Evolution of glomerulopathies associated with rheumatoid arthritis
PDF (Español)
PDF
HTML (Español)

Supplementary Files

Carta de presentación (Español)

Keywords

Rheumatoid arthritis
glomerulopathies
urinary sediment
MDRD
renal failure.

How to Cite

1.
Daza JL, De La Cruz Y, Marín C, Zapata M, Segovia F, Daza LJ, De rosa G, Galindo J. Evolution of glomerulopathies associated with rheumatoid arthritis. Rev. Colomb. Nefrol. [Internet]. 2018 Jan. 18 [cited 2024 Mar. 29];5(1):36-42. Available from: https://revistanefrologia.org/index.php/rcn/article/view/295

Abstract

Introduction: Rheumatoid arthritis is one of the most common clinical syndromes within rheumatological conditions and its association with glomerular diseases is rare.

Objective: To describe the histopathological findings in renal biopsies in patients with rheumatoid arthritis and to correlate them with the clinical and laboratory manifestations at the beginning, at 6 months and at one year of follow-up.

Patients and Methods: This is a retrospective observational study conducted in the Hospital de Clinicas “Jose De San Martin” in Buenos Aires, Argentina; Where we included 41 patients diagnosed with RA (ACR 1987) in a period of 20 years. Histopathological diagnoses of membranous nephropathy (MN), minimal change disease (MCD), secondary amyloidosis (AA), focal and segmental glomerulosclerosis (FSGS); mesangial glomerulopathy (MGP) and glomerulonephritis with extracapillary proliferation (GNEC) were included. Histopathological description, different treatments, years of evolution of rheumatoid arthritis Clinical and laboratory characteristics were analyzed during the first 6 months and one year of follow-up in order to determine the progression of renal failure calculated through the formula of MDRD of 4 variables (Modification of diet in renal disease) and the increase of proteinuria.

Results: The most frequent histological finding was amyloidosis with 34,1 % (n=14), followed by mesangial glomerulopathy 21,9 % (n=9), membranous nephropathy 19,5 % (n=8), glomerulonephritis with extracapillary proliferation 12,1 % (n=5), focal and segmental glomerulosclerosis 7,3 % (n=3) and minimal change disease 8,2 % (n=2). Nephrotic syndrome was the most frequent presentation in patients with amyloidosis in 85,7 %, microhematuria occurred in 100 % of patients with MPG and in 80 % of patients with GNEC. In patients with AA, moderate to severe interstitial fibrosis occurred in 85,7 %, followed by GNEC and NM with 80 % and 40 % respectively. The 24-hour proteinuria, creatinine and glomerular filtration rate estimated by MDRD at 6 months and 12 months were evaluated. Concluding, that patients with AA, FSGS and GNEC had greater progression of renal failure at 12 months; the opposite occurred in patients with minimal change disease (MCD) and mesangial glomerulopathy (MGP) who had a lower progression of renal failure at one year of follow-up; There was a correlation in the glomerulopathies that had greater deterioration of the renal function had greater interstitial tubule involvement as was the case of amyloidosis. The glomerulopathies that presented greater proteinuria at the beginning were membranous nephropathy, amyloidosis and minimal change disease. Both membranous nephropathy and minimal change disease had partial remission at one year, in contrast to amyloidosis, which showed progression of proteinuria at 12 months of follow-up.

Conclusion: The glomerulopathies that presented greater progression of renal failure at 1 year based on the estimation by MDRD 4, had a higher renal tubular interstitial involvement in renal biopsy and these were amyloidosis (AA), segmental focal glomerulosclerosis (FSGS), glomerulonephritis with proliferation extracapillary On the other hand, those with the best evolution in relation to the degree of proteinuria and the glomerular filtration rate determined by the MDRD4 equation were mesangial glomerulopathy, minimal change disease, and membranous nephropathy.

https://doi.org/10.22265/acnef.5.2.295
PDF (Español)
PDF
HTML (Español)

References

1. Karstila K, Korpela M, Sihvonen S, Mustonen J. Prognosis of Clinical Renal Disease and Incidence of New Renal Findings in Patients with Rheumatoid Arthritis: Follow-Up of a Population-Based Study. Clin Rheumato. 2007;26(12):2089-2095.
http://doi.org/10.1007/s10067-007-0625-y

2. Hickson LJ, Crowson CS, Gabriel SE, McCarthy JT, Matteson EL. Development of Reduced Kidney Function in Rheumatoid Arthritis. Am J Kidney Dis. 2014;63(2):206-213.
http://doi.org/10.1053/j.ajkd.2013.08.010

3. Yoshinaga Y, Nishiya K, Yamamura M, Hatano M, Ogura T, Takaoka M, et al. Study of Urinary ?ndings and Renal Functions in Patients with Rheumatoid Arthritis [en Japonés]. Kidney Dialysis. 1989;26:477-482.

4. Hill AJ, Thomson RJ, Hunter JA, Traynor JP. The Prevalence of Chronic Kidney Disease in Rheumatology Outpatients. Scott Med J. 2009;54(2):9-12. http://doi.org/10.1258/rsmsmj.54.2.9

5. Symmons DP, Jones MA, Scott DL, Prior P. Long Term Mortality Outcome in Patients with Rheumatoid Arthritis: Early Presenters Continue to Do Well. J Rheumatol. 1998;25(6):1072-1077.

6. Laasko M, Mutru O, Isomaki H, Koota K. Mortality from Amyloidosis and Renal Disease in Patients with Rheumatoid Arthritis. Ann Rheum Dis. 1986;45(8):663-667.

7. Adu D, Tse WY. Rheumatoid Arthritis, Mixed Connective Tissue Disease, and Polymyositis. in: Adu D, Emery P, Madaio MP, editores. Rheumatology and the Kidney. New York: Oxford University Press; 2001. p. 293-302.

8. Fogazzi G. The Urinary Sediment. An Integraded View. 3a ed. Milan: Elsevier; 2009.

9. Fogazzi GB, Grignani S: Urine microscopic analysis: An art abandoned by nephrologists? Nephrol Dial Transplant. 1998;13:2485-2487.

10. Hall CL, Fothergill NJ, Blackwell MM, Harrison PR, MacKenzie JC, MacIver AG. The Natural Course of Gold Nephropathy: Long Term Study of 21 Patients. Br Med J (Clin Res Ed). 1987;295(6601):745-748.

11. Hall CL, Jawad S, Harrison PR, MacKenzie JC, Bacon PA, Klouda PT, MacIver AG. Natural Course of Penicillamine Nephropathy: A Long Term Study of 33 Patients. Br Med J (Clin Res Ed). 1988;296(6629):1083-1086.

12. Bourke BE, Woodrow DF, Scott JT. Proteinuria in Rheumatoid Arthritis-Drug-Induced or Amyloid? Ann Rheum Dis. 1981;40(3):240-244.

13. Helin HJ, Korpela MM, Mustonen JT, Pasternack AI. Renal Biopsy Findings and Clinicopathologic Correlations in Rheumatoid Arthritis. Arthritis Rheum. 1995;38(2): 242-247.
No national or foreign publication may partially or totally reproduce or translate Revista Colombiana de Nefrología articles or abstracts without prior written permission from the journal’s Editorial Board.

Dimensions


PlumX


Downloads

Download data is not yet available.