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Nephrolithiasis for the Internist

Rajiv Kumar

Divisions of Nephrology and Endocrinology

Departments of Medicine, Biochemistry and Molecular Biology

Mayo Clinic, Rochester

Meira and Shaul G. Massry Visiting Professorship

Dr. Massry has had an exceptionally distinguished career. He has received honorary doctorates from

universities across Europe and has been the recipient

of numerous awards from universities and societies

throughout the world. Dr. Massry was the Editor-in-

Chief of the American Journal of Nephrology, and

of Mineral and Electrolyte Metabolism. He is the co-

Editor of the Textbook of Nephrology.

Dr. Massry is a past President of the National Kidney

Foundation, American Society of Renal Biochemistry

and Metabolism, International Society of Nutrition and

Metabolism in Renal Diseases, International Society of

Uremia Research and Toxicity, and International

Association of the History of Nephrology. Dr. Massry

has been a frequent guest speaker at national and

international meetings and a visiting professor at many

universities across the globe. He has published over

600 scientific papers, 111 chapters in books and edited

32 books.

Shaul G. Massry, M.D. , Professor

Emeritus of Medicine and Physiology

& Biophysics at the Keck School of

Medicine, University of Southern

California and Emeritus Chief of the

Division of Nephrology (1974-2000).

Mayo Clinic Rochester

Disclosures

• None

Objectives

• Familiarize you with recent trends in kidney

stone prevalence

• Discuss the pathogenesis of kidney stones

• Review diagnostic tests required to assess

kidney stones

• Review medical therapeutic interventions

which will reduce stone recurrence

Case 1

• You are asked to evaluate an 85 yo female with a history of Crohn's disease with multiple ileal resections and an ileal transverse colostomy. 122 cm of the ileum have been resected. At the present time the patient does not have any diarrhea, but she has had frequent loose stools in the past.

• She was evaluated in the ED for left-sided ureteric colic three weeks ago. She underwent a cystoscopy, left retrograde pyelogram, left flexible ureteroscopy, laser lithotripsy and basket extraction of stones from her left ureter. A ureteral stent was placed. Since then, she has been asymptomatic. Chemical analysis of her stones has been performed.

• The patient does take vitamin D and calcium for treatment of osteoporosis, but she has not been hypercalcemic or hypercalciuric per report. There is also a history of vitamin C use. Oral fluid intake is low.

Case 1

• VITAL SIGNS. Height 15.0 cm; weight 58.0 kg; BMI 24.2 kg/m2; temp 36.8 C; BP 99/55 mmHg; P 56 bpm, regular.

• PHYSICAL EXAMINATION. Negative except for colostomy and multiple abdominal surgical scars.

Case 1 contd.

Stone analysis is likely to reveal:

• Ca oxalate monohydrate and Ca oxalate dihydrate

• 100% uric acid

• Struvite (Ca-Mg-NH4) stone

• Brushite (Ca phosphate)

• Hydroxyapaptite

Case 1 contd.

You would recommend treatment with which of the following?

• A high fluid intake – 2.5 L/day or more

• A low oxalate diet

• Calcium carbonate 1gm po tid

• All of the above

• None of the above

Case 2

• You are asked to evaluate an 80 yo female with a history of recurrent kidney stones. Recently, she underwent a cystoscopy and laser lithotripsy for a L ureteral stone. Two and four years prior to seeing you, she had extracorporeal shock wave lithotripsy for stones in the left and right renal pelvis, respectively.

• With respect to risk factors for stones, she has a two-year history of intermittent hypercalcemia with serum Ca values as high as 11.1 mg/dL and a non-suppressed PTH. She also has a history of gout dating back twenty years, for which she takes colchicine when she has an acute attack, and for which she is on chronic allopurinol. She has not had any recent gouty attacks. With respect to medications, she takes no vitamin D, calcium, or vitamin C. She has taken prednisone in the past for a short period of time.

Case 2

• There is no history of ulcerative colitis, regional ileitis, malabsorption, or diarrhea.

• Her diet does not reveal a high oxalate or purine precursor intake. She is on treatment at the present time with Urocit-K 20 mEq PO t.i.d. as well as allopurinol.

Case 2 contd.

• VITAL SIGNS: Height: 167.3 cm. Weight: 97.60 kg. BSA(G): 2.16 M2. BMI: 34.870 KG/M2. Temperature: 36.8 °C. Blood Pressure: 141/68 mmHg. Pulse Rate: 78/minute, regular. PHYSICAL EXAMINATION: There was a left parotid mass approximately 3 cm in diameter. No nodes were felt. No other neck masses noted. The rest of the exam was normal. Labs:

PTH 120

Case 2 contd.

Case 2 contd.

Chest x-ray; 2 views: Prominent fat pad right

cardiophrenic angle. Slight scarring or atelectasis in

the right middle lobe. Calcified granuloma left lower

lobe. Mild thoracolumbar curve.

ECG normal.

Case 2 contd. ACE – 71 U/L (nl 8-53); PTH-RP < 0.2 pmol/L (nl - < 2.0 pmol/L); whole

molecule PTH – 120 pg/mL (nl 5-65 pg/mL); serum monoclonal protein

by immunofixation small IgG l.

Parathyroid scan performed with technetium 99m sestamibi and

I-123 including SPECT imaging. Subtraction imaging showed a

discordant area of increased sestimibi uptake test posterior to the

inferior pole of the right thyroid lobe consistent with an abnormal

parathyroid gland. In addition there was increased sestamibi localization

posterior to the left inferior lobe of the thyroid that is less certain but

worrisome for a second abnormal parathyroid gland. No additional foci

of discordant sestimibi uptake.

Ultrasound of the neck demonstrated a 6 mm by 8mm x 9 mm hypoechoic

nodule posterior to the lower right thyroid lobe which could be a

parathyroid adenoma. There was also a 6 mm x 7 mm hypoechoic nodule in

the posterior portion of the inferior left thyroid lobe which is

likely a benign thyroid nodule. Small area of calcification in the mid

left thyroid lobe which was not associated with a focal nodule. No

cervical adenopathy.

Case 2 contd.

• An endocrine surgeon performed a two gland parathyroidectomy with resolution of hypercalcemia and subsequent stone activity.

Intra-operative Neck Vein PTH, pg/mL

Baseline

PTH

10 minutes 15 minutes

254 48 40

Post-op Ca 9.0 mg/dL.

Pathology of parathyroid glands: A. Parathyroid, left

superior, parathyroidectomy: Normocellular parathyroid

gland (50.0 milligrams). B. Parathyroid, left inferior,

biopsy: Normocellular parathyroid tissue. C. Parathyroid,

right superior, parathyroidectomy: Hypercellular

parathyroid (230.0 milligrams). D. Parathyroid, right

inferior, parathyroidectomy: Hypercellular parathyroid

(240.0 milligrams).

Case 2 contd.



• 100% uric acid



• Hydroxyapaptite

Nephrolithiasis is Common, Costly and Preventable

• Nephrolithiasis is a common disorder (yearly incidence of nephrolithiasis in the US is ~ 0.5%) that is associated with considerable morbidity and economic cost.

• In the USA the economic cost is estimated at between $2.1 and $5.3 billion billion per year, with the vast majority ($4.5 billion) attributed to direct medical/urological costs.

• Strategies to accurately diagnose the type of stones and institute measures to prevent stone recurrence will have a great impact on reducing costs associated with this illness.

The Prevalence of Nephrolithiasis has Increased

• The prevalence of nephrolithiasis in the United States and Europe has increased in the two decades between 1970-1990 from about 3% to about 5%.

Percent Prevalence of History of

Kidney Stones 1976-1980 and 1988-1994

Statmatelou, Kidney International 63: 2003

Incidence of Kidney Stones

1950-1974 and 1970-2000 in Rochester, MN

Lieske et al, Kidney International (2006) 69, 760–764.

• Better diagnostic tools

• Life style

• Dietary habits

• Obesity

Why the “Stone Boom”?

Life Style Risk Factors for Stone Formation

• Low water intake : low volume and infrequent intake increased urine supersaturation

• Consumption of food rich in calories and salt, and low in fiber and alkali hypercalciuria, deficiency in urinary stone inhibitors

• Sedentary lifestyle obesity

Stone Episodes and Obesity

Siener R, Obesity Res, 12: 106-113, 2004

BMI and Relative Risk of Symptomatic Stones

Taylor E, JAMA, 293(4), 455-462 2005

Urine Composition with Obesity

• Decreased Urine pH

• Elevated urinary excretion of

Sodium

Calcium (men > women)

Phosphate, sulfate

Uric acid

Oxalate (women)

Siener R, Obesity Research 12:106-113, 2004

Nephrolithiasis is Associated with an Increase in the Incidence of CKD

Rule et al, Clin J Am Soc Nephrol, 6:2069-2075, 2011.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3156433/

Nephrolithiasis is Associated with an Increased Incidence of Myocardial

Infarction

Rule et al, J Am Soc Nephrol. 2010 Oct;21(10):1641-4.

Composition of Kidney Stones

Percentage of stones Characteristics

Crystal type

Calcium oxalate monohydrate

40-60% Radio-opaque, well-circumscribed

Calcium oxalate dihydrate 40 to 60% Radio-opaque

Calcium phosphate, apatite, Ca10[PO4]6[OH]2

20-60% Radio-opaque

Calcium phosphate, Brushite, CaHPO4.2H2O

2-4% Radio-opaque

Uric Acid 5-10% Radiolucent

Struvite (magnesium ammonium phosphate)

5-15% Can be staghorn

Cystine 1.0-2.5% Mildly radio-opaque

Ammonium urate 0.5-1 .0%

Mixed stones

Calcium oxalate-phosphate 35-40% Radio-opaque

Mixed uric acid-calcium oxalate

5% Radio-opaque

Herring et al, J. Urol, 88:545, 1962; Mandel et al, J. Urol, 142-1513, 1989; Mandel et al, J. Urol, 142:1516,1989

Pathophysiology of Stones

A number of metabolic abnormalities are associated with the occurrence of renal calculi.

• Increased urinary concentration of solutes due to a reduction in fluid intake and urine volume.

• Metabolic abnormalities: Hypercalciuria, hypocitraturia, hyperoxaluria, hyperuricosuria, and altered urinary pH.

Individuals at Increased Risk for Stone Formation

• Hypercalciuria

• Hypocitraturia

• Hyperparathyroidism

• Hyperoxaluria

• GI diseases (Colitis, Crohn’s, malabsorption)

• Surgery for obesity

• Family History

• Gout/hyperuricosuria/Uric acid

• Infected stones

• Genetically determined

•Cystinuria

•Primary Hyperoxaluria

•RTA Type I

•2,8 Dihydroxyadenine

•Xanthine

Pathophysiology of Renal Stones Cause Pathophysiology Stone

Composition Clinical Clues

All Stones

Low urine volume (raises concentration of solutes)

Reduced intake or increased loss of water

Renal water conservation All stones Urine volume less than 1 L per day and osmolality greater than 600 mOsm/Kg

Calcium stones

Hypercalciuria (raises saturation of calcium salts)

Absorptive hypercalciuria

Increased absorption in intestine

Calcium oxalate or calcium phosphate

Urine Ca >6 mmol/liter (240 mg) per day

Renal leak Loss of Ca in via kidney Urine Ca >6 mmol/liter (240 mg) per day

HPT Increased absorption in the intestine and increased bone resorption

High PTH concentrations and high 1, 25(OH)2D concentrations.

Immobilization Increased bone resorption High U Ca

Excess sodium in diet

Sodium induced hypercalciuria

Increased urine Na

Excess protein or acid in diet

Protein induced bone loss and renal leak

Urine NH4 increased, high urine sulfate, low urine pH

Range of monogenic disorders

Bone loss, gut hyper-absorption and various combinations

Pathophysiology of Renal Stones Cause Pathophysiology Stone

Composition Clinical Clues

Calcium stones

Hypocitraturia (increases urinary ionized Ca, reduces inhibitor activity against Ca salts)

Renal tubular acidosis (distal type)

Abnormal renal defense of acid-base balance

Calcium phosphate

Urine citrate concentrations less than 1.7 mmol/day.

High urine pH

High acid load (absence of detectable acidemia)

Physiological hypocitraturia

Calcium phosphate and calcium oxalate

Urine citrate concentrations less than 1.7 mmol/day.

High urine pH

Hyperoxaluria (raises saturation of calcium oxalate)

Excess of dietary oxalate

Increased delivery of luminal oxalate

Calcium oxalate Urine oxalate greater than 0.4 mmol/day

Bowel disease (malabsorption, gastric bypass procedures)

Reduced formation of luminal/intestinal Ca-oxalate complexes

Calcium oxalate Urine oxalate greater than 0.4 mmol/day

Increased endogenous production of oxalate

Primary hyperoxaluria, type I and 2

Hyperuricosuria (Na urate precipitation causes nidation of Ca salts)

High purine intake High purine intake Raised production & excretion of sodium urate

Urinary uric acid excretion of greater than 600 mg/day

Gout, Myeloproliferative disease, enzymatic defect, uricosuric drugs, renal leak

Increased excretion of uric acid

Hyperuricosuria, serum uric acid may be decreased

Pathophysiology of Renal Stones

Cause Pathophysiology Stone Composition

Clinical Clues

Uric acid stones

Low urine pH or hyperuricosuria

High acid load, metabolic syndrome, other causes of hyperuricosuria

Urate salts are converted to uric acid which is insoluble and low urinary pH

Uric acid Low urine pH, less than 5.5

Cystine stones

Cystinuria Congenital mutations of di-basic amino acid transportersubunits

Increased urinary cystine and other of basic amino acids

Cystine Urine cystine greater than 150 μmol/mmol creatinine

Infection-related stones

Urinary tract infection

Urea-splitting organisms

Production of ammonium and bicarbonate ions from urea

Magnesium ammonium phosphate, carbonate apatite

High urinary pH, pyuria, positive cultures for organism producing urease

Kidney Stone Management

Recognize Risks

Manage risks

Monitor

Evaluation of the First Stone

First Stone Episode

Determine Metabolic Activity

Dual Energy CT

Urinalysis

Urine chemistries

Diet

Fluid

3-6 month follow-up

No growth

Monitor every 1-2 years

Metabolic activity

Treatment options

Chemical Evaluation of Stones

• Serum

•Ca, Pi

•PTH

•Vitamin D Metabolites

•Uric Acid

•Na, K, Cl, HCO3

• Urine

•pH

•Sediment

•Osmolality

•Gram’s stain

•Culture

• 24hr urinary profile

•Volume

•Calcium

•Citrate

•Oxalate

•Phosphorus

•Sodium

•Magnesium

•Urinary supersaturation

• Radiological Studies

•Dual energy CT

•CT Urogram

Renal Stone Characterization Using DECT

Uric acid calculus

Non-uric acid/

Calcium calculus

Hartman et al. Radiologic Clinics of North America 2012 vol:50 iss:2 pg:191 -205

Renal Stone Characterization Using DECT

Ca oxalate

calculus Hydroxyapaptite

calculus

Liu et al, Academic Radiology, 20, 1521–1525, 2013

General Measures for the Treatment of Renal Stones: Lifestyle changes

These interventions are applicable to all stones

• BMI 18-25 kg/m2

• Balancing excess fluid loss

• Dietary changes

• Physical activity

General Measures: Dietary Prevention of Stone Formation


• Fluid • Total intake: 2.5-3.0 L/day

• Urine output: 2.0-2.5 L/day

• Intake balanced throughout the day

• Neutral beverages

General Measures: Dietary Prevention of Stone Formation


• Limit animal protein: 0.8-1.0 grams/Kg/day

• Limit sugar and fat content

• Limit sodium: 4-5 grams/day Calcium: 1,000-1,200 mg/day (not with absorptive hypercalciuria)

• Limit oxalate intake

• Rich in vegetable fiber

• Rich in alkaline potassium

General Measures: Restriction of Dietary Animal Protein and Sodium

A high intake of animal proteins/purine precursors

• Increases urinary uric acid excretion

• Decreases urinary pH

• Decreases urinary citrate excretion

• Increases urinary calcium excretion

A high intake of sodium chloride

• High salt diet – increases urinary calcium excretion

Dietary Animal Proteins

and Salt:

Risks for Stone

Formation

Kok D at al. J Clin Endocrinol Metab. 71:661. 1990

A High Calcium Intake is Associated with Reduced Urinary Oxalate Excretion

Von Unruh G, et al, JASN 15(6), 1567-73, 2004

Specific Measures for the Treatment of Nephrolithiasis

Lifestyle or Dietary Modification

Pharmacological Treatment

Low urine volume Increase fluid intake to 2.5-3 liters per day

Increased Fluid Intake

Hypercalciuria Sodium moderation less than 150 mmol per 24 hours

Protein moderation

Hydrochlorothiazide or indapamide + potassium alkali (potassium citrate 5-10 mEq p.o. t.i.d.)

Hyperoxaluria Restriction of dietary oxalate

Avoidance of calcium restriction

Low-fat intake in malabsorption syndrome

Calcium supplementation in malabsorption syndrome or following bypass surgery

Pyridoxine for primary hyperoxaluria; liver kidney transplantation

Specific Measures for the Treatment of Nephrolithiasis

Lifestyle or Dietary Modification

Pharmacological Treatment

Hyperuricosuria Purine restriction Potassium citrate, other alkalinizing agents such as Bicitra

Allopurinol

Low urinary pH Protein restriction Potassium citrate

Cystinuria High fluid intake Potassium citrate, D-penicillamine, b-mercaptopropionyl glycine

Urinary Tract Infection Antibiotics

Specific Measures For Calcium Oxalate Stones

Assessment of Risk factors

• Hypercalciuria, Hyperoxaluria, Hyperuricosuria, Hypocitraturia

• Low urine volume

• Diet: Low fluids, High salt, High protein, High sugar

• Family History

• Sex

Measures Which Decrease the Risk of Recurrent Calcium Oxalate Stone Disease

• Low animal protein diet

• Low salt diet

• Increased fluids 2.5-3 L/day

• Normal Ca intake (1 g/day)

A High Calcium Intake is Associated with Reduced Urinary Oxalate Excretion

Von Unruh G, et al, JASN 15(6), 1567-73, 2004

Management of Calcium Oxalate Stones: Urinary Profiles, Risks and Interventions

• Hypercalciuria –

• Hydrochlorothiazide 25-50 mg/d

• Indapamide 1.25 mg/d

• Chlorthalidone 50 mg/d

• Potassium citrate 5-10 mEq p.o. t.i.d.

• Hypocitraturia –

• Lower dietary animal protein


Management of Calcium Oxalate Stones: Urinary Profiles, Risks and Interventions

• Hyperoxaluria –

• Calcium 500 mg/day with meals

• Magnesium 200 - 400 mg/day

• Hyperuricosuria –


• Allopurinol 100 mg/day

• Hypomagnesiuria –

• Magnesium 200 - 400 mg/day

Nephrolithiasis and Hyperoxaluria are Complications of Bariatric Surgery

• Although there is a decrease in overall mortality and

an improvement in lipid and carbohydrate

metabolism in patients after RYGB surgery, the

incidence of nephrolithiasis and hyperoxaluria

increases post-RYGB surgery.

• In a recent study of 4,639 RYGB patients who had

undergone bariatric surgery and 4,639 obese control

patients, Matlaga et al noted that 7.65% (355 of

4,639) of RYGB patients developed urolithiasis

compared to 4.63% (215 of 4,639) of the obese

control patients in the control group (Matlaga et al J. Urol, 2009).

Kidney Stones Associated with Malabsorption and Gastric Bypass Surgery:

Hyperoxaluric Stone Disease

• Increased oxalate absorption from the colon

• Excess free fatty acids – fat malabsorption

• Bind calcium and magnesium

• Leave free oxalate to be absorbed

• Fatty acids and bile salts increase colonic oxalate absorption



• Increase in Urinary supersaturation

• Decreased water absorption – low urine volumes

• Decreased absorption of crystallization inhibitors:

• Magnesium, phosphate, pyrophosphate



• Urinary Profile

•Hypocalciuria

•Hypomagnesiuria

•Hypocitraturia

•Hyperoxaluria

•Low urine volumes

•Acidic urine

• Treatment

•Correct underlying malabsorption

•Dietary calcium

•Magnesium sup.

•Citrate

•Low oxalate diet

•Increase fluids

•Decrease dietary fat

•Cholestyramine

Kidney Stones Associated with Bowel Disease: Uric Acid Stones

• Etiology: low urine output and acidic urine

• Colectomy with ileostomy – loss of fluid and alkali

• Treatment

• Alkalinize the urine

• Fluids

• Allopurinol

Stones Associated with an Acidic Urine: Uric Acid Stones

• 5-10% of all stones

• With gout, 25% form uric acid stones

• Etiology:

• Low urine volume

• Acidic urine

• Chronic diarrhea – colectomy and ileostomy

• Excess protein intake

Stones Associated with an Acidic Urine: Uric Acid Stones

• Treatment: dissolve and prevent

• Increase fluid intake and decrease protein intake

• Alkalinize the urine – citrate

• Allopurinol

Stones with an Acidic Urine: Cystine Stones

• 1% of Kidney stones formers

• Autosomal recessive : homozygotes – stones

• Defect in intestinal and renal absorption of cystine, ornithine, lysine, and arginine (COLA)

• Diagnosis:

• Crystalluria on UA – hexagonal

• Cystinuria ( 400mg/day)

• Family History

Stones with an Acidic Urine Cystine Stones

• Treatment

• Alkalinize urine to > 7.0

• Chelators: tiopronin or penicillamine (+ pyridoxine)

Stones Associated with an Alkaline Urine :Calcium Phosphate Stones

• RTA type I

• Hyperparathyroidism

• Use of absorbable alkali (Tums, Rolaids, Alka- Seltzer)

• Medullary Sponge Kidney

Stones Associated with an Alkaline Urine: RTA Type I

• Hyperchloremic Hyperkalemic Metabolic Acidosis

• Nephrocalcinosis

• Urinary Profile

• Hypercalciuria

• Hypocitraturia

• Urine pH always > 5.3

Stones Associated with an Alkaline Urine: RTA Type I

• Treatment

• High fluid intake

• Correct acidosis: K citrate

Stones Associated with an Alkaline Urine: Struvite Stones

• Magnesium ammonium phosphate stones

• All are infected

Proteus, other gram-negative organisms

• 10% of all kidney stones / 50% are bilateral

• Urine Profile : pH 8.0

• Treatment:

• Preoperative antibiotics

• Surgical removal of all stone material

• Post-op bacterialcidal antibiotics for 6-12 months

Hyperparathyroidism and Kidney Stones

The association is well-recognized – “stone, bones, groans”

etc. The association first recognized in the case of Captain

Martell by Dr. Eugene F. DuBois in 1926. Captain Martell

had become disabled by demineralization of the skeleton in

association with hypercalcemia over many years. He had

several episodes of flank pain, kidney calcification and

stones. He was extensively studied at the MGH and

eventually, a parathyroid adenoma was removed from the

mediastinum at his seventh operation in 1932 with

correction of his serum calcium.

Interestingly, in 1925 in Europe, Felix Mandl, had removed a

parathyroid tumor from a patient with kidney stones and a

bony disorder, with marked clinical improvement.

Hyperparathyroidism and Nephrolithiasis

• Only 15-20% of patients with HPT develop stones.

• The reason for this might be that patients with

stones have a concomitant increase in their

1,25(OH)2D concentrations and increase in

intestinal Ca absorption.

Broadus et al , N Engl J Med 1980; 302:421-426.

Treatment of Stone with HPT

• Identify aberrant gland

• Parathroidectomy

•Oxalate is poorly absorbed from the alimentary tract.

About 10-20 percent of the oxalate excreted in the

urine is dietary in origin, the vast majority being

endogenously derived.

•About 40 percent of oxalate production appears to be

derived from glycine metabolism.

•Most oxalate precursors are metabolized via

glyoxylate and/or glycolate the oxidation of which is

the main regulatory step in the metabolism of

carbohydrates to oxalate.

Primary Hyperoxaluria

Oxalate Metabolism

Metabolism of Oxalate

Aronson PS, Kidney International 2006

•PH1 is caused by a functional deficiency of the liver-specific

peroxisomal enzyme alanine:glyoxylate aminotransferase (AGT)

•PH2 by a deficiency of the cytosolic enzyme glyoxylate

reductase (GR) and hydroxypyruvate reductase (HPR).

•One-third of PH1 patients have significant levels of AGT catalytic

activity due to a unique intracellular protein trafficking defects in

which AGT is erroneously localized to the mitochondria.

Oxalate Metabolism

C. J. Danpure

Treatment Stones and PH

• Pyridoxine

• Hepatic or hepatic/renal

transplantation

Surgical Therapy

• Obstruction

• Persistent severe hematuria

• Persistent metabolic activity despite

maximal medical therapy

Case 1

• Patient with long standing Crohn’s disease and an intact colon.

Case 1 contd.



• 100% uric acid



• Hydroxyapaptite

Case 1 contd.

On a 24 hour urine you would expect to see which of the following:

• Hyperoxaluria

• Hyper-uricosuria

• Hypercalciuria

• Hypo-citraturia



Case 1 contd.

You would recommend treatment with:

• A high fluid intake – 2.5 L/day or more

• A low oxalate diet

• Calcium carbonate 1gm po bid or tid



Case 2

• Patient with primary HPT

Case 2 contd.



• 100% uric acid



• Hydroxyapaptite

Summary

• Nephrolithiasis is increasing in frequency

• Metabolic abnormalities can and should

be identified in the urine and serum to guide

therapy

• A treatment program can be designed based

on findings

• Serial follow-up is necessary

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