Step 1: Begin with the chemistry. Purines are broken down through hypoxanthine and xanthine to uric acid, a reaction catalysed by xanthine oxidase. Gout appears when the body either makes too much urate or clears too little of it. Step 2: The defining laboratory feature and the true engine of the disease is a high serum urate level, written as $[\text{urate}]_{serum} > 6.8\ mg/dL$, the saturation point. Past this point urate precipitates as monosodium urate crystals. Step 3: Those crystals are phagocytosed by neutrophils, which release inflammatory mediators and cause the painful acute attack. Hence the metabolic root is the elevated urate concentration, option c. Step 4: Reject the distractors: blocking xanthine oxidase (option b) is the basis of allopurinol THERAPY and would drop urate, not cause gout; stones (option a) and interstitial nephropathy (option d) are downstream consequences. The printed key (b) is medically wrong. \[\boxed{\text{Increase in serum urate concentration}}\]