The initial evaluation of a patient presenting with newly diagnosed kidney stones should be aimed at identifying factors predisposing to stone formation and should be performed in the context of stone composition, if a stone analysis is available. The medical history may reveal stone-relevant medical conditions including type 2 diabetes, obesity, bone disease/osteoporosis, neoplasm, endocrine disorders including hyperthyroidism and primary hyperparathyroidism, distal renal tubular acidosis (RTA), gastrointestinal (GI) malabsorptive states, and recurrent or persistent UTI. Relevant surgical history, including urologic and GI surgery, should be elicited as well. Indeed, malabsorptive bariatric surgery has been associated with a four- to six-fold increased risk of nephrolithiasis.79, 80 An inventory of prescribed medications, over-the-counter medications, and supplements should be reviewed to identify any potential pharmacologic contribution to stone risk. For example, carbonic anhydrase inhibitors including acetazolamide,81 topiramate,82 and zonisamide83 have been associated with lithogenic urinary alterations and a significantly increased risk of subsequent symptomatic kidney stones. Uricosuric medications should be noted as they may contribute to hyperuricosuria. In addition, some uncommon poorly soluble, renally excreted medications including older protease inhibitors such as indinavir and some antibiotics may directly precipitate in urine and form kidney stones.84 Limited data have identified an increased risk of kidney stones with excessive intake of supplemental vitamin C85 and supplemental calcium.86 Excessive vitamin D supplementation should be assessed. Family history should be reviewed for history of nephrolithiasis, gout, or multiple endocrine neoplasia (in view of its association with primary hyperparathyroidism), and may suggest inherited monogenic stone disease as further explored in Statement 7. Dietary history should elicit estimates of fluid intake, fruits and vegetables, dietary calcium, ketogenic diet, and proclivities for oxalate-rich, high purine, high protein (particularly from animal sources), and/or sodium-rich foods. Physical examination may reveal conditions associated with an increased risk of stones, such as obesity. Furthermore, evidence of GI reconstructive procedures may raise suspicion for high fluid losses, such as high output ostomies in those with ileostomy/colostomy. Baseline laboratory testing should include serum chemistries and UA. Serum chemistry studies will reveal electrolyte abnormalities, such as hypercalcemia, that may contribute to calcium stone formation through hypercalciuria and may suggest primary hyperparathyroidism or sarcoidosis. Indeed, serum calcium has been cited as the most important serum test in patients presenting with stones.87 Additionally, hypokalemia, particularly when associated with low serum bicarbonate, may implicate distal RTA or chronic diarrhea. Serum chemistry testing may include uric acid to identify hyperuricemia, and serum glucose to identify hyperglycemia, both of which may be associated with kidney stones.88, 89 Serum creatinine allows for assessment of renal function, as it may impact the type or dose of medications used for stone prevention. Elevated creatinine revealing CKD may also prompt consideration of testing for genetic diseases such as primary hyperoxaluria and Dent’s Disease. Dipstick UA can suggest a UTI which should prompt a urine culture. Additionally, urine-specific gravity provides an estimate of urinary concentration and reflects the balance between fluid intake and fluid loss, and urinary pH may raise suspicion of pH-dependent stones such as uric acid, calcium phosphate, and struvite stones. Urine microscopy may reveal crystalluria, and in particular, identification of pathognomonic cystine or struvite crystals.90