The condition arises due to excessive activation of the thiazide-sensitive Na/Cl cotransporter (NCC) in the distal convoluted tubules, leading to increased NaCl reabsorption, reduced excretion of K+ and H+, and subsequent manifestations including high blood pressure, hyperkalemia, hyperchloremic metabolic acidosis, suppressed renin levels, and variable aldosterone levels. The gene discussed is REN; the disease is Hyperkalemia.