0.4). The median age in the three groups was 6, 7 and 7.5 years in MCD, mesPGN and FSGS, respectively, with no statistical difference. The median age in the controls was eight years. The duration of illness was similar in all the three groups (eight months in MCD, nine months in mesPGN and ten months in FSGS). No significant difference was found between the groups with regard to duration of illness. Edema was the most frequent clinical symptom, followed by hematuria and hypertension.

The NS was classified as steroid resistant (SRNS) in 67% of the cases, frequently relapsing in 23% of the patients and steroid dependent in 10% of the patients.

Biochemical parameters

All patients had hypoproteinemia and hypo-albuminemia (mean serum protein 5.04 ± 0.72 g/dL; serum albumin 0.98 ± 0.42 g/dL). The mean 24-h urinary protein excretion was 3.53 ± 2.26 g/24-h in these patients. Hypercho-lesterolemia (serum cholesterol >250 mg/dL) was demonstrated in 28 of 30 cases.

Renal function was assessed by serum creatinine and calculation of GFR. The mean serum creatinine was 0.86 ± 0.6 mg/dL, ranging from 0.67 ± 0.33 mg/dL in MCD to 0.64 ± 0.24 mg/dL in mesPGN and 1.25 ± 0.93 mg/dL in FSGS. The difference in serum creatinine between MCD and FSGS was statistically significant (P = 0.012). The calculated GFR in these patients ranged from 102.22 ± 26.82 mL/min in MCD to 95.6 ± 24.38 in mesPGN and 76.76 ± 38.81 in FSGS. The difference in GFR between the three groups was not statistically significant.

Renal histologic features

The degree of tubular atrophy was absent to minimal in patients with MCD (0 in nine cases, 0.5 in three cases and 1 in one case). In the mesPGN group, three patients had no tubular atrophy while two patients had grade 0.5 atrophy, one each had grade 1 and grade 4 tubular atrophy. In comparison, only one renal biopsy in the FSGS group had grade 0 tubular atrophy. Two biopsies showed 0.5+ atrophy, four had grade 1, two grade 2 and one grade 4 tubular atrophy. The degree of tubular atrophy was significantly higher in the FSGS compared with the MCD group (P = 0.001). However, the difference between MCD and mesPGN ( P = 0.112) as well as that between FSGS and mesPGN (P = 0.113) was not significant.

Immunofluorescence showed mesangial IgM deposits in 21 of 30 cases, while the remaining nine cases showed absence of deposits. None of the renal biopsies showed any staining for IgA, IgG or C3.

Morphometric analysis

PTC density in the control biopsies was 604.26 ± 16.49 per mm 2 [Figure 1]b. In comparison, biopsies with MCD had PTC density of 539.9 3 ± 54.89 [Figure 1]c while mesPGN showed PTC density of 563.9 ± 54.58 per mm 2 . Biopsies with FSGS showed capillary density of 460.65 ± 53.32 per mm 2 [Figure 1]d. On statistical analysis, PTC density was lower in the MCD (P = 0.019) and FSGS (P = 0.001) groups compared with the control group.

Comparison between the groups of NS revealed a significant difference in PTC density between MCD and FSGS (P = 0.005) and between mesPGN and FSGS (P = 0.003). The difference between MCD and mesPGN was not significant (P = 0.498).

The mean percentage of interstitial fibrosis [Figure 2]a and b ranged from 7.25 ± 2.3 in MCD to 7.73 ± 3.67 in mesPGN and 16.63 ± 6.0 in FSGS group. On statistical analysis, the interstitial matrix was more in MCD (P = 0.043) and FSGS (P = 0.005) compared with that in the control biopsies. Between the groups of NS, interstitial fibrosis was significantly higher in FSGS compared with MCD (P = 0.002) and mesPGN (P = 0.003).
Figure 2. Masson's trichrome-stained section highlighting the interstitial fibrosis (a, ×200) with quantification by image analysis software (b).

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Correlation was attempted between PTC density and renal function. A negative correlation was observed between PTC density and serum creatinine (Spearman's correlation P = 0.027) and degree of proteinuria (P = 0.048) in our cases. On the other hand, GFR showed a positive correlation with PTC density (Spearman's rho, P = 0.038). Tubular atrophy was inversely related to PTC density (P = 0.039). Although interstitial fibrosis showed an inverse association with PTC density, the association did not reach statistical significance (P = 0.102).

Ultrastructural features

Electron microscopic features could be evaluated in ten cases of MCD, five cases of mesPGN and ten cases of FSGS. Five cases could not be evaluated due to the presence of medulla in two biopsies and poor preservation in three biopsies. The number of PTCs studied in each case varied from one to three.

In biopsies with MCD and mesPGN, the PTC contour was normal [Figure 3]a. The endothelial luminal surface showed normal cytoplasmic projections. Focal accumulation of pinocytotic vesicles was seen. Basal lamina thickness varied from 0.5 to 1.5 μm. No splitting or multilayering of basement membrane was seen [Figure 3]b.
Figure 3. Electron micrographs showing a peritubular capillary with normal basal lamina in a control case (a, ×35000). A case of minimal change disease with normal appearing basal lamina (b, ×71000). A case of focal segmental glomerulosclerosis demonstrating abnormal contour of peritubular capillary (c, ×18000) and double-layered basal lamina (d, ×44000).

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The luminal contour of PTCs was distorted [Figure 3]c. Endothelial cell thickness was highly variable with normal fenestrations and focal serration of abluminal border. Pinocytotic vesicles were clustered at places, along with lipid vacuoles. The basal lamina thickness varied from 0.5 to 3.5 μm. Splitting and multi-layering of the basal lamina was seen in three of ten cases [Figure 3]d.


   Discussion Top


NS is a clinico-pathological entity comprising nephrotic range proteinuria (>40 mg/m 2 / hr), hypoalbuminemia (serum albumin <2.5 g/dL in children) and peripheral edema. The causes of NS include both primary and secondary glomerular diseases. A study by Gulati et al in 2006 showed MCD to be the most common pathologic diagnosis in children with NS aged below eight years, while FSGS was most frequent in those aged above beyond eight years. [1] Several reports since 1999 have suggested that the incidence of FSGS may be increasing in children and adults. [11] The prognosis of NS in children depends on the clinical as well as the pathologic features. Among the latter, interstitial fibrosis has been shown to correlate with serum creatinine at presentation and predict end-stage renal disease. [2] The development of tubulo-interstitial changes has been attributed to the combined effects of proteinuria (tubular uptake of filtered proteins or toxins and macrophage recruitment) and obstruction of efferent blood flow by global glomerulosclerosis. [3] Recent studies have demonstrated that injury and loss of PTCs lead to tubulo-interstitial cellular hypoxia, and this correlates with fibrosis and tubular atrophy. [4],[12] The significance of loss of PTCs has been shown in rat models of obstructive nephropathy, glomerulonephritis and chronic kidney disease. [13],[14],[15] Similar results have also been demonstrated in human studies in ischemic renal failure, IgA nephropathy and chronic allograft nephropathy. [16],[17],[18] Earlier studies evaluating PTCs employed 1-μm semithin sections stained with silver. [19] Seron et al, in 1990, utilized endothelial immunostaining to identify PTCs and showed the correlation of number of capillary cross-sections with plasma creatinine and GFR. [10] In a study by Saowanee et al, an inverse correlation of PTC flow and relative area of renal cortical interstitium was found. [20] An elegant study by Futrakul et al in 2000 showed the presence of normal PTC flow in MCD with an intact tubulo-interstitial structure. A substantial reduction in PTC flow seen in steroid-resistant mesPGN correlated with mild interstitial fibrosis, while severe reduction in flow associated with FSGS was denoted with a higher frequency of tubulo-interstitial fibrosis. [5] In the present study, we found a lower PTC density in MCD and FSGS compared with the controls. In addition, FSGS showed a significantly lower PTC density than both MCD and mesPGN. The degree of tubular atrophy was inversely correlated with PTC density. These findings represent a histological correlate of the previous studies evaluating PTC flow and suggest an association between tubulo-interstitial changes and PTC density in the cortical interstitium. Correlation of PTC density with clinical parameters revealed a negative correlation with serum creatinine and a positive association with GFR. However, few questions remain unanswered: Is significant PTC loss early in FSGS? Is this PTC loss responsible for tubulo-interstitial insult in FSGS? These can be answered only with follow-up biopsies. A clinical study in 2004 showed that therapy with vasodilators like angiotensin II receptor antagonists, angiotensin converting enzyme inhibitors and calcium channel blockers lead to reduction in efferent arteriolar resistance and increase in PTC flow and GFR in patients with FSGS. [21] These results suggest that correction of hemodynamic maladjustment may prevent renal disease progression in FSGS. However, a histopathologic demonstration of the effect of this vasodilation on interstitial changes has not been performed till date.

An ultrastructural study of PTC exclusively in children with NS has not been reported in the published literature. PTC structure has been evaluated in renal transplant patients along

with native kidney biopsies. In their study, PTC reduplication was seen in only one case of MCD and no change was seen in FSGS. [6] In contrast, PTC reduplication was noted in three cases of FSGS in our study. The basal lamina thickness was also increased. Biopsies with MCD and mesPGN did not reveal PTC reduplication. This reduplication was identified as a characteristic ultrastructural feature of renal allografts with transplant glomerulopathy. [22] Endothelial injury with release of mitogenic peptide, endothelin-1, has been implicated in the pathogenesis of PTC reduplication. [23] A study in a rat model of remnant kidney showed that administration of vascular endothelial growth factor (VEGF) led to a decrease in the PTC rarefaction and less interstitial type III collagen. The authors thus concluded that VEGF treatment reduced renal fibrosis and stabilized renal function in a remnant kidney model. [24] Such a therapeutic effect needs to be explored in nephrotic syndrome patients.

In conclusion, the present study reiterates the loss of PTCs in the renal cortical tissue of children with nephrotic syndrome, especially biopsies showing focal segmental glomerulosclerosis. This loss correlated with GFR, serum creatinine, degree of interstitial fibrosis and tubular atrophy. In addition, this study demonstrates prominent ultrastructural changes in PTC in NS. Thus, these results highlight the importance of an intact PTC network in pediatric NS.

 
   References Top

1.Gulati S, Sengupta D, Sharma RK, et al. Steroid resistant nephrotic syndrome: Role of histopathology. Indian Pediatr 2006;43:55-60.  Back to cited text no. 1
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2.Wehrmann M, Bohle A, Held H, Schumm G, Kendziorra H, Pressler H. Long term prognosis of focal sclerosing glomerulonephritis: An analysis of 250 cases with particular regard to tubulo-interstitial changes. Clin Nephrol 1990; 33:115-22.  Back to cited text no. 2
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3.Eddy AA. Molecular basis of renal fibrosis. Pediatr Nephrol 2000;15:290-301.  Back to cited text no. 3
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4.Norman JJ, Fine LG. Intrarenal oxygenation in chronic renal failure. Clin Exp Pharmacol Physiol 2006;33:989-96.  Back to cited text no. 4
    
5.Futrakul N, Yenrudi S, Sensirivatana R, et al. Peritubular capillary flow determines tubulointerstitial disease in idiopathic nephrotic syndrome. Ren Fail 2000;22:329-35.  Back to cited text no. 5
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6.Gough J, Yilmaz A, Miskulin D, et al. Peritubular capillary basement membrane reduplication in allografts and native kidney disease: A clinicopathologic study of 278 consecutive renal specimens. Transplantation 2001;71: 1390-3.  Back to cited text no. 6
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7.Primary nephrotic syndrome in children: clinical significance of histopathologic variants of minimal change and of diffuse mesangial hypercellularity. A Report of the International Study of Kidney Disease in Children. Kidney Int 1981;20:765-71.  Back to cited text no. 7
    
8.Churg J, Habib R, White RH. Pathology of the nephrotic syndrome in children: A report for the International Study of Kidney Disease in Children. Lancet 1970;760:1299-302.  Back to cited text no. 8
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9.Pirani CL, Pollack VE, Schwartz FD. The reproducibility of semi-quantative analysis of renal histology. Nephron 1964;29:230-7.  Back to cited text no. 9
    
10.Seron D, Alexopoulos E, Raftery MJ, Hartley B, Cameron JS. Number of interstitial capillary cross-sections assessed by monoclonal antibodies: Relation to interstitial damage. Nephrol Dial Transplant 1990;5:889-93.  Back to cited text no. 10
    
11.Srivastava T, Simon SD, Alon US. High incidence of focal segmental glomerulosclerosis in nephrotic syndrome of childhood. Pediatr Nephrol 1999;13:13-8.  Back to cited text no. 11
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12.Choi YJ, Chakraborty S, Nguyen V, et al. Peritubular capillary loss is associated with chronic tubulointerstitial injury in human kidney: Altered expression of vascular endothelial growth factor. Hum Pathol 2000;31:1491-7.  Back to cited text no. 12
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13.Ohashi R, Shimizu A, Masuda Y, et al. Peritubular capillary regression during the progression of experimental obstructive nephropathy. J Am Soc Nephrol 2002;13:1795-805.  Back to cited text no. 13
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14.Ohashi R, Kitamura H, Yamanaka N. Peritubular capillary injury during the progression of experimental glomerulonephritis in rats. J Am Soc Nephrol 2000;11:47-56.  Back to cited text no. 14
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15.Thomas SE, Anderson S, Gordon KL, Oyama TT, Shankland SJ, Johnson R. Tubulointerstitial disease in aging: Evidence for underlying peritubular capillary damage, a potential role for renal ischemia. J Am Soc Nephrol 1998; 9:231-42.  Back to cited text no. 15
    
16.Basile DP. Rarefaction of peritubular capillaries following ischemic acute renal failure: A potential factor predisposing to progressive nephropathy. Curr Opin Nephrol Hypertens 2004;13:1-7.  Back to cited text no. 16
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17.Namikoshi T, Satoh M, Horike H, et al. Implication of peritubular capillary loss and altered expression of vascular endothelial growth factor in IgA nephropathy. Nephron Physiol 2006;102:9-16.  Back to cited text no. 17
    
18.Ishii Y , Swada T , Kubota K, Fuchinoue S, Teraoka S, Shimizu A. Injury and progressive loss of peritubular capillaries in the development of chronic allograft nephropathy. Kidney Int 2005;67:321-32.  Back to cited text no. 18
    
19.Bohle A, von Gise H, Mackensen-Haen S, Stark-Jakob B. The obliteration of the post-glomerular capillaries and its influence upon the function of both glomeruli and tubuli. Functional interpretation of morphologic findings. Klin Wochenschr 1981;59:1043-51.  Back to cited text no. 19
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20.Yenrudi S, Laohapaibul A, Kittidiwit W, Suteparuk S, Futrakul N. A correlation between renal morphology and renal circulation in pediatric nephrotic syndrome. Ren Fail 2001; 23:85-90.  Back to cited text no. 20
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21.Futrakul N, Futrakul P, Siriviriyakul P. Correction of peritubular capillary flow reduction with vasodilators restores function in focal segmental glomerulosclerotic nephrosis. Clin Hemorr Microcirc 2004;31:197-205.  Back to cited text no. 21
    
22.Racusen LC, Solez K, Colvin RB, et al. The Banff 97 working classification of renal allograft pathology. Kidney Int 1999;55:713-23.  Back to cited text no. 22
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23.Simonson MS, Emancipator SN, Knauss T, Hricik DE. Elevated neointimal endothelin-1 in transplantation-associated arteriosclerosis of renal allograft recipients. Kidney Int 1998; 54:960-71.  Back to cited text no. 23
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24.Kang DH, Hughes J, Mazzali M, Schreiner GF, Johnson RJ. Impaired Angiogenesis in the Remnant Kidney Model: II. Vascular Endothelial Growth Factor Administration Reduces Renal Fibrosis and Stabilizes Renal Function. J Am Soc Nephrol 2001;12:1448-57.  Back to cited text no. 24
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Correspondence Address:
Amit K Dinda
Department of Pathology, All India Institute of Medical Sciences, Ansari Nagar, New Delhi - 110 029
India
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DOI: 10.4103/1319-2442.118091

PMID: 24029259

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