Indian Journal of Rheumatology

BRIEF REPORT
Year
: 2017  |  Volume : 12  |  Issue : 3  |  Page : 156--159

Renal function in Ankylosing Spondylitis


Renu Saigal1, Arun Kumar Agrawal2, Laxmikant Goyal2, Abhishek Agrawal2, Naveen Gupta2,  
1 Department of Medicine, IMSRC, Jaipur National University, Jaipur, Rajasthan; Department of Medicine, SMS Medical College, Jaipur, Rajasthan, India
2 Department of Medicine, SMS Medical College, Jaipur, Rajasthan, India

Correspondence Address:
Renu Saigal
33, Muktanand Nagar, Gopalpura Byepass, Tonk Road, Jaipur - 302 018, Rajasthan
India

Abstract

Background: To study renal functions in patients with ankylosing spondylitis (AS) and compare with matched healthy controls and correlation between renal function parameters and disease activity markers. Methods: Renal functions of forty cases with AS and the same number of age- and sex-matched individuals were evaluated. Disease activity was assessed using Bath Ankylosing Spondylitis Disease Activity Index, Bath Ankylosing Spondylitis Functional Index, Bath Ankylosing Spondylitis Metrology Index scores, C-reactive protein, and erythrocyte sedimentation rate. Results: Among AS cases, 31 AS cases (77.50%) had renal function abnormalities including hematuria (20%), proteinuria (30%), albuminuria (52.50%), increased 24 h urine protein (22%), raised serum creatinine (17%), and reduced glomerular filtration rate (GFR) (37%). Among healthy controls, 20/40 (50%) had renal function abnormalities including albuminuria (15%), raised serum creatinine (7.50%), and reduced GFR (20%). Abnormal renal functions were significantly more in AS cases (31/40, 77%) than healthy controls (20/40, 50%) (P < 0.05). Renal function abnormalities were more frequent among AS cases having elevated markers of disease activity. Renal abnormalities were more prevalent in cases taking nonsteroidal anti-inflammatory drugs (NSAIDs) for < 48 months than cases taking these drugs for ≥48 months, suggesting that these renal abnormalities were probably not due to NSAIDs-induced nephropathy but may be due to AS itself. Conclusions: In this study with small number of participants abnormalities in the renal function were common in patients with AS. No significant correlation was found between renal functions and markers of disease activity.



How to cite this article:
Saigal R, Agrawal AK, Goyal L, Agrawal A, Gupta N. Renal function in Ankylosing Spondylitis.Indian J Rheumatol 2017;12:156-159


How to cite this URL:
Saigal R, Agrawal AK, Goyal L, Agrawal A, Gupta N. Renal function in Ankylosing Spondylitis. Indian J Rheumatol [serial online] 2017 [cited 2020 Nov 24 ];12:156-159
Available from: https://www.indianjrheumatol.com/text.asp?2017/12/3/156/205162


Full Text

Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized by progressive ankylosis of the axial skeleton, asymmetric peripheral arthritis associated with various extra-articular manifestations such as uveitis, renal, cardiac, and pulmonary manifestations.[1],[2],[3]

Renal failure has been identified as an important cause of premature mortality in AS.[4],[5] The renal abnormalities reported in AS include renal amyloidosis, analgesic-induced nephropathies such as acute renal failure, acute and chronic types of tubulointerstitial nephritis, papillary necrosis, and glomerulonephritis with subendothelial deposits of immunoglobin A (Ig A) and complements.[2],[4],[5],[6]

Using sensitive and reliable tests of renal function assessment, patients of AS with renal dysfunction can be identified at an early stage, and appropriate measures can be taken to prevent the progression of renal disease and development of end-stage renal disease. Looking at very few studies reported on renal function in AS patients in India, this study was carried out to evaluate renal functions in AS patients and to compare these with matched normal controls.

 Methods



This hospital-based study was carried out in forty patients with AS (diagnosed according to the modified New York criteria)[7] from the rheumatology clinic, at a tertiary care hospital in North India. The same numbers of age- and sex-matched healthy controls were recruited from the hospital staff. Main exclusion criteria for both the groups were diabetes mellitus, hypertension, urinary tract infection, gout, urolithiasis, and renal function alteration due to presumably known cause other than AS. The approval from institutional ethics committee and written informed consent from all the study participants were obtained.

Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), and Bath Ankylosing Spondylitis Metrology Index (BASMI) scores were calculated for each patient using preformed questionnaires and physical examination. C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and human leukocyte antigen (HLA) B-27 status were determined for each patient. ESR was measured using Westergren method and CRP by turbidimetry, and the presence of HLA B-27 was tested using polymerase chain reaction technique.

All participants underwent various renal function tests including urine examination, albuminuria, 24 h urine protein, and serum creatinine level. Serum creatinine was measured using Jaffe's picrate colorimetric method and levels >1.2 mg/dl were considered abnormal. The presence of proteinuria on dipstick test (at least 1 + or more) and/or microscopic hematuria (≥5 red blood cells [RBCs] per high-power field) in ≥3 consecutive urinalysis was considered abnormal. Albuminuria was quantified in the form of albumin-to-creatinine ratio (ACR) using Clinitek 100 reagent strips. ACR <30 μg/mg indicates normal albuminuria while microalbuminuria (ratio between 30 and 300 μg/mg) and macroalbuminuria (ratio >300 μg/mg) were considered abnormal. Twenty-four-hour urine protein was measured by pyrogallol red colorimetric method. Values >300 mg/day were considered abnormal. Glomerular filtration rate (GFR) was calculated using Cockcroft–Gault formula. GFR <90 ml/min/1.73 m2 was taken as reduced GFR.

Statistical analysis

Continuous variables were expressed as mean ± standard deviation. Pairs of groups were compared using Student's t-test for a normally distributed continuous variables. The “Chi-square” test was used for categorical variables as needed. Pearson's coefficient was used to investigate the correlation between two variables. Statistical significance was set at P < 0.05.

Ethical approval

This study was approved by the institutional ethics committee. Written informed consent from all the study participants were obtained.

 Results



In this study, mean age of individuals in both groups was 27.85 ± 9.10 years, male:female ratio was 12.3:1, and mean duration of AS was 57.93 ± 50.71 months. Thirty-two patients were HLA B-27 positive (80%). The differences in 24 h urine protein and GFR among AS cases and healthy controls were significant [Table 1].{Table 1}

Twenty-four-hour urine protein was significantly higher in AS patients and GFR (ml/min) was significantly reduced in AS patients as compared to controls [Table 1].

The frequency of hematuria and albuminuria and raised 24 h urine proteins were significantly more in AS cases as compared to healthy group. Although serum creatinine >1.2 mg% and reduced GFR < 90 ml/min was found in a higher number of AS patients as compared to controls, it was not significant (P > 0.05). Overall abnormal renal functions were seen significantly more in AS patients (31/40) as compared to controls (20/40) [Table 1].

Renal abnormalities were more prevalent in cases taking nonsteroidal anti-inflammatory drugs (NSAIDs) for <48 months duration than cases taking these drugs for ≥48 months but without a significant difference (P > 0.05) [Table 2].{Table 2}

We did not observe any significant difference in renal abnormalities between AS cases who were taking and those who were not taking sulfasalazine (P > 0.05), suggesting that sulfasalazine intake did not have any effect on renal functions in our study [Table 2].

Serum creatinine had a positive correlation with duration of disease and Bath indices. Twenty-four-hour urine protein had a positive correlation with duration of disease, BASDAI, BASFI and negative correlation with BASMI score. GFR had a negative correlation with duration of disease, ESR, BASDAI, BASFI (r = −0.087), and BASMI scores. However, none of these correlations were found statistically significant [Table 3].{Table 3}

 Discussion



This study reported significantly higher frequency of abnormal renal function in AS cases (31/40, 77.50%) as compared to healthy controls (20/40, 50%) (P< 0.05).

Previous studies have shown renal function abnormalities in a smaller proportion (8%–35%) of cases of AS, and they did not compare renal functions in AS cases with healthy controls.[1],[2],[8],[9] Our patients of AS were also of younger age (mean age 27.84 ± 9.28 years) and with lesser duration of disease (57.93 ± 50.71 months) than previous studies (mean age 32–48.3 years, mean duration of disease 8.53–15.4 years).[1],[10],[11],[12]

The frequency of microscopic hematuria was 8/40 in AS cases (20%) in our study. This was more than other studies (1.8%–17.8%)[1],[8],[9],[11],[12],[13] but less than some studies (21–21.5%).[2],[10] Five cases showed hematuria had dysmorphic RBCs, suggesting glomerular involvement in AS.

Proteinuria (>300 mg/day) was also more frequent in AS patients in our study as compared to other studies.[1],[8],[9]

Increased albuminuria (ACR >30 μg/mg) was present in 21 AS cases in the present study while it was found in only 10% cases by Vilar et al.[2]

We found higher proportion of AS cases having raised serum creatinine (7/40) as compared to healthy controls (3/40). Raised serum creatinine was found in lesser proportion of AS patients in earlier reports.[1],[2]

Reduced GFR was observed in 15 cases (35%) of AS, which was more than healthy controls. However, other authors did not find any impairment in GFR among AS cases [14] and while in one study it was reported in only 4/40 (10%) cases.[2]

No statistically significant correlation was found between duration of disease, ESR, BASDAI, BASFI, and BASMI scores and renal function parameters (serum creatinine, 24 h urine proteins and GFR) (P > 0.05).

Renal abnormalities were more prevalent in cases taking NSAIDs for <48 months duration than cases taking these drugs for ≥ 48 months but without a significant difference (P > 0.05), suggesting that these renal abnormalities were probably not due to NSAIDs-induced nephropathy but may be due to AS itself.

We performed renal biopsy in the only patient having proteinuria >1 g/24 h. Biopsy showed renal amyloidosis. Many studies had reported renal amyloidosis in AS varying from 1.1% to 6.1%.[9],[15]

This study was only an observation study with small number of participants. A follow-up study with a large sample size will be more informative about renal abnormalities in AS.

Since we excluded other possible causes or conditions predisposing to renal abnormalities such as diabetes mellitus, hypertension, urolithiasis, gout, and urinary tract infections and the abnormal findings could not be explained by NSAIDs- or sulfasalazine-induced nephropathy, the renal abnormalities observed in our study seem to be purely due to AS itself.

In conclusion, renal function abnormalities were found in significantly more number of patients with AS as compared to healthy controls. In the present study no significant correlation was found between renal function and markers of disease activity. In view of this it might be prudent to assess a patient with AS from renal point of view as there might be occult renal involvement.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

References

1Lange U, Stapfer G, Ditting T, Geiger H, Teichmann J, Müller-Ladner U, et al. Pathologic alterations of the heart and the kidney in patients with ankylosing spondylitis. Eur J Med Res 2007;12:573-81.
2Vilar MJ, Cury SE, Ferraz MB, Sesso R, Atra E. Renal abnormalities in ankylosing spondylitis. Scand J Rheumatol 1997;26:19-23.
3Nabokov AV, Shabunin MA, Smirnov AV. Renal involvement in ankylosing spondylitis (Bechterew's disease) Nephrol Dial Transplant 1996;11:1172-5.
4Wollheim FA Ankylosing spondylitis. In: Kelley WN, Harris ED Jr., Ruddy S, Sledge CB, editors. Textbook of Rheumatology. 4th ed. Philadelphia: WB Saunders Company; 1993. p. 943-60.
5Mittal VK, Malhotra KK, Bhuyan UN, Malaviya AN. Kidney involvement in seronegative spondarthritides. Indian J Med Res 1983;78:670-5.
6Strobel ES, Fritschka E. Renal diseases in ankylosing spondylitis: Review of the literature illustrated by case reports. Clin Rheumatol 1998;17:524-30.
7van der Linden S, Valkenburg HA, Cats A. Evaluation of diagnostic criteria for ankylosing spondylitis. A proposal for modification of the New York criteria. Arthritis Rheum 1984;27:361-8.
8Lee SH, Lee EJ, Chung SW, Song R, Moon JY, Lee SH, et al. Renal involvement in ankylosing spondylitis: Prevalence, pathology, response to TNF-a blocker. Rheumatol Int 2013;33:1689-92.
9Samia B, Hazgui F, Abdelghani KB, Hamida FB, Goucha R, Hedri H, et al. Renal abnormalities in ankylosing spondylitis. Nephrol Ther 2012;8:220-5.
10Peeters AJ, van den Wall Bake AW, van Albada-Kuipers GA, Westedt ML, Brand R, Breedveld FC, et al. IgA containing immune complexes and hematuria in ankylosing spondylitis. A prospective longitudinal study. J Rheumatol 1988;15:1662-7.
11Wall BA, Agudelo CA, Pisko EJ. Increased incidence of recurrent hematuria in ankylosing spondylitis: A possible association with IgA nephropathy. Rheumatol Int 1984;4:27-9.
12Jones DW, Mansell MA, Samuell CT, Isenberg DA. Renal abnormalities in ankylosing spondylitis. Br J Rheumatol 1987;26:341-5.
13Rodrigues CE, Vieira WP, Bortoluzzo AB, Gonçalves CR, da Silva JA, Ximenes AC, et al. Low prevalence of renal, cardiac, pulmonary, and neurological extra-articular clinical manifestations in spondyloarthritis: Analysis of the Brazilian registry of spondyloarthritis. Rev Bras Reumatol 2012;52:375-83.
14Calin A. Renal glomerular function in ankylosing spondylitis. Scand J Rheumatol 1975;4:241-2.
15Dönmez S, Pamuk ÖN, Pamuk GE, Aydogdu E, Inman R. Secondary amyloidosis in ankylosing spondylitis. Rheumatol Int 2013;33:1725-9.