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146 NEPHROLITHIASIS

146 NEPHROLITHIASIS
Harrison’s Manual of Medicine

146

NEPHROLITHIASIS

Signs and Symptoms
Stone Composition
Workup
Bibliography

Renal calculi are common, affecting ~1% of the population, and recurrent in more than half of pts. Stone formation begins when urine becomes supersaturated with insoluble components due to (1) low volume, (2) excessive excretion of selected compounds, or (3) other factors (e.g., urinary pH) that diminish solubility. Approximately 75% of stones are Ca-based (the majority are Ca oxalate; also Ca phosphate and other mixed stones), 15% struvite (magnesium- ammonium-phosphate), 5% uric acid, and 1% cystine, depending on the metabolic disturbance(s) from which they arise.
Signs and Symptoms
Stones in the renal pelvis may be asymptomatic or cause hematuria alone; with passage, obstruction may occur at any site along the collecting system. Obstruction related to the passing of a stone leads to severe pain, often radiating to the groin, sometimes accompanied by intense visceral symptoms (i.e., nausea, vomiting, diaphoresis, light-headedness), hematuria, pyuria, UTI, and, rarely, hydronephrosis. Staghorn calculi are associated with recurrent UTI with urea- splitting organisms (Proteus, Klebsiella, Providencia, Morganella, and others).
Stone Composition
Most stones are composed of Ca oxalate. These may be associated with hypercalciuria or hyperoxaluria. Hypercalciuria can be seen in association with a very high Na diet (or exogenous saline administration), furosemide or other loop diuretic therapy, distal (type I) renal tubular acidosis (RTA), sarcoidosis, Cushing’s syndrome, conditions associated with hypercalcemia (e.g., primary hyperparathyroidism, vitamin D excess, milk-alkali syndrome), or may be idiopathic.
Hyperoxaluria may be seen with intestinal (especially ileal) malabsorption syndromes (e.g., inflammatory bowel disease, pancreatitis), due to the binding of intestinal Ca by fatty acids within the bowel lumen to form soaps, allowing free oxalate to be absorbed (and then excreted via the urinary tract). Ca oxalate stones may also form due to (1) a deficiency of urinary citrate, an inhibitor of stone formation that is underexcreted with metabolic acidosis; and (2) hyperuricosuria (see below). Ca phosphate stones are much less common and tend to occur in the setting of an abnormally high urinary pH (7–8), usually in association with a complete or partial distal (type I) RTA.
Struvite stones form in the collecting system when infection with urea-splitting organisms is present. Struvite is the most common component of staghorn calculi and obstruction. Risk factors include previous UTI, nonstruvite stone disease, urinary catheters, neurogenic bladder (e.g., with diabetes or multiple sclerosis), and instrumentation.
Uric acid stones develop when the urine is saturated with uric acid in the presence of dehydration and an acid urine pH. Pts with myeloproliferative disorders (esp. after treatment with chemotherapy), gout, acute and chronic renal failure, and following cyclosporine therapy often develop hyperuricemia and hyperuricosuria and are at risk for stones if the urine volume diminishes. Hyperuricosuria without hyperuricemia may be seen in association with certain drugs (e.g., probenecid, high-dose salicylates).
Cystine stones are the result of a rare inherited defect of renal and intestinal transport resulting in overexcretion of cystine. Stones begin in childhood and are a rare cause of staghorn calculi; they occasionally lead to end-stage renal disease. Stones are more likely to form in acidic urinary pH.
Workup
Although some have advocated a complete workup after a first stone episode, others would defer that evaluation until there has been evidence of recurrence or if there is no obvious cause (e.g., low fluid intake during the summer months with obvious dehydration). Table 146-1 outlines a reasonable workup for an outpatient with an uncomplicated kidney stone.

Table 146-1 Workup for an Outpatient with a Renal Stone

TREATMENT
Treatment of renal calculi is often empirical, based on odds (Ca oxalate most common stones) or clinical Hx. Sometimes a stone is recovered and can be analyzed for content. Stone analysis is advisable, especially for pts with more complex presentations or recurrent disease. An increase in fluid intake to at least 2.5–3 L/d is advisable, regardless of the type of stone. Conservative recommendations for pts with Ca oxalate stones (i.e., low salt, low fat, moderate protein diet) are thought to be healthful in general and therefore probably advisable in pts whose condition is otherwise uncomplicated. Table 146-2 outlines stone-specific therapies for pts with complex or recurrent nephrolithiasis.

Table 146-2 Specific Therapies for Nephrolithiasis

Bibliography

For a more detailed discussion, see Asplin JR, Coe FL, Favus MJ: Nephrolithiasis, Chap. 279, p. 1615, in HPIM-15.

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3 comments on “146 NEPHROLITHIASIS

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