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BRIEF REPORT
Year : 2020  |  Volume : 3  |  Issue : 2  |  Page : 75-77

Degree of proteinuria as a predictor of severity in diffuse proliferative glomerulonephritis: An experience from Sri Lanka


1 Department of Pathology, Faculty of Medicine, University of Peradeniya, Kandy, Sri Lanka
2 Department of Pediatrics, Faculty of Medicine, University of Peradeniya, Kandy, Sri Lanka
3 Department of Emergency Medicine, Teaching Hospital Peradeniya, Peradeniya, Sri Lanka

Date of Submission25-Apr-2020
Date of Decision18-Jul-2020
Date of Acceptance09-Dec-2020
Date of Web Publication31-Dec-2020

Correspondence Address:
Kanchana Sanjeewani Liyanaarachchi
Department of Pathology, Royal Surrey County Hospital, Guilford, England
Sri Lanka
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2589-9309.305917

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  Abstract 


Acute glomerulonephritis (AGN) or infection-related glomerulonephritis (IRGN) is the leading cause of acute nephritic syndrome in developing countries. We examined for differences in histopathological pattern and severity of injury in 48 patients with IRGN, categorized by the degree of proteinuria as nonnephrotic and nephrotic range, and compared the levels of serum albumin and degree of tubular injury between the two groups. Patients with nephrotic range proteinuria had a more severe glomerular and tubular injury and had double contours more often than patients with nonnephrotic range proteinuria.

Keywords: Diffuse proliferative glomerulonephritis, hypoalbuminemia, infection-related glomerulonephritis, nephrotic range proteinuria


How to cite this article:
Liyanaarachchi KS, Ratnatunga NV, Thalgahagoda RS, Galliyadda AB. Degree of proteinuria as a predictor of severity in diffuse proliferative glomerulonephritis: An experience from Sri Lanka. Asian J Pediatr Nephrol 2020;3:75-7

How to cite this URL:
Liyanaarachchi KS, Ratnatunga NV, Thalgahagoda RS, Galliyadda AB. Degree of proteinuria as a predictor of severity in diffuse proliferative glomerulonephritis: An experience from Sri Lanka. Asian J Pediatr Nephrol [serial online] 2020 [cited 2021 Jan 23];3:75-7. Available from: https://www.ajpn-online.org/text.asp?2020/3/2/75/305917




  Introduction Top


Acute diffuse proliferative glomerulonephritis (AGN) or infection-related glomerulonephritis (IRGN) is the leading cause of acute nephritis in developing countries.[1] The condition primarily affects children, usually between 5 and 15 years of age, and represents 50%–90% of pediatric acute nephritis.[2],[3],[4],[5] Patients typically present with abrupt onset of macroscopic or microscopic hematuria, hypertension, oliguria, and azotemia. While urinary excretion of protein usually ranges from 0.5 to 3 g daily, nephrotic range proteinuria (>3.5 g/day) may also occur.[2]

The aim of this study was to examine for glomerular and tubular changes in relation to the degree of proteinuria and to see whether hypoalbuminemia can predict the severity of histological changes in patients with IRGN. This would be important in resource-constrained countries where facilities for kidney biopsy are limited.


  Methods Top


This retrospective descriptive study included children under 14 years of age who were diagnosed with IRGN and also had a rapid rise in serum creatinine that indicated need for kidney biopsy. Light microscopy findings in 48 kidney biopsies were studied on slides stained with hematoxylin and eosin and methenamine silver. Features of IRGN on light microscopy included mesangial cell proliferation, endothelial cell swelling, and leukocytic infiltration of the tuft Immunofluorescence, showed immune complexes containing immunoglobulin (Ig) G and C3. IgA and IgM deposits were insignificant or absent.

The presence of crescents and necrotizing lesions with glomerular capillary obliteration were considered as severe glomerular injury, while all the other glomerular lesions were considered as nonsevere glomerular injury. Glomerular basement membrane changes of double contouring were documented. Tubulorrhexis was considered as severe tubular injury, while epithelial cell injury, dilatation, and tubulitis were considered nonsevere tubular injuries. These histological changes were compared between patients with nephrotic range proteinuria (Group 1) and nonnephrotic range proteinuria (Group 2). Levels of serum albumin between groups were compared using the independent sample t-test; P < 0.05 was considered as statistically significant. Data analysis was done using Microsoft Statistical Package for Social Science (SPSS) version 21 (IBM Corp., Armonk, NY).


  Results Top


Nephrotic range proteinuria was present in 27 (56%) of 48 patients. Levels of serum albumin were significantly lower in patients with IRGN with nephrotic range proteinuria (Group 1) than in those with nonnephrotic range proteinuria (Group 2; mean: 28.2 g/L vs. 32.2 g/L; mean difference: -3.8 g/L; 95% confidence interval: -7.4–-0.56; P = 0.023). Severe glomerular injuries were seen in 10 (37%) patients in Group 1 and 6 (29%) patients in Group 2. Glomerular capillary double contours were seen in 5 and 2 patients, respectively, while crescents were present in 4 and 1 patient, respectively. Tubular injury was present in 14 (52%) patients in Group 1 and 8 (38%) patients in Group 2. Severe tubular injury was noted in 4 (28.5%) and none (0%) patients in the respective groups.


  Discussion Top


Childhood IRGN is usually a self-limiting illness with favorable prognosis, especially in children. While kidney biopsy is not performed in typical cases, it is necessary in patients with atypical presentation, including those with nephrotic range proteinuria and a significant rise in creatinine. Information on correlation between clinical presentation and severity of histopathological lesions in such biopsies would be useful in guiding case management and might avoid need for kidney biopsy, especially in resource-limited settings. Since nephrotic range proteinuria is not a typical finding in uncomplicated IRGN, its presence might indicate a different diagnosis with a different plan of management and prognosis. Uncommonly, such patients may mistakenly be managed as nephrotic syndrome, with corticosteroids which are quite unnecessary in IRGN.[2]

Typical histological features in uncomplicated IRGN are endothelial and mesangial cell proliferation with leukocytic infiltration of the tuft and normal tubules, indicating nonsevere lesions. Even in patients with IRGN complicated with nephrotic range proteinuria, we did not find severe glomerular lesions in 63% of patients. Double contouring of the basement membrane, considered a hallmark of membranoproliferative glomerulonephritis, is reported in patients with IRGN and persistent glomerulonephritis[6] or resolving lesions.[7] We observed double contours as well as crescents in IRGN, more often in patients with nephrotic range proteinuria than in those with nonnephrotic range proteinuria. Not unexpectedly, the level of serum albumin was highest in patients with IRGN and nonnephrotic range proteinuria without crescents and lowest in those with nephrotic range proteinuria and crescents. [Table 1]
Table 1: Mean serum albumin levels in relation to crescents and tubular injury

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Previous studies on histology of IRGN predominantly report findings in glomeruli and no striking changes in the tubulointerstitium.[8],[9] However, we found severe tubular injury, such as tubulorrhexis, was associated with heavy proteinuria, and glomerular crescents. Similarly, Lewy et al. found a significant correlation between tubular damage and proteinuria in biopsies of 46 children with IRGN,[10] while previous studies report minimal tubular injury in patients with IRGN and its presence was observed chiefly in biopsies with severe renal damage such as crescents.[10] However, we found tubular injury in a high proportion of biopsies in patients with nephrotic range proteinuria even in the absence of crescents. It remains unclear whether severe proteinuria itself may injure tubules.

Our findings indicate that severe proteinuria reflects severe glomerular injury in patients with IRGN and is associated with tubular injury. Patients with heavy proteinuria, therefore, warrant long-term follow-up. The lack of electron microscopic findings is an important limitation of this study.

Acknowledgment

We especially thank Mrs. Nadeeka Herath, medical laboratory assistant, for the technical assistance with the renal biopsies.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
El-Desoky SM, Al-Sulimani LK, Alkhatieb MT, Alhasan KA, Albanna AS, Kari JA. Pediatric acute poststreptococcal glomerulonephritis: A single-center experience. Asian J Pediatr Nephrol 2019;2:36-40.  Back to cited text no. 1
  [Full text]  
2.
Adedoyin OT, Afolayan FM, Buhari MO, Abdulkadir MB, Ibrahim OR, Akintade OO, et al. Acute glomerulonephritis mimicking nephrotic syndrome. Niger J Paediatr 2016;43:95-8.  Back to cited text no. 2
    
3.
Vinen CS, Oliveira DB. Acute glomerulonephritis. Postgrad Med J 2003;79:206-13.  Back to cited text no. 3
    
4.
Welch TR. An approach to the child with acute glomerulonephritis. Inter J Pediatr 2012;2012:426192.  Back to cited text no. 4
    
5.
Rosai J, Ordonez NG. Urinary tract kidney, renal pelvis, and ureter; bladder. In: Rosai J, editor. Rosai and Ackerman's Surgical Pathology. 10th ed. New York: Elsevier; 2011, p. 1125-6.  Back to cited text no. 5
    
6.
Vernon KA, Jorge EG, Hall AE, Fremeaux-Bacchi V, Aitman TJ, Cook HT, et al. Acute presentation and persistent glomerulonephritis following streptococcal infection in a patient with heterozygous complement factor h–related protein 5 deficiency. Am J Kidney Dis 2012;60:121-5.  Back to cited text no. 6
    
7.
Turner NN, Lameire N, Goldsmith DJ, Winearls CG, Himmelfarb J, Remuzzi G. Oxford Text Book of Clinical Nephrology. 4th ed. Oxford, UK: Oxford University Press; 2015.  Back to cited text no. 7
    
8.
Clark G, White RH, Glasgow EF, Chantler C, Cameron JS, Gill D, et al. Post streptococcal glomerulonephritis in children: Clinico-pathological correlations and long-term prognosis. Pediatr Nephrol 1988;2:381-8.  Back to cited text no. 8
    
9.
Hutt MS, White RH. A clinico-pathological study of acute glomerulonephritis in east african children. Arch Dis Child 1964;39:313-23.  Back to cited text no. 9
    
10.
Lewy JE, Salinas-Madrigal L, Herdson PB, Pirani CL, Metcoff J. Clinico-pathologic correlations in acute poststreptococcal glomerulonephritis. A correlation between renal functions, morphologic damage and clinical course of 46 children with acute post streptococcal glomerulonephritis. Medicine (Baltimore) 1971;50:453-501.  Back to cited text no. 10
    



 
 
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