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Saudi Journal of Kidney Diseases and Transplantation
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LETTER TO THE EDITOR  
Year : 2021  |  Volume : 32  |  Issue : 2  |  Page : 588-589
Renal lesions in rheumatoid arthritis: Variants and risk factors


Department of Nephrology, Tareev Clinic of Internal Diseases, Sechenov First Moscow State Medical University, Moscow, Russia

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Date of Web Publication11-Jan-2022
 

How to cite this article:
Chebotareva NV, Guliaev SV, Androsova TV, Moiseev SV. Renal lesions in rheumatoid arthritis: Variants and risk factors. Saudi J Kidney Dis Transpl 2021;32:588-9

How to cite this URL:
Chebotareva NV, Guliaev SV, Androsova TV, Moiseev SV. Renal lesions in rheumatoid arthritis: Variants and risk factors. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 Jan 23];32:588-9. Available from: https://www.sjkdt.org/text.asp?2021/32/2/588/335478


To the Editor,

Recently, Fayed et al published some interesting data on the effect of therapy on kidney involvement in patients with rheumatoid arthritis (RA).[1] The authors showed that 10.4% patients with RA had chronic kidney disease (CKD) before treatment and 89.6% after starting treatment. Amyloidosis (28.1%) was the most common variant in RA patients followed by mesangioproliferative nephritis (19.1%), membranous nephropathy (6.1%), crescents nephritis (16.8%), focal segmental glomerulosclerosis (18.6%), and minimal changes (11.7%). In addition, the authors showed that hydroxychloroquine and leflunomide can be associated with membranous nephropathy, infliximab - with focal segmental sclerosis and amyloidosis in RA patients. However, etanercept appears not to be connected with kidney impairment.[1]

We also examined 242 patients with RA between 2017 and 2019. Eighty-six out of 242 (35.5%) patients had various variants of kidney damage. In our study amyloidosis was also the most common histologic pattern in 86 (35.5 %), followed by chronic glomerulonephritis (CGN) in 14 (16.3 %) and tubulo-interstitial nephritis in nine (10.4%) cases. Mesangial glomerulonephritis was most frequent in patients with glomerulonephritis. Mesangioproliferative GN (MPGN) was diagnosed in seven patients (6 – IgA nephropathy, 1 – IgM nephropathy), MPGN in two, minimal change disease in one, membranous nephropathy in one, nephrosclerosis due to GN in three.

The development of amyloidosis in our study was associated with a persistent increase in C-reactive protein (CRP) levels and with a duration of RA (more than 11 years). CGN developed earlier (average 5 years) after the debut of RA. But, we found no link between histological forms of CGN and therapy.

In our study 40 (46.5%) patients had a decrease in glomerular filtration rate (GFR) <60 mL/min/m2 only (CKD 3–4 stages). No kidney biopsies were performed in these cases because no urine abnormalities were detected. We found that age, duration of the disease, arterial hypertension, and lipid disorders, i.e. common cardiovascular risk factors, were significant independent risk factors for GFR decline in patients with RA. There were also found correlations between GFR levels and CRP (Rs = 0.43, P = 0.048) levels.

The persistence of chronic inflammation may play a role in the development of CKD in RA. It has been shown that elevated levels of CRP, as well as high levels of interleukin-6 (IL-6) and TNF-alpha, may be risk factors for CKD.[2] CRP can directly affect the tubulo-interstitium through the deposition in the tubular epithelium and can cause interstitial inflammation and fibrosis in RA.[3],[4] Amyloidosis is caused by deposition of AA amyloid fibrils in renal tissue. These fibrils derive from the acute-phase serum amyloid A protein and may be controlled by treatment. The pathogenesis of GN in RA remains unknown. The influence of a high level of IL-6 in mesangial proliferation has been discussed.[5] However, podocytopathies (focal segmental glomerulosclerosis and membranous nephropathy) without mesangial proliferation were also described in RA. The influence of therapy has also been discussed.[1],[6] Thus, further studies are needed to determine the factors that influence the renal lesion in RA.


   Compliance with Ethical Standards Top


The study was approved by the Ethics Committee of the Sechenov University. All subjects provided informed written consent before participation in the study that conformed to the Declaration of Helsinki.

Conflict of interest: None declared.



 
   References Top

1.
Fayed A, Shaker A, HamzaWM, Wadie M. Spectrum of glomerulonephritis in Egyptian patients with rheumatoid arthritis: A university hospital experience. Saudi J Kidney Dis Transpl 2019;30:803-11.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
Shankar A, Sun L, Klein BE, et al. Markers of inflammation predict the long-term risk of developing chronic kidney disease: a population-based cohort study. Kidney Int 2011;80:1231-8.  Back to cited text no. 2
    
3.
Schwedler SB, Guderian F, Dämmrich J, Potempa LA, Wanner C. Tubular staining of modified C-reactive protein in diabetic chronic kidney disease. Nephrol Dial Transplant 2003; 18:2300-7.  Back to cited text no. 3
    
4.
Li ZI, Chung AC, Zhou L, et al. C-reactive protein promotes acute renal inflammation and fibrosis in unilateral ureteral obstructive nephropathy in mice. Lab Invest 2011;91:837- 51.  Back to cited text no. 4
    
5.
Rops AL, Jansen E, van der Schaaf A, et al. Interleukin-6 is essential for glomerular immunoglobulin A deposition and the development of renal pathology in Cd37- deficient mice. Kidney Int 2018;93:1356-66.  Back to cited text no. 5
    
6.
Góis M, Carvalho F, Sousa H, Ferreira AC, Sousa J, Nolasco F. Renal involvement in rheumatoid arthritis: analysis of 53 renal biopsies. Port J Nephrol Hypert 2017;31:25- 30.  Back to cited text no. 6
    

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Correspondence Address:
Natalia V Chebotareva
Department of Nephrology, Tareev Clinic of Internal Diseases, Sechenov First Moscow State Medical University, Moscow
Russia
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DOI: 10.4103/1319-2442.335478

PMID: 35017360

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