allopurinol and Polycystic-Kidney-Diseases

Hyperuricemia is a common feature in patients with chronic kidney disease (CKD). Hyperuricemia has been associated with increased cardiovascular mortality in the general population, but less is known about this association in patients with CKD.. To explore possible associations of serum uric acid with all-cause mortality and comorbidity in patients with CKD, we studied 294 incident patients with CKD stage 5 (185 men; age, 53 +/- 12 years) starting renal replacement therapy with a median glomerular filtration rate of 6.4 mL/min/1.73 m(2) (0.11 mL/s/1.73 m(2); range, 0.8 to 14.3 mL/min/1.73 m(2) [0.01 to 0.24 mL/s/1.73 m(2)]). Survival was determined from the day of examination and during a mean follow-up period of 27 months (range, 3 to 72 months); 94 patients died. Patients were divided into 3 groups based on serum uric acid levels (low quintile, 3 middle quintiles, and high quintile).. In a nonadjusted analysis, patients in the high quintile, followed by patients in the low quintile, had greater all-cause mortality compared with patients in the 3 middle quintiles (log-rank test chi-square, 6.8; P = 0.03). After adjusting for age, sex, glomerular filtration rate, cholesterol level, phosphate level, C-reactive protein level, cardiovascular disease, diabetes mellitus, diuretics, and allopurinol treatment, the association showed a "J-shaped" association with hazard ratios of 1.96 (confidence interval, 1.10 to 3.48; P = 0.02) for the high quintile and 1.42 (confidence interval, 0.76 to 2.66; P = not significant) for the low quintile. Moreover, uric acid levels correlated positively with levels of triglycerides, phosphate, C-reactive protein, and intracellular adhesion molecule 1 and negatively with levels of calcium, high-density lipoprotein cholesterol, and apolipoprotein A.. Serum uric acid levels showed a J-shaped association with all-cause mortality, with the lowest risk in the 3 middle quintiles. Moreover, uric acid level was associated with calcium/phosphate metabolism, dyslipidemia, and inflammation.

Topics: Adult; Aged; Allopurinol; Antimetabolites; Cause of Death; Comorbidity; Confounding Factors, Epidemiologic; Diabetic Nephropathies; Diuretics; Female; Follow-Up Studies; Glomerulonephritis; Humans; Hyperuricemia; Male; Middle Aged; Nutritional Status; Phosphates; Polycystic Kidney Diseases; Proportional Hazards Models; Prospective Studies; Renal Insufficiency, Chronic; Renal Replacement Therapy; Survival Analysis; Triglycerides; Uric Acid

A 43 year old female patient with chronic renal failure originated from polycystic kidney disease was admitted with pancytopenia. Prior to the admission, she had a history of taking allopurinol for 3 months. Allopurinol was discontinued immediately and she was treated with blood transfusion (platelet and RBC) and fluoxymesterone. The lymphocyte stimulation tests were negative for allopurinol and oxipurinol. The determination of serum levels of allopurinol and oxipurinol was disclosed to be not so high compared with other patients treated with allopurinol. On 45th day after admission, she was transfused with bone marrow from her elder brother. Thereafter bone marrow finding of the patient began to improve despite the lack of bone marrow engraftment. For further improvement, pulse treatment with corticosteroid was carried out. Although the pathophysiology of allopurinol-induced aplastic anemia remains unknown, it is interesting to note that bone marrow transfusion and pulse treatment with corticosteroid seemed effective in this case.

Topics: Adult; Allopurinol; Anemia, Aplastic; Blood Transfusion; Bone Marrow Transplantation; Female; Humans; Kidney Failure, Chronic; Methylprednisolone; Polycystic Kidney Diseases