nephrolithiasis medical management

1: NephrolithiasisMedical Management Common Ambulatory Topics Andrea L. Banks, MD April 1, 2008

3: Clinical Case HPI A 34 year-old white man comes to your office complaining of severe left flank pain that began this morning. The pain comes and goes in waves. He also notes nausea and vomiting. He has not had any change in his urination. The pain has now resolved. He denies any fevers or chills. PMHx HTN Medications Atenolol

4: Clinical Case (cont.) SHx Smoker Exam Afebrile, tachycardic Well-appearing, in no obvious pain Otherwise normal

5: Demographics Estimated 5% prevalence in general population More prevalent in men Risk factors Family history Gout Primary hyperparathyroidism Prolonged immobilization RTA Excess dietary meat Excess dietary sodium

6: Stone Composition Calcium oxalate 70% Calcium phosphate 5-10% Uric acid 10% Struvite 15-20% Cystine 1%

7: Clinical Presentation Pain Paroxysms of severe pain lasting 20-60 minutes Originates in flank and radiates to groin Location may vary as stone migrates Hematuria Gross or microscopic Nausea/vomiting Dysuria and urgency (less common)

8: Diagnosis Non-contrasted helical CT scan Gold standard Specificity nearly 100% Also detects signs of urinary tract obstruction Ultrasound Misses small stones and ureteral stones Test of choice in pregnancy KUB Misses radiolucent stones (uric acid) IVP

9: KUB - Calcium Oxalate Stone

10: Non-constrast CT scan

11: Stone Size <5 mm 90% pass spontaneously Alpha-blockers can increase chance of passage >10 mm <10% chance of spontaneous passage

12: Acute Treatment Increase fluid intake to goal of 2 L urine output per day Pain control NSAID�s, opioids Hospitalization if severe

13: Returning to the Clinical Case Labs CBC: normal BMP: normal, calcium normal U/A: few RBC�s Imaging Non-constrast CT showed a 4mm non-obstructing calculus in the left ureter

14: Returning to the Clinical Case You send the patient home with PO pain medication and instructions to increase fluid intake. You tell him the stone should spontaneously pass. He calls the office the next week reporting he is feeling well.

15: Work-up: the first episode Confirm the diagnosis Radiographic evidence of stone Comprehensive metabolic evaluation is not cost effective after first episode Consider straining urine for stone Composition analysis Consider minimal labs Urinalysis, routine electrolytes, calcium (iPTH if Ca is elevated)

16: Prevention: after the first episode Increase urine output to 2 L per day Reduces urinary saturation of stone-forming salts Water is most important; orange juice, coffee, and alcohol have been proven beneficial Dietary modifications Calcium Should not restrict calcium as it binds oxalate in the gut Decrease sodium intake Enhances calcium reabsorption Decrease meat intake Protein intake decreases urinary pH and increases uric acid

17: Back to the case. . . Your patient returns one year later with complaints that he is �passing another kidney stone�. Non-constrast CT confirms the diagnosis. The acute episode resolves with conservative management. He asks what can be done to prevent further episodes.

18: Work-up: recurrent episodes Relapse rate of 50% in first 5-10 years after first episode Strain urine for stone retrieval Composition analysis Laboratory data Calcium, bicarbonate, creatinine, chloride, potassium, magnesium, phosphate, uric acid, BUN iPTH and vitamin D in hypercalcemic patients

19: Work-up: recurrent episodes 24-hour urine collections for: Volume pH Calcium Creatinine Sodium Phosphate Citrate Uric acid Cystine Oxalate

20: Calcium oxalate stones Hypercalciuria Primary hyperparathyroidism Intestinal hyperabsorption Idiopathic Treat with thiazide diuretics (increases Ca reabsorption in distal tubule) Decrease sodium intake Hypocitraturia (citrate inhibits calcium salt formation) RTA Idiopathic Treat with potassium citrate Hyperoxaluria Enteric hyperabsorption Decrease oxalate intake, increase calcium intake (binds enteric oxalate)

21: Uric acid stones Hyperuricosuria Gout Low urinary pH Malignancy Treatment Allopurinol for hyperuricemia Potassium citrate to raise urinary pH

22: Struvite stones Consist of magnesium, ammonium, and calcium phosphate Not associated with metabolic abnormalities intrinsic to the patient Recurrent UTI with urea-splitting organisms Proteus Ureaplasma

23: Staghorn Calculus

24: Cystine stones Autosomal recessive disorder leading to decreased cystine resorption in the kidney Often first presents in childhood Hydration, urine alkalinization, cystine binders

25: Back to the case. . . Stone analysis Calcium oxalate 24-hour urine Hypercalciuria Treatment Continue increased fluid intake Add thiazide diuretic Decrease sodium intake

26: When to refer to Urology. . . Outpatient Stone >10 mm Failure to pass symptomatic stone after conservative management Shock wave lithotripsy Ureteroscopic lithotripsy Percutaneous nephrolithotomy Laparascopic stone removal

27: When to refer to Urology. . . Urgent inpatient Bilateral obstructing stones Intractable pain Urosepsis Acute renal failure Anuria

28: Take home points Calcium oxalate stones are the most common type Non-contrast CT is test of choice for diagnosis Increase fluid intake for acute treatment and prevention Only limited evaluation necessary after the first episode

29: References Kidney stones: pathophysiology and medical management. Lancet 2006; 367: 333-44. Medical management of common urinary calculi. Amer Fam Phys, 2006; 74(1): 86-94. Medical management of stone disease. Curr Opin Urol, 2003; 13: 229-233. Pathophysiology and management of calcium stones. Urol Clin N Am, 2007; 34: 323-334. Management of kidney stones. BMJ 2007; 334: 468072. The contemporary management of renal and ureteric calculi. BJU 2006; 98: 1283-1288. Up To Date Online, Version 15.3.