Nephrolithiasis

Published on 02/03/2015 by admin

Filed under Endocrinology, Diabetes and Metabolism

Last modified 02/03/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1573 times

CHAPTER 17

Nephrolithiasis

1. Define hypercalciuria, kidney (renal) stones, renal calculi, nephrolithiasis, urolithiasis, renal lithiasis, and nephrocalcinosis.

Hypercalciuria is urinary calcium excretion greater than 300 mg/day in men and greater than 250 mg/day in women. A more accurate definition is urinary calcium excretion greater than 4 mg per kg of ideal body weight per day in either sex. A good estimate of the 24-hour urine calcium excretion is 1.1 times the calcium-to-creatinine ratio (Ca/Cr) on a random urine specimen. For example, if urine calcium is 20 mg/dL and urine creatinine is 70 mg/dL, then the Ca/Cr would be 20:70 or 0.286 g (286 mg/day). The estimated 24-hour urinary calcium excretion would be 1.1 × 286 = 315 mg/day. Kidney stones, renal calculi, nephrolithiasis, urolithiasis, and renal lithiasis are synonymous terms that define the clinical syndrome of formation and movement of stones in the urinary collecting system. Renal calculi are abnormally hard, crystalline, insoluble substances that form in the renal collecting system. Nephrocalcinosis is deposition of calcium salts in the renal parenchyma.

2. Who is at risk for the development of kidney stones?

The average prevalence of kidney stones in the United States is approximately 5%, with the lifetime risk for a stone being 13% in men and 7% in women. The yearly cost of kidney stone disease in the United States is more than $5 billion. Fifty percent of patients with kidney stones have a recurrence within 5 to 10 years. Stones occur most often between ages 20 and 60 years and occur in Caucasians more than other ethnicities. Women have had more stones in recent years, possibly because of increased calcium and protein intake and greater exercise with the potential for dehydration. Review of nephrolithiasis in the Women’s Health Initiative suggests that hormone replacement therapy is a risk for renal stones. Other risks for stones include a family history of stones, obesity, diabetes mellitus, hypertension, autosomal dominant polycystic kidney disease, medullary sponge kidney, renal tubular acidosis, urine volume less than 2 L/day, dietary sodium greater than 2 g/day, low water intake, and high protein intake (see question 4).

3. What are the compositions and approximate frequencies of kidney stones in the United States?

There are six major types of stones, as outlined in Figure 17-1, which also shows the approximate frequency of occurrence of each type of stone.

4. What are the main causes of nephrolithiasis?

5. Describe the conditions associated with both renal stone disease and hypercalciuria.

6. What are the most important causes of normocalciuric calcium nephrolithiasis?

7. Describe the process of renal stone formation.

Initially, urinary crystallization or precipitation of sparingly soluble salts and acids occurs. Nucleation follows as the initial crystals and urinary matrix ions form a stable framework for crystal enlargement through growth and aggregation. After they are sufficiently large, crystals become trapped in a narrow portion of the urinary collecting system (often at the end of collecting ducts), forming a nidus for further stone growth. Alternatively, crystals form in the medullary interstitium, are extruded, and adhere to the renal papilla and form a Randall’s plaque nidus for further crystal accumulation and stone growth. Once stone growth occurs, the stone may detach from the renal papilla, move distally, and cause obstruction. Common sites for obstruction are the ureteropelvic junction, midureter, and ureterovesical junction.

8. Discuss the pathophysiologic factors that influence the formation of renal stones.

Renal stones result from hereditary or acquired disorders causing supersaturation of stone precursors, deficiency of stone inhibitors, and possibly excess promoters. Supersaturation causes crystallization with mineral precursors, such as calcium and oxalate. Calcium oxalate crystals bind to anionic, sialic acid–containing glycoproteins on the apical surfaces of renal tubular epithelial cells, allowing further growth. Other factors that increase stone formation include urinary stasis (medullary sponge kidney), decreased flow (obstruction), increased urine ammonium (infection), dehydration (concentrated urine), and increased urinary alkalinity (renal tubular acidosis [RTA]). Type I RTA promotes stone formation through the increased release of calcium and phosphorus from bone to buffer the acidemia, with resulting hypercalciuria and hyperphosphaturia. The acidemia enhances proximal tubule reabsorption of citrate with resulting hypocitraturia. The alkaline urine of RTA promotes precipitation of calcium phosphate stones. Acidemia with a positive urine anion gap (UNa + UK − UCl) is a clue to the presence of RTA.

9. What are the main chemical precursors of renal stones?

10. What are the main inhibitors of renal stone formation? How do they work?

11. What is nephrocalcin? What role does it play in the formation of renal stones?

12. What are the promoters of renal stone formation?

13. How does the kidney handle calcium?

14. Calculate the normal filtered and excreted load of calcium per day.

The serum calcium concentration is normally 10 mg/dL. The kidney filters complexed and free calcium, which makes up 60% of the total, or 6 mg/dL. The normal glomerular filtration rate (GFR) is 120 mL/min. Thus the filtered load of calcium is 6 mg/100 mL × 120 mL/min × 1440 min/day = 10,368 mg/day. Because the kidney reabsorbs 98% of the filtered calcium, only 2% is excreted. Thus normally the kidney excretes about 200 mg of calcium/day (10,368 mg/day × 0.02 = 207 mg/day). If the excreted calcium level increases to 5%, the urinary calcium level increases to 500 mg/day.

15. How do the serum calcium level and dietary sodium intake affect hypercalciuria?

16. Describe the etiology and pathophysiology of IH.

IH affects 10% of the general population and 40% of stone formers. The four types of IH are AH-I to AH-III and RH. AH-I and AH-II result from increased intestinal sensitivity to calcitriol with intestinal calcium hyperabsorption and higher numbers of vitamin D receptors in osteoblasts, causing greater bone resorption and resorptive hypercalciuria. The latter accounts for decreased bone mass seen in many patients with AH-I and some of those with AH-II. AH-III, an unusual disorder, is due to a renal phosphate leak with urinary loss of phosphate, decreased serum phosphate, and increases in renal calcitriol production and intestinal calcium absorption. The level of the phosphaturic factor, fibroblast growth factor-23, is increased in some patients with calcium nephrolithiasis, hypophosphatemia, and renal phosphate leak. RH is characterized by impaired tubular reabsorption of calcium, which causes a decrease in serum calcium, elevations in parathyroid hormone (PTH) and calcitriol, and increases in bone resorption and intestinal calcium absorption.

17. Distinguish among the various forms of IH.

18. When is it necessary to distinguish among the various forms of IH?

19. Explain the differences in serum levels of phosphorus and PTH in AH-III and RH.

Buy Membership for Endocrinology, Diabetes and Metabolism Category to continue reading. Learn more here