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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