The key concept is that the kidney cannot distinguish lithium from sodium in the proximal tubule. Anything that makes the body retain sodium will simultaneously make it retain lithium. Diuretics, by promoting natriuresis and shrinking the extracellular volume, trigger a compensatory upregulation of proximal sodium reabsorption; lithium piggybacks on this process and its renal excretion drops sharply. Since lithium already has a dangerously narrow margin between therapeutic and toxic plasma concentrations, this reduced clearance can quickly push levels into the toxic zone, producing coarse tremor, ataxia, confusion and cardiac disturbances. That is why a diuretic is the antihypertensive to steer clear of when a patient is on lithium. By contrast, the centrally acting agent clonidine, the beta-adrenergic blockers and the calcium channel blockers do not meaningfully alter renal lithium handling and are far safer choices for blood-pressure control in such patients. \[\boxed{\text{Diuretics}}\]