|Year : 2018 | Volume
| Issue : 6 | Page : 1506-1510
|Periarticular calcification mimicking inflammatory polyarthritis in chronic kidney disease
Kumari Naidoo1, Kwazi C. Z. Ndlovu2, Girish M Mody1
1 Department of Rheumatology, School of Clinical Medicine, University of KwaZulu-Natal and Inkosi Albert Luthuli Central Hospital, Durban, South Africa
2 Department of Nephrology, School of Clinical Medicine, University of KwaZulu-Natal and Inkosi Albert Luthuli Central Hospital, Durban, South Africa
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|Date of Submission||05-Dec-2017|
|Date of Decision||25-Jan-2018|
|Date of Acceptance||01-Feb-2018|
|Date of Web Publication||27-Dec-2018|
| Abstract|| |
Periarticular calcification is a frequent radiographic manifestation in chronic kidney disease (CKD). However, clinical presentation as inflammatory periarthritis, tenosynovitis, and bursitis is unusual. A 34-year-old man with CKD on dialysis for three years presented with painful swollen joints. His adherence to regular dialysis, phosphate binders, Vitamin D supplements, and antihypertension therapy was poor. He had swelling of the right thumb, index, and little fingers; periarticular swelling of the left middle finger and right little toe; and extensor tenosynovitis of the wrists and right olecranon bursitis. Laboratory investigations showed the following: urea 36 mmol/L; creatinine 1764 umol/L; serum urate 0.37 mmol/L; corrected calcium 1.76 mmol/L; phosphate 4.32 mmol/L; 25-dihydroxycholecalciferol 30 ng/mL; and parathyroid hormone 104 pmol/L. Radiographs showed periarticular calcification corresponding to the sites of inflammation. The inflammation resolved with oral steroids. In our patient, deranged mineral and bone metabolism contributed to periarticular calcification at multiple sites, mimicking inflammatory polyarthritis.
|How to cite this article:|
Naidoo K, Ndlovu KC, Mody GM. Periarticular calcification mimicking inflammatory polyarthritis in chronic kidney disease. Saudi J Kidney Dis Transpl 2018;29:1506-10
|How to cite this URL:|
Naidoo K, Ndlovu KC, Mody GM. Periarticular calcification mimicking inflammatory polyarthritis in chronic kidney disease. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2019 Jun 27];29:1506-10. Available from: http://www.sjkdt.org/text.asp?2018/29/6/1506/248309
| Introduction|| |
We report the case of a patient with chronic renal failure who presented with calcific periarthritis, tenosynovitis, and bursitis, mimicking inflammatory polyarthritis. Although there are isolated reports of tumoral calcinosis and calcific periarthritis, presentation with bursitis, tenosynovitis, and periarthritis is rare since the original small cases series of five patients by Caner and Decker in 1964 and two patients by Mirahmadi et al in 1973.,
| Case Report|| |
A 34-year-old Indian male with chronic renal failure on renal replacement therapy for three years was referred to the rheumatology department for suspected inflammatory polyarthritis.
He had a history of renal disease since childhood but did not attend regular follow-up. He presented with advanced renal failure in November 2014 and required emergency dialysis. The kidneys were shrunken and unsuitable for renal biopsy. The results of laboratory tests were as follows: urea 23.6 mmol/L, creatinine 1215 umol/L, calcium 1.8 mmol/L, phosphate 1.99 mmol/L, and parathyroid hormone (PTH) 93.6 pmol/L. Further diagnostic workup failed to reveal a cause for his renal failure. He was initially treated with hemodialysis (HD) and then maintained on continuous ambulatory peritoneal dialysis (CAPD). He was on phosphate binders, alpha-calcidol, and treatment for hypertension. His adherence to therapy was poor.
He presented in October 2016 with a three-month history of progressive pain and swelling involving the hands, wrists, and right elbow. He also had a one-week history of severe pain and swelling in the right small toe. He did not have morning stiffness, skin rashes, eye problems, inflammatory backache, diarrhea, or genitourinary symptoms. There was no family history of arthritis.
He was apyrexial, the nails were white, and the skin and eyes were normal. He had diffuse swelling of the right thumb and little fingers with swelling over the proximal phalanx of the index finger. There was firm discrete swelling around the metacarpophalangeal joints of the left index and middle fingers [Figure 1]a. He also had bilateral extensor tenosynovitis over the dorsum of the hands and wrists [Figure 2]a, right olecranon bursitis [Figure 3]a, and acute inflammation of the right little toe.
|Figure 1: Shows the clinical and radiographic appearance of the hands with periarticular swelling and calcification.|
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|Figure 2: Shows swelling of the dorsum of the left wrist with calcification over the dorsal and volar aspect.|
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|Figure 3: Shows right olecranon bursitis with calcification around the head of the radius and ulna.|
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Laboratory tests showed an anemia of 7.5 g/dL, an elevated urea of 36 mmol/L, crea-tinine of 1764 umol/L, a normal urate of 0.37 mmol/L, a low corrected calcium of 1.76 mmol/L, and marked hyperphosphatemia of 4.32 mmol/L. The level of 25-dihydroxychole-calciferol was 30 ng/mL. There was secondary hyperparathyroidism (PTH 104 pmol/L) with a normal Sestamibi scan. The rheumatoid factor, anti-cyclic citrullinated peptide anti-bodies, and antinuclear factor were negative. The erythrocyte sedimentation rate (120 mm/h) and the C-reactive protein (12 mg/dL) were elevated.
Radiographs of the hands showed soft-tissue swelling of the right thumb and proximal phalanx of the index and little fingers. Calcium deposits were seen around the metacarpo-phalangeal joints of the index and middle fingers on the left and the proximal inter-phalangeal joint of the index finger on the right [Figure 1]b. Calcification was also present over the dorsum of the wrist [Figure 2]b, the head of the radius and ulna [Figure 3]b, and around the right little toe.
There was complete resolution of the inflammation with a two-week course of cortico-steroids. The serum phosphate fell to 2.24 mmol/L on regular HD, dietary restriction of phosphate, premeal timing of the phosphate binder, and low-dose alpha-calcidol. He did not experience any further episodes of peri-articular inflammation. It is likely that iatro-genic factors contributed to his presentation because at the time of presentation with periarticular calcification, he was on alpha-calcidol 0.25 μg/day despite his high calcium phosphate product.
| Discussion|| |
Deranged mineral and bone metabolism in chronic kidney disease (CKD) produces a wide spectrum of musculoskeletal symptoms, due to involvement of the bones, joints, and muscles and the occurrence of soft-tissue calcification. They may have a considerable impact on the quality of life of CKD patients.
The pathogenesis of extraosseus calcification is multifactorial, and possible mechanisms include hyperphosphatemia, hypercalcemia (often a consequence of excessive administration of calcium and Vitamin D), deficiencies in calcium regulatory proteins, hyperparathy-roidism, and chronic inflammation. The sites of extraosseus calcification include the soft tissues, viscera, and vasculature. The occurrence of vascular calcification, an established cardiovascular risk factor, is associated with increased mortality in CKD., A patient with systemic lupus erythematosus who had early and disseminated calcifications of vascular and periarticular soft tissues related to CKD-mineral and bone disorder (MBD) was reported by Yildiz et al in 2014.
The Kidney Disease: Improving Global Outcomes clinical guidelines set target levels for calcium, phosphate, and PTH for patients with CKD-MBD. Liu et al showed that achieving target levels for serum phosphate was associated with greatest reduction in all-cause mortality in patients on HD. However, the multinational OCEANOS study showed that greater vigilance is necessary as only 13.7% of the 2247 participants achieved all the three biochemical targets.
Periarticular calcification is a common radiological finding in patients with CKD and has been reported in 32% of a series of 241 patients by Andresan and Nielsen. It is usually asymptomatic, with tumoral calcinosis being the most frequent clinical presentation. Tumoral calcinosis is most commonly seen in patients with CKD and has been reported in 0.5-1.2% of patients on HD.,, Periarticular calcification is rarely associated with acute inflammation of the soft-tissue structures around the joints.
In 1964, Caner and Decker described a series of five patients with renal failure, presenting with periarthritis, tenosynovitis, and bursitis, in association with calcific nodules and radiological soft-tissue calcification. The episodes were monoarticular, had a predilection for the hands and wrists, and were recurrent. In 1973, Mirahmadi et al described a series of nine patients on HD, who developed tenosynovitis/ tendinitis, two of whom also had periarthritis. Moskowitz et al reported a patient with CKD and periarticular inflammation who showed clinical and radiological improvement with correction of hyperphosphatemia. Chalmers et al identified periarticular calcification in 12 of the 19 patients who developed joint inflammation while on peritoneal dialysis. Since then, there have only been isolated case reports of periarticular inflammation in association with calcification in CKD., Reports of extra-osseus calcification presenting as periarthritis, bursitis, and tenosynovitis, mimicking an inflammatory polyarthritis, are very uncommon.
Although hyperuricemia and gout occur in patients with CKD, the presence of peri-articular calcification rather than tophi or the typical erosive changes would make gout unlikely. While radiographic chondrocalci-nosis may be detected in patients with CKD, Yildiz et al noted that acute pseudogout is rare and usually presents as a monoarthritis or oligoarthritis. In a literature review in 2014, Jimbo et al noted that there were only seven cases of pseudogout reported in patients with CKD. Unfortunately, analysis of the synovial fluid from the olecranon bursitis was not undertaken in our patient. In the absence of analysis of the synovial fluid, gout and pseudogout could not be definitively excluded as contributory factors to the clinical presentation in our patient. Despite this limitation, our patient had an uncommon presentation with periarthritis, bursitis, and tenosynovitis.
In conclusion, we highlight an unusual presentation of periarticular calcification at multiple sites which responded to corticosteroid therapy. A good response was maintained with counseling, regular dialysis, and effective control of mineral metabolism.
| Acknowledgment|| |
The authors would like to thank Mr. Fundile Habana for assistance with the preparation of this manuscript.
| Consent|| |
Consent for publication was obtained from the patient and the Biomedical Research Ethics Committee of the University of KwaZulu-Natal.
| Source(s) of Support|| |
Financial support for a research assistant was obtained from the Aaron Beare Family Chair of Rheumatology Endowment Fund.
Conflict of interest
Dr. Kumari Naidoo and Dr. Kwazi C. Z. Ndlovu report no conflict of interest. Prof. Girish M. Mody has received honoraria from AstraZeneca (South Africa) and GlaxoSmithKline.
| References|| |
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Prof. Girish M Mody
Department of Rheumatology, University of KwaZulu-Natal and Inkosi Albert Luthuli Central Hospital, Durban 4001
[Figure 1], [Figure 2], [Figure 3]
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