Renal outcomes of gout and hyperuricemia

Fessel, W. J.

doi:10.1016/0002-9343(79)90076-7

Cited by 181 publications

(58 citation statements)

References 12 publications

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“…However, large numbers of patients with asymptomatic hyperuricemia followed for long periods of time failed to exhibit an increased incidence of gout or kidney stones [30, 31], and the risk of renal disease developing remained low, unless the serum urate was very high. These observations seem consistent with the very infrequent development of significant renal disease in patients with gout – even in those who did not receive treatment [32, 33, 34]. …”

Section: Spectrum Of ‘Chronic Hyperuricemic Nephropathy’supporting

confidence: 76%

Hyperuricemic Nephropathies

Steele¹

1998

Nephron

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This review explores the relationship between uric acid or urate and the pathogenesis of renal impairment. The following points and conclusions are emphasized: (1) uric acid is an end product of purine degradation in humans and normally depends upon renal excretion for the majority of its elimination from the body; (2) massive urate overproduction – usually occurring acutely because of tumor lysis, rhabdomyolysis, or some other cause of rapid nucleic acid turnover or tissue destruction – tends to cause acute renal failure because of an increase of intratubular uric acid precipitation and obstruction; (3) chronic urate overproduction (with increased urate excretion) is more likely to be associated with stones or gout than with acute renal failure; (4) chronic asymptomatic hyperuricemia is unlikely to cause renal disease, gout, or stones, but is associated with cardiovascular impairment over the long term, and (5) asymptomatic hyperuricemia may serve as an indicator of renal vascular disease, or, to the extent that it may reflect insulin-induced acceleration of renal tubule urate reabsorption, hyperuricemia may serve as an indicator of insulin resistance. Therefore chronic asymptomatic hyperuricemia may predict the adverse cardiovascular consequences of insulin resistance.

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Section: Spectrum Of ‘Chronic Hyperuricemic Nephropathy’supporting

confidence: 76%

Hyperuricemic Nephropathies

Steele¹

1998

Nephron

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“…Thus, increased uric acid levels might have a pathogenic role in the development and progression of both CKD and cardiovascular disease, and thereby underlie the proposed cardio-renal connection, rather than merely reflecting an impaired renal excretion of uric acid [11]. Indeed, hyperuricemia has been associated with progression of kidney disease in diabetic nephropathy [12] and individuals with normal kidney function [13], although data surrounding this relationship are contradictory [14,15,16] and the clinical significance of an increase in uric acid levels within normal limits remains unclear. However, recent cohort studies by cross-sectional analysis demonstrated a close association between serum uric acid and CKD in the general population [17,18,19].…”

Section: Introductionmentioning

confidence: 99%

Uric Acid Levels Predict Future Development of Chronic Kidney Disease

et al. 2011

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Aims: Increased uric acid levels are associated with kidney dysfunction. We tested the hypothesis that uric acid level predicts future development of chronic kidney disease (CKD) in the general population. Methods: For this study, we enrolled 7,078 consecutive subjects with normal estimated glomerular filtration rates (eGFR; ≧60 ml/min/1.73 m²) who visited our hospital for a yearly health checkup (age: 52.8 ± 10.7 years; female: 35.8%). Subjects underwent a routine physical examination and laboratory assessment of cardiovascular disease risk factors at enrollment, and were followed up for 1,694 days (median) with the endpoint being the development of CKD (eGFR <60 ml/min/1.73 m²). The impact of uric acid and other cardiovascular risk factors at baseline on the future development of CKD were assessed. Results: During the follow-up period, 417 male (9.2%) and 151 female subjects (6.0%) developed CKD. Univariate logistic regression analysis revealed a significant association between the onset of CKD and age, male gender, body mass index, blood pressure, fasting plasma glucose, dyslipidemia and uric acid. Multiple logistic regression analysis revealed that new-onset CKD was independently correlated with the baseline uric acid level after adjustment for possible factors. Subanalysis showed similar results in subjects with normal uric acid levels (male: ≤7.0 mg/dl; female: ≤6.0 mg/dl; n = 6,223). Conclusion: Uric acid is an independent predictor of future development of CKD. Whether preventing an increase in uric acid levels reduces the incidence of CKD must be clarified by prospective follow-up studies.

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“…1 ]. In contrast, many authors advocated that neither sustained hyperuricemia nor gout per se would independently affect the renal function [7][8][9][10][11], When renal failure developed in gouty patients, it was usually ascribed to some complicated associated medical conditions such as hypertension (HTN), diabetes mellitus, and arteriosclero sis [7][8][9]11]. Linnane et al [12] and Verger et al [13] claimed that most cases exhibiting urate deposits in the renal medulla were frequently associated with preexisting and nongouty renal diseases.…”

Section: Introductionmentioning

confidence: 99%

Renal Function in Gout Patients

et al. 1995

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Patients with gouty arthritis were examined at Veterans General Hospital to evaluate whether their renal function is impaired and to define the factor(s), if any, of renal function deterioration. A total of 152 cases were included in the study, and the patients were divided into two groups. One group (n = 80) exhibited pure gout without any associated medical problems or preexisting renal disorders. The second group (n = 72) included patients with gout and hypertension. The group with pure gout was further stratified into patients with tophi (n = 21) and those without (n = 59). Seventy-two sex- and age-matched normal adults served as the control group. We found (l)that the renal function was impaired in the pure-gout group when compared with sex-and age-matched normal individuals (serum creatinine 1.56 ± 0.64 vs. 0.90 ± 0.16mg/dl, p = 0.0001; creatinine clearance 59.91 ± 30.90 vs. 97.10 ± 27.19 ml/min, p = 0.0001); (2) that the renal function was significantly more aggravated in patients with clinically visible tophi than in those without (gout with tophi vs. gout without tophi: serum creatinine 1.89 ± 0.90 vs. 1.44 ± 0.48 mg/dl p = 0.040; creatinine clearance 47.27 ± 31.90 vs. 64.40 ± 29.53 ml/min, p = 0.030), and (3) that a further significant decline of the renal function was noted in gouty patients with an associated medical illness, i.e., hypertension (gout with hypertension vs. pure gout: serum creatinine 2.10 ± 0.97 vs. 1.56 ± 0.64 mg/dl, p = 0.0001; creatinine clearance 45.06 ± 24.69 vs. 59.91 ± 30.90 ml/min, p = 0.0029). From image studies, i.e., renal sonogram and KUB film, it was determined that 19 out of 21 cases with tophaceous gout had highly echogenic and radiolucent lesions scattered over the corticomedullary junctions of both shrunken kidneys. Renal biopsy was performed in 4 such patients with tophaceous gout and impaired renal function, and pathological investigation disclosed a mixture of tubular, interstitial, and vascular lesions. Most importantly, the presence of urate deposits with giant cell reaction in the medullary interstitium was characteristic in all our patients. A fairly satisfactory association could be found with clinically visible tophi, with radiolucent and highly echogenic lesions in the kidneys, and with the distinctive presence of urate deposits in the renal medulla. This paper draws attention to the importance that gouty kidney, lead poisoning, or genetic factors may play a role in the pathogenesis of renal disorder of gouty patients.

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Renal outcomes of gout and hyperuricemia

Cited by 181 publications

References 12 publications

Hyperuricemic Nephropathies

Hyperuricemic Nephropathies

Uric Acid Levels Predict Future Development of Chronic Kidney Disease

Renal Function in Gout Patients

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