Abstract

Introduction: Uric acid is a product of purine metabolism and elevated serum concentration are very common in, and linked with hypertension and chronic kidney disease, conditions associated with heavy health burden and cardiovascular complications particularly in sub Sahara Africa. An assessment of factors relating hyperuricemia to hypertension and chronic kidney disease would therefore be necessary as way of mitigating the poor quality of life, morbidity and mortality associated with these diseases in low income nations. Methods: A single centre, descriptive comparative study in which the demographic, clinical and laboratory data of hypertensive and non-dialyzed chronic kidney disease (CKD) patients were analyzed. Serum biochemical parameters with uric acid, hematocrit and urine dip strip protein were assessed. Predictors of hyperuricemia were determined using multivariate analysis. Results: One hundred and thirty nine hypertensives and 69 CKD were studied. The mean age of the participants was 54.3 ± 11.7 years, hypertensives (52.9 ± 15.7 years) and CKD (57.3 ± 16.1 years). Both groups had more males, P = 0.8. Majority (78.3%) of the CKD cohorts had stage 4 or 5 (non-dialyzed) disease. The systolic and diastolic blood pressure, creatinine and uric acid were lower in hypertension than in CKD, P = 0.07, P = 0.05, P < 0.001 and P = 0.004 respectively. The hematocrit, albumin and GFR were higher in HTN than CKD, P < 0.001, P < 0.001 and P < 0.001 respectively. The prevalence of hyperuricemia was 56.2%. The mean uric acid was 505.9 ± 23.6 mmol/L, 382 7 ± 10.5 mmol/L for hypertensive and 755.9 ± 14.8 mmol/L for CKD, P < 0.001. The prevalence of systolic HTN, proteinuria, hypoalbuminemia and anemia were 51%, 75%, 46% and 59%, and were higher in males. Hyperuricemia was related to advancing age, proteinuria, elevated creatinine, hypoalbuminemia, anemia and hypertriglyceridemia. Proteinuria (OR—4.66, 95% CI—2.42 - 9.65), elevated creatinine (OR—3.12, 95% CI—2.40 - 6.92), hypoalbuminemia (OR—2.92, 95% CI—1.83 - 5.78) and anemia (OR—4.01, 95% CI—3.78 - 7.99) independently predicted hyperuricemia. Conclusion: Hyperuricemia is commoner in CKD than hypertension and was higher in males and positively correlated with the blood pressure, proteinuria and creatinine, but negatively related to hematocrit, albumin and glomerular filtration rate. Independent predictors of hyperuricemia were proteinuria, elevated creatinine, hypoalbuminemia and anemia. Measures are needed to prevent and treat hyperuricemia to reduce the health burden associated with hypertension and CKD.

Highlights

  • Uric acid is a product of purine metabolism and elevated serum concentration are very common in, and linked with hypertension and chronic kidney disease, conditions associated with heavy health burden and cardiovascular complications in sub Sahara Africa

  • The prevalence of hyperuricemia in HWCKD mirrors that found by Cannon et al [27] but higher than the 41.4% (35% in males, 43% in females) found in a nationwide survey of Taiwanese hypertensives [28], higher than the 38.7% found in the Chinese hypertensive population [29], and much higher than the 14% reported by Fan et al [30]

  • It is higher than the 67% reported by Doualla et al [5] in Cameroon, another low income nation, higher than the 47.5% found by Adejumon et al [4] in Nigeria, higher than the 60% found in Italy, and much higher than the 15.2% reported in Chad

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Summary

Introduction

Uric acid is a product of purine metabolism and elevated serum concentration are very common in, and linked with hypertension and chronic kidney disease, conditions associated with heavy health burden and cardiovascular complications in sub Sahara Africa. A definitive causative relationship has not been established between hyperuricemia and HTN or CKD, the associations between hyperuricemia and HTN, and with CKD are reported to be mediated through chronic inflammatory changes with renal microvascular injury involving the endothelium induced by the activation of the renin angiotensin aldosterone system (RAAS) [6] This occurs mostly in the intracellular and intravascular spaces and an end point of this inflammatory state is endothelial injury, release of vasoactive cytokines, atherosclerosis and increased cardiovascular risk profile [7].

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