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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Massive periarticular calcinosis of the soft tissues is a unique but not rare radiographic finding. On the contrary, tumoral calcinosis is a rare familial disease. Unfortunately, the term tumoral calcinosis has been liberally and imprecisely used to describe any massive collection of periarticular calcification, although this term actually refers to a hereditary condition associated with massive periarticular calcification. The inconsistent use of this term has created confusion throughout the literature. More important, if the radiologist is unfamiliar with tumoral calcinosis or disease processes that mimic this condition, then diagnosis could be impeded, treatment could be delayed, and undue alarm could be raised, possibly leading to unwarranted surgical procedures. The soft-tissue lesions of tumoral calcinosis are typically lobulated, well-demarcated calcifications that are most often distributed along the extensor surfaces of large joints. There are many conditions with similar appearances, including the calcinosis of chronic renal failure, calcinosis universalis, calcinosis circumscripta, calcific tendonitis, synovial osteochondromatosis, synovial sarcoma, osteosarcoma, myositis ossificans, tophaceous gout, and calcific myonecrosis. The radiologist plays a critical role in avoiding unnecessary invasive procedures and in guiding the selection of appropriate tests that can result in a conclusive diagnosis of tumoral calcinosis.
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PMID:Tumoral calcinosis: pearls, polemics, and alternative possibilities. 1670 60

Here, we report a case of matrix stone in a 32-year-old man with diabetes, gout, and chronic renal failure. The patient complained of pain in the left flank. He had undergone an operation for bilateral vesicoureteral reflex at the age of 17 and matrix stone discharge was repeated. Computed tomography revealed a soft tissue mass in the right hydroureter. Percutaneous ureteral lithotripsy was performed successfully. Analysis of the stone components revealed the stone to be composed entirely of protein. Radiological imaging of matrix stones may be difficult to separate from urothelial cancers.
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PMID:[Matrix stone: a case report]. 1675 27

The etiology and mechanisms of Achilles, patellar and quadriceps tendon ruptures are very similar. Age dependent changes in tendon structure and disorders such gout, diabetes, rheumatic diseases and chronic renal failure are associated causes. The main mechanism of rupture is indirect trauma. Although clinical diagnosis is easy, ruptures are still frequently missed. Sonography is the main standard diagnostic tool. MRI is indicated only in special cases. Open operative repair is the most common treatment for quadriceps and patellar tendon ruptures. Treatment of Achilles tendon ruptures is moving towards an individualized choice of therapy. Percutaneous and other "minimally invasive" techniques will play an increasingly important role.
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PMID:[Damage to large tendons: Achilles, patellar and quadriceps tendons]. 1678 38

Hyperuricemia and gout are common complications in adult renal transplant recipients. In pediatric recipients, however, hyperuricemia seems to be rare, but data are scarce. Thirty-two children (21 males, 11 females) were investigated for a median time of 4.8 years (range: 0.4-11.2 years) following renal transplantation. The median age of this pediatric study group was 13.9 years (range: 5.7-20.3 years), and the calculated glomerular filtration rate (GFR) was 61 ml/min per 1.73 m(2) (range:12-88 ml/min per 1.73 m(2)). All patients were given calcineurin inhibitors, with 22 and ten children receiving cyclosporine A (CSA) and tacrolimus (TAC), respectively. The median plasma uric acid was 385 micromol/l (range: 62-929 micromol/l); 15 children (47%) were above the age-related normal range. Only one patient experienced gouty arthritis. There was a significant correlation between plasma uric acid concentration and both time span after transplantation and plasma creatinine, and an inverse correlation to GFR (p<0.05). No significant correlation was found between plasma uric acid and body mass index (BMI). Plasma uric acid concentrations were neither different among CSA- and TAC-treated children, nor did they correlate with drug exposure or blood trough levels of CSA or TAC. Plasma uric acid concentration was not different when compared to children with chronic renal failure (CRF) of a similar degree in native kidneys. We conclude that hyperuricemia is common among pediatric renal transplant recipients and rather a consequence of chronic renal transplant dysfunction than the use of calcineurin inhibitors. Gout, however, is rare.
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PMID:Hyperuricemia and gout following pediatric renal transplantation. 1694 31

Gout continues to be a health problem around the world, and the treatment may turn into a real challenge when the patient presents a certain degree of chronic renal failure (CRF). We discuss a case of tophaceous gout in a 68-year-old male patient without urolithiasis and with uric acid (UA) underexcretion and CRF (creatinine clearance of 42 ml/min). Uricosuric treatment with benzbromarone and urinary alkalinization was administered, and acute gouty attacks improved substantially. Subsequently, allopurinol was added to the treatment to accelerate tophi reduction in the hands, feet, elbows and knees. After 30 months of treatment, serum UA declined from 10 to 3.2 mg/dl. Urinary UA excretion of 0.44 g/24 h in the baseline rose to 0.85 g/24 h, returning to the baseline value after 30 months. UA clearance tripled, rising from 3.05 ml/min before treatment to 9.48 ml/min, and remained at this level. It is worth stressing that even in cases of severe tophaceous gout, the response to clinical treatment may be satisfactory with substantial reduction of tophi and full acute gouty attack remission even in patients presenting a certain degree of CRF.
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PMID:Excellent response to the clinical treatment of tophaceous gout. 1704 91

A case of colchicine-induced rhabdomyolysis is reported. A 79-year-old man with ischemic heart disease, chronic atrial fibrillation, chronic renal failure, hypothyroidism, and gout arthritis was hospitalized because of fatigue, myalgia, and leg weakness, shortly after starting treatment with colchicine. Investigation confirmed the diagnosis of rhabdomyolysis, and discontinuation of colchicine resulted in resolution of clinical and biochemical features of rhabdomylysis. Colchicine-induced rhabdomyolysis is a rare complication, and the postulated mechanisms and risk factors for this severe complication are discussed.
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PMID:Colchicine-induced rhabdomyolysis. 1761 11

Gout is one of the most common inflammatory arthritides, which is considered to be a true crystal deposition disorder caused by the formation of monosodium urate crystals in and around joints. A number of epidemiological studies from a diverse range of countries suggest that gout has increased in prevalence and incidence in recent years and that the clinical pattern of gout is becoming more complex. In particular, the greatest increase has been observed in primary gout in older men. Robust epidemiological studies have established risk factors for gout including genetic factors, excess alcohol consumption, purine-rich diet, the metabolic syndrome (obesity, hypertension, hyperlipidemia and insulin resistance), use of diuretics and chronic renal failure. Trends in alcohol use, diet, obesity and the metabolic syndrome in the general population might explain changes in the prevalence and incidence of gout in the community. Osteoarthritis, which is thought to predispose patients to monosodium urate crystal deposition in their joints, is becoming more prevalent as a consequence of increased longevity. In hospital settings, widespread diuretic use, increasing prevalence of end-stage renal failure and the success of organ transplant programmes have led to an increase in clinical complexity. Suboptimal management of gout is likely to have contributed to the rise in the prevalence of clinically overt, symptomatic, chronic gout.
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PMID:The changing epidemiology of gout. 1788 62

Familial juvenile hyperuricemic nephropathy (FJHN) and medullary cystic kidney disease type 2 (MCKD2) are autosomal dominant disorders characterized by juvenile hyperuricemia of the underexcretion type, juvenile gout and chronic renal failure in the adult. FJHN/MCKD2 constitute diseases caused by mutations of the human uromodulin (UMOD) gene that encodes uromodulin, the most abundant glycoprotein in normal human urine. The mutations affect the transport of uromodulin, resulting in the accumulation of uromodulin in the kidneys of FJHN/MCKD2 patients. The purpose of this study was to confirm the accumulation of uromodulin in the kidneys of transgenic mice harboring the mutant human UMOD gene with mouse UMOD gene promoter, and to determine the relationship between its accumulation and the effect on uromodulin transport. The mutant human UMOD mRNA and its protein were expressed in the kidneys of transgenic mice. Moreover, the staining of human uromodulin was colocalized with that of mouse uromodulin. Although the human UMOD mRNA levels increased, the protein levels did not change and the accumulation of human uromodulin was not observed. However, the mouse uromodulin consists of two forms, 103 and 117 kDa, and the 103 kDa protein was gradually increased in the kidneys of transgenic mice. Human and mouse uromodulins in the kidneys of transgenic mice were mainly detected in the Triton X-100 insoluble microsomal fraction. Therefore, the progressive accumulation of uromodulin was observed in the plasma membrane of the kidneys of transgenic mice but the accumulated uromodulin protein was not that encoded by the transgene.
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PMID:Progressive accumulation of intrinsic mouse uromodulin in the kidneys of transgenic mice harboring the mutant human uromodulin gene. 1831 Sep 1

The overall incidence of nephrolithiasis-related acute and chronic renal failure is poorly known and surely underestimated. However, obstructive nephropathy represents a potentially curable form of kidney disease that often requires for managing an instrumentation of urinary tract. Rasburicase is an enzyme that transforms uric acid to allantoin, a compound more water soluble that will be excreted by the kidney more easily. Rasburicase has been proven to be an effective therapy for prevention of tumour lysis syndrome. But it also represents an interesting new option in managing hyperuricemia in patients with severe tophaceous gout. We administered rasburicase intravenously (0.20 mg/kg/day, for 2 days) in 2 adults with acute obstructive nephropathy from renal calculi, which was receiving temporary haemodialysis. Rasburicase produced a sharp polyuria 12-18 hours after its administration accompanied with a fast reduction of serum creatinine levels, that returned to normal range without further dialysis. If we suppose that rasburicase can pass through glomerular filter by its relatively low molecular weight, it could dissolve tubular uric acid crystals in acute renal failure associated to tumour lysis syndrome, providing the restoration of renal function. But we also could postulate that rasburicase can act in urinary tract, fragmentating renal calculi, promoting relief of obstructive uropathy and the resolution of renal failure. We suggest rasburicase should be tried in this new indication to prove its potential efficacy.
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PMID:[Efficacy of rasburicase therapy in obstructive renal failure secondary to urolithiasis: a novel therapeutic option]. 1833 40

Familial juvenile hyperuricemic nephropathy (FJHN) is an autosomal-dominant disease characterized by hyperuricemia of underexcretion type, gout, and chronic renal failure. Recent discovery of uromodulin mutations as a cause of FJHN and MCKD2 led a new concept, i.e. uromodulin-associated kidney disease (UAKD). The genotype-phenotype correlation and genetic heterogeneity of FJHN are reviewed.
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PMID:[Familial juvenile hyperuricemic nephropathy (FJHN)]. 1840 15


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