Non-crystalline and crystalline rheumatic disorders in chronic kidney disease

Sarraf, Pasha; Kay, Jonathan

doi:10.1007/s11926-008-0038-1

Cited by 14 publications

(18 citation statements)

References 97 publications

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“…Further, self-report could overinflate the prevalence of gout in the US as several studies show low validation rates with self-reported gout [53,54]. It should be noted that pseudogout is also associated with CKD [55] and in the absence of confirmatory arthrocentesis could be misclassified as gout. However, in sensitivity analyses using a more specific definition of gout, we observed the same relationship between CKD stages and gout.…”

Section: Discussionmentioning

confidence: 99%

Association of kidney disease with prevalent gout in the United States in 1988–1994 and 2007–2010

Juraschek

Kovell

Miller

et al. 2013

Seminars in Arthritis and Rheumatism

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Objective To determine the prevalence of gout associated with progressive degrees of kidney disease in the US population. Methods We performed a cross-sectional analysis among non-institutionalized adults (age 20 and older) of the National Health and Nutrition Examination Surveys in 1988–1994 and 2007–2010. Gout status was ascertained by self-report of physician-diagnosed gout. Chronic kidney disease (CKD) was defined in stages based on estimated glomerular filtration rate (GFR) and single albuminuria measurements (albumin-to-creatinine ratio). Prevalence ratios comparing successive categories of GFR, albuminuria, and CKD as well as temporal trends over a 22-year interval were determined via Poisson regression. Results In the US, the crude prevalence of gout was 2–3% among participants without CKD, 4% among participants with CKD stage 1, 6–10% for stage 2, 11–13% for stage 3, and over 30% for stage 4. The adjusted prevalence ratio comparing the CKD stage 4 stratum to participants without CKD was 3.20 (95% CI: 1.96, 5.24) in 2007–2010 and remained significant even after adjustment for serum uric acid. Notably, there was a statistically significant, progressively greater adjusted prevalence ratio of gout associated with successively lower categories of GFR and higher categories of albuminuria. Conclusions Among US adults, there exists a strong dose–response association between impaired renal function and prevalent gout. Health providers should be aware of the elevated burden of gout among patients with CKD especially when evaluating new onset joint pain and swelling.

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Section: Discussionmentioning

confidence: 99%

Association of kidney disease with prevalent gout in the United States in 1988–1994 and 2007–2010

Juraschek

Kovell

Miller

et al. 2013

Seminars in Arthritis and Rheumatism

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“…Oxalate arthritis may result from deposition of calcium oxalate crystals within bones, tendons, cartilage, and synovium. From these sites the crystals are thought to gain entry into the synovial fluid where they invoke an inflammatory response 44 causing joint effusions and arthralgias 45, 46 . Alternatively, supersaturation of calcium oxalate within the synovial fluid itself may lead to local crystal formation, especially when fluid is removed during dialysis, a phenomenon referred to as articular hyperconcentration 47 .…”

Section: Signs and Symptomsmentioning

confidence: 99%

“…Typical joint involvement includes the proximal interphalangeal and metacarpophalangeal joints, knees, elbows and ankles 48 . X-rays of the joints in hyperoxaluria may reveal calcification around the joints and within tendon sheaths and soft tissue 45 . Chondrocalcinosis of the metacarpophalangeal and metatarsophalangeal joints may be seen 48 .…”

Section: Signs and Symptomsmentioning

confidence: 99%

“…X-ray imaging reveals fractures, pseudofractures 45 , sclerosis, cystic bone changes, subperiosteal resorption adjacent to oxalate deposits 48, 49 , dense metaphyseal bands 50 and increased bone density 51 (see Figure 1). Calcium oxalate has a tendency to crystallize in previously damaged joints, such as distal and proximal interphalangeal joints involved in osteoarthritis, thus presenting as soft tissue calcification about the degenerated joint 47 .…”

Section: Signs and Symptomsmentioning

confidence: 99%

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Update on Oxalate Crystal Disease

et al. 2013

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Oxalate arthropathy is a rare cause of arthritis characterized by deposition of calcium oxalate crystals within synovial fluid. This condition typically occurs in patients with underlying primary or secondary hyperoxaluria. Primary hyperoxaluria constitutes a group of genetic disorders resulting in endogenous overproduction of oxalate, whereas secondary hyperoxaluria results from gastrointestinal disorders associated with fat malabsorption and increased absorption of dietary oxalate. In both conditions oxalate crystals can deposit in the kidney leading to renal failure. Since oxalate is primarily renally eliminated, it accumulates throughout the body in renal failure, a state termed oxalosis. Affected organs can include bones, joints, heart, eyes and skin. Since patients can present with renal failure and oxalosis before the underlying diagnosis of hyperoxaluria has been made, it is important to consider hyperoxaluria in patients who present with unexplained soft tissue crystal deposition. The best treatment of oxalosis is prevention. If patients present with advanced disease, treatment of oxalate arthritis consists of symptom management and control of the underlying disease process.

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“…Similar to HH the prevalence of hyperparathyroidism in patients with CC is low 10. The association between hypomagnesia and CC has been mainly demonstrated in patients with Gitelman’s or Bartter syndrome 10 11. Given the low incidence of sporadic CC in patients under the age of 55, current opinion is that it is reasonable to screen such patients with CC for the above metabolic conditions.…”

Section: Discussionmentioning

confidence: 92%