CHAPTER 22 Renal Disorders 545
Excessive bone resorption caused by immobility, bone disease, hyperparathyroidism, and renal tubu- lar acidosis are all predisposing risk factors to calcium stone formation. Gout predisposes persons to uric acid stone formation. Gastrointestinal malabsorption due to inflammatory bowel disease or bariatric surgery also predisposes persons to nephrolithiasis. Indinavir, a drug used for HIV infection, predisposes individuals to cal- cium stones. Urinary tract infection (UTI) and alkaline urine can predispose individuals to struvite (magnesium ammonium phosphate) stones, which are usually large.
Struvite stones account for 15% of cases and are associated with chronic UTI and specific urine pH. Usual organisms include Proteus, Pseudomonas, and Klebsiella species; urine pH is typically alkaline, greater than 7. The bacteria possess the enzyme urease, which can react with urea in the urine to form ammonia and carbon dioxide. Ammonia makes the urine alkaline. Uric acid stones account for 6% of renal calculi and are associated with high purine intake, malig- nancy, and gout. Purines are derived from the DNA of animal cells or cancer cells. High purine levels in the bloodstream occur with high ingestion of meats or whenever there is high cellular breakdown, as in treat- ment of malignancy. Approximately 25% of patients with uric acid stones have gout, which is caused by hyperuricemia. Cystine stones account for 2% of renal calculi and arise because of failure of renal tubular reabsorp- tion of cystine, an amino acid, into the blood. Urine becomes supersaturated with cystine, with resultant crystal deposition. There are three main theories regarding the for- mation of renal calculi. The first theory proposes that there is supersaturation of the urine by stone-forming crystalline constituents. Crystals can act as a nucleus, upon which more crystalline constituents settle and build into a calculus. Depending on where it is formed, in the renal pelvis or ureter, the calculus becomes impacted in a site in the ureter as it passes along with urine toward the urinary bladder. The second theory proposes that there is a depo- sition of calcium phosphate, a normal compound from breakdown of bone, onto an area of tubule cell membranes in the renal papilla, an area of kidney that empties into the minor calyx. The calcium phosphate compound collects layers of collagenous material and cellular debris, at which point it is called a Ran- dall plaque, within the subepithelial membrane. The plaque collects layers of crystalline elements, becomes a calculus, and eventually erodes through the urothe- lium of the renal pelvis to enter the ureter. The third theory suggests that persons with neph- rolithiasis have a deficiency of one or all proteins that inhibit stone formation. The kidney is supposed to secrete three types of stone-inhibitors: nephrocalcin, Tamm–Horsfall mucoprotein, and uropontin. Regardless of etiology or composition, a renal cal- culus flows into the ureter, becomes impacted, and causes an obstruction. As the stone travels down the ureter, it scrapes against the ureter’s membrane, caus- ing minor bleeding into the urine and intense pain. The ureter spasms around the stone, causing a colicky type of pain. Obstruction of urine can lead to increased pressure within the kidney. Based upon the degree of obstruction, the stone can cause backpressure into the renal pelvis, a condition called hydronephrosis. Hydronephrosis occurs when edema and distention of the renal pelvis interfere with renal blood flow and function (see Fig. 22-10). Prolonged hydronephrosis
CLINICAL CONCEPT Struvite stones commonly cause staghorn calculi, which can fill the entire renal pelvis (see Fig. 22-9).
Pathophysiology The formation of renal calculi involves many different factors that include dietary and intestinal absorption factors, endocrine abnormalities, crystalline compo- nents in the blood, constituents of urine, pH of urine,
urinary tract structures, and heredity. The most common renal calculi are:
• Calcium stones • Struvite stones • Uric acid stones • Cystine stones
Seventy-five percent of renal calculi consist of calcium; most are composed of calcium oxalate. The cause for these stones is attributed to hyperabsorption of calcium and oxalate from the gastrointestinal tract.
FIGURE 22-9. X-ray showing staghorn calculus. A staghorn calculus is a large calcification that occupies the renal pelvis. (From Scott Camazine/Science Source.)
Powered by FlippingBook