A kidney stone most commonly presents with severe flank pain, sudden in onset, and is often associated with nausea and vomiting. The radiation of the pain may provide some clue as to where in the urinary tract the stone is lodged. Stones in the ureteropelvic junction cause flank pain that may radiate to the groin, whereas those lodged in the narrowest portion of the ureter, where it enters the bladder, are associated with signs of bladder irritation (dysuria, frequency, and urgency). Struvite-carbonate stones are, on occasion, incidentally discovered on abdominal radiograph. A careful abdominal examination and, in women, a pelvic examination are important to rule out other potential causes of abdominal pain.

A. Laboratory evaluation should include a complete blood cell count, serum chemistries, and urinalysis. The white blood cell count may be mildly elevated but is generally less than 15,000/mm³. A white blood cell count greater than 15,000/mm³ is suggestive of another intra-abdominal cause or an associated infection behind an obstructing calculus. An elevation of the serum blood urea nitrogen (BUN) and creatinine concentrations indicates prerenal azotemia, parenchymal renal disease, or obstruction of
a solitary functioning kidney. A urinalysis should be performed routinely in any patient with abdominal pain. Microscopic hematuria is observed in approximately 90% of patients with renal colic.

B. Once the diagnosis is suspected based on the history, physical examination, and preliminary laboratory studies, establishing a definitive diagnosis is the focus of the next stage of the evaluation.

1. A flat radiographic plate of the abdomen is often obtained and is capable of identifying radiopaque stones (calcium oxalate, calcium phosphate, struvite-carbonate, and cystine) that are ???2 mm in size. It will miss radiolucent stones, the most common of which are composed of uric acid, and stones that overlie the bony pelvis. For these reasons, an abdominal flat plate is most valuable in ruling out other intra-abdominal processes.

2. An ultrasonographic examination of the genitourinary tract often identifies stones in the renal pelvis; however, most of the stones are lodged in the ureter, and the ultrasonographic examination often misses these.

3. The intravenous pyelogram (IVP) was formerly considered the gold standard for the diagnosis of nephrolithiasis and is still of considerable value in the acute setting. Although the stone itself may not be visualized on IVP, the site of obstruction is regularly identified. Structural or anatomic abnormalities that may be present in the urinary tract and renal or ureteral complications can be recognized. Disadvantages of the IVP include the need for intravenous contrast and the prolonged waiting time often required to visualize the collecting system on the side of the obstruction.

4. Spiral computed tomography (CT) is the test of choice in the patient with suspected renal colic. The advantages of spiral CT include higher sensitivity, faster scan times, and lack of need for contrast.

C. Management. After the diagnosis is established, subsequent management is determined by (a) the presence or absence of associated pyelonephritis; (b) whether parenteral narcotics are required for pain control; and (c) the likelihood of spontaneous stone passage. Obstructing calculi can be managed with observation alone if pain can be controlled with oral analgesics and spontaneous passage is likely. Extracorporeal shock wave lithotripsy or ureteroscopic lithotripsy may need to be employed for stones lodged in the upper ureter. Calculi in the lower ureter can be removed by cystoscopy and ureteroscopy. Hospital admission is necessary if there is evidence of renal parenchymal infection; when nausea, vomiting, or severe pain precludes oral analgesic use; or the stone is unlikely to pass spontaneously. The likelihood of spontaneous passage is determined by stone size and location in the ureter (Table 6-1). Small stones in the distal ureter will likely pass, whereas large stones in the upper ureter will likely require urologic consultation and intervention. α1-Receptor antagonists, such as tamsulosin, and calcium channel blockers can be used to aid stone passage (medical expulsive therapy).

A. Calcium-containing stones make up 90% of all stones and are generally composed of a mixture of calcium oxalate and calcium phosphate. In mixed stones, calcium oxalate usually predominates, and pure calcium oxalate
stones are more common than pure calcium phosphate stones. Calcium phosphate tends to precipitate in alkaline urine, as occurs with renal tubular acidosis (RTA), whereas the precipitation of calcium oxalate does not vary with pH. Because urine is acidic in most patients, calcium oxalate stones are more common. The major risk factors for the formation of calciumcontaining stones include hypercalciuria, hypocitraturia, hyperuricosuria, hyperoxaluria, low urine volume, and medullary sponge kidney. These risk factors can occur either alone or in combination. Their relative frequency is shown in Table 6-2.

1. Hypercalciuria is often defined as urinary calcium excretion greater than 250 mg/24 hours in women and greater than 300 mg/24 hours in men. Hypercalciuria is present in approximately two-thirds of patients with calcium-containing stones and may result from an increased filtered load, decreased proximal reabsorption, or decreased distal reabsorption. Proximal calcium reabsorption parallels sodium. Any situation that decreases proximal sodium reabsorption such as extracellular fluid (ECF) volume expansion also decreases proximal calcium reabsorption. Distal tubular calcium reabsorption is stimulated by parathyroid hormone (PTH), thiazides, and amiloride and inhibited by acidosis and phosphate depletion.

Hypercalciuria may be idiopathic or secondary to primary hyperparathyroidism, RTA, sarcoidosis, immobilization, Paget’s disease, hyperthyroidism, milk-alkali syndrome, and vitamin D intoxication. The idiopathic group makes up 90% of all hypercalciuria. This category of patients is characterized by increased 1,25(OH)₂ vitamin D₃ concentration, suppressed PTH, and reduced bone mineral density. Three potential pathophysiologic mechanisms are postulated: increased intestinal calcium absorption; decreased renal calcium or phosphorus reabsorption; and enhanced bone demineralization. On the basis of a fast-and-calcium-load study, some authors advocate subdividing idiopathic hypercalciuria into
absorptive hypercalciuria type I (due to primary intestinal calcium hyperabsorption with low-normal PTH), type II (dietary calcium-dependent hypercalciuria), type III (intestinal calcium hyperabsorption induced by elevated calcitriol levels secondary to renal phosphate leak), and renal leak hypercalciuria. Patients with absorptive hypercalciuria have exaggerated intestinal calcium reabsorption, which can be reduced in some by dietary calcium restriction. Some authors have expressed concern over the potential long-term effects of dietary calcium restriction. Patients with idiopathic hypercalciuria often have reduced bone mass and are in negative calcium balance, which may be further exacerbated by a low-calcium diet. In addition, a reciprocal relationship exists between free calcium and free oxalate in the intestinal lumen. Calcium acts to bind oxalate in the intestine and reduce absorption. If oral calcium intake is reduced, oxalate remains free in the intestinal lumen and its absorption increases. However, this may be reduced by concomitant oxalate restriction. Finally, as shown in Table 6-3, most randomized controlled trials demonstrating that a given pharmacologic intervention reduces the risk of calcium-containing stones did not subdivide patients based on results of a calcium load study. Whether patients with recurrent calcium oxalate stone formation should ingest a diet that is either liberal or restricted in calcium remains controversial and will be further discussed in the section on therapy.

In primary hyperparathyroidism, filtered calcium load is increased as a result of bone calcium release and increased intestinal calcium absorption mediated by 1,25(OH)₂ vitamin D₃. In those patients with hypercalciuria, the increase in filtered calcium load overcomes distal PTH action to increase tubular calcium reabsorption. In RTA, the decreased systemic pH results in increased calcium release from bone. In addition, acidosis directly inhibits distal nephron calcium reabsorption.

Macrophages in sarcoidosis produce 1,25(OH)₂ vitamin D₃, which leads to increased intestinal calcium absorption. Immobilization, Paget’s disease, and hyperthyroidism cause hypercalciuria by releasing calcium from bone and increasing filtered calcium load.

2. Hypocitraturia. It is defined as less than 320 mg citrate excretion/day. Citrate combines with calcium in the tubular lumen to form a nondissociable but soluble complex. As a result, less free calcium is available to combine with oxalate. Citrate also prevents nucleation and aggregation of calcium oxalate. Chronic metabolic acidosis from any cause enhances proximal tubular citrate reabsorption and decreases urinary citrate concentration; this is the mechanism whereby chronic diarrhea, RTA, and increased dietary protein load result in hypocitraturia. Another important cause of hypocitraturia is hypokalemia, which increases expression of the sodium-citrate cotransporter present in the proximal tubular luminal membrane.