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NEPHROLITHIASIS / RENAL STONES YOUR LECTURER :

Kidney stones

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Page 1: Kidney stones

NEPHROLITHIASIS / RENAL STONESNEPHROLITHIASIS / RENAL STONES

YOUR LECTURER :

YOUR LECTURER :

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NEPHROLITHIASISNEPHROLITHIASIS

- Magnitude of Stone disease: 1 out of 5 will have urologic stone in a lifetime 7 to 10 of every 1000 hosp. admissions(USA) 4/5 cases are male; peak age 25 - 35 years (prime of life)

Stones may injure kidneys, produce Renal Failure by infection or obstruction, cause severe pain or worrisome bleeding. More morbidity occurs than death or ESRD (accounts for 2-3% only of all-cause CKD) Majority of cases, stone dse will accelerate; complex etiology; overall hx is of chronicity and hope of waning as age progresses is for the majority, unrealistic.

Recurrence is the rule: one stone every 2-3 years Average recurrence: 50% within 5 yrs; 60% in 10 yrs

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MANIFESTATIONS :• Asymptomatic - as long as stone remains attached to renal papillae• Hematuria - may be isolated or associated with pain• Obstruction - typically produce pain from acute obstruction anywhere

from ureteropelvic to ureterovesical junction called renal colic which gradually increases severity over 30 mins to a plateau.

• Stone passage - pain begins at flank then moves downward and laterally along anterior abdomen to loin, testis or vulva. Stone lodged in ureterovesical junction

present as frequency, urgency or dysuriamistaken as UTI.

• Staghorn calcuili - can be struvite, cystine or uric acid stones grown too large, usually in the presence of urease + organisms

• Nephrocalcinosis - multiple papillary calcifications commonly seen in RTA and medullary sponge kidneys.

• Sludge - precipitate plug of uric acid or cystine crystals• Infection – flank pain, fever, chills, nausea/vomiting,

hypogastric pain

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Hydronephrosis causes tubular dilatation with cellular atrophy.

    after 2-3 days,blunting of the renal papillae with gradual atrophy of renal tissue

     in 7 days, atrophy is seen up to the distal nephron

     by 14 days, progressive dilatation of the distal tubules with atrophy up to proximal tubules

- at 28 days, 50% loss of the medulla with marked atrophy of proximal tubules and thinning of the cortex. Glomerular damage occurs after 28 days of obstruction

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In one study of 75 patients with ureteral stones who were followed prospectively, the average time for stone passage in patients with stones that were 2 mm in diameter or smaller, 2 to 4 mm, and greater than 4 mm was 8, 12, and 22 days, respectively

Pain control – Both NSAIDs and narcotics have traditionally beenused for pain control in patients with acute renal colic and in prospective studies are equally effective. One study compared indomethacin (100 mg) by rectal suppository or I.V. morphine (5 mg then up to two additional 2.5 mg doses if needed). There was no significant difference between the two. A second RCT found that I.V. Ketorolac (60 mg initial dose) had superior pain relief compared with I.V. meperidine (50 mg initial dose). Alternative opiates include tramadol and fentanyl , used alone or in conjunction with NSAIDs.

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NSAIDs have advantage of decreased ureteral smooth muscle tone. On the other hand, in patients w/ preexisting renal disease, NSAIDs impair the kidney's autoregulatory response to acute obstruction and induce acute renal failure.

Moreover, NSAIDs should be stopped 3 days before ESWL to minimize the risk of bleeding, owing to antiplatelet effect.

Newer COX-2 inhibitors have promise in acute colic pain relief withless antiplatelet effect, but to date there are no good studies norguideline recommendations.

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50% of patients have only 1 stone.• Waiting for a 2nd stone before metabolic workup is reasonable because of attitudinal behavior and low incidence of renal impairment; except a.) < 25 or > 60 yo b.) strong family history

c.) preexisting renal disease

• Analysis of stones passed out spontaneously - may NOT be useful. 80% stones are Ca++ oxalate, no matter the primary d/o. This won’t alter the workup in recurrent stone dse. Ex: hyperuricosuria causes calcareous stones 4x more than uric acid stones by enhancing Ca oxalate precipitation and adsorbing urinary stone inhibitors such as citrate However, as with crystalluria, will give a clue to the underlying metabolic d/o, such as with cystine and struvite stone formers.

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MgNH4CaPO4 /struvite“coffin lid” crystals

Cystine“hexagon” crystals

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STONE DISSOLUTION (Medical) OR SURGERY- 1924, Cromwell dissolved cystine stones in mercuchrome & alkali- 1940, Suby and Albright used “chemolysis” to dissolve phosphate

calculi by nephrostomy tube irrigation- Percutaneous technics now allow stone extraction or disintegration

so that only < 10% of cases require open stone surgery.- Advent of ESWL 1980 allowed stone disruption and elimination of

surgery. Drawback: $ 5-9,000 although less thanendourologic stone removal costing $ 6-10,000.Locally, ESWL = P 45,000 ; NL = P 30-60,000

- Presently, renal calculi is preventable with selective medical therapy designed to correct underlying metabolic disorders or derangements in urinary biochemistry.

Consensus Conference on Prevention and Treatment of Kidney Stones – “ Current medical therapy will NOT dissolve most stones. Rather, aimed at inhibiting stone growth and preventing formation of new stones.”

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Lithotripsy CANNOT replace medical prevention. Surgery & medical Rx complementary. Medical Rx effectively: 1. prevents recurrence 2. reduces need for surgery 3. avoids renal colic 4. correct extrarenal manifestations of a systemic disease 5. cost effective = $ 1,000 for comprehensive metabolic eval’n

and $ 300 per year for selective medical Rx

ESWL for stones < 2 cm dia; bigger stones and lower pole stones > 1 cm require repeat procedures. Ureteral stones pass out spontaneously if < 5 mm. ESWL and invasive procedures may be delayed for 3-4 days w/o causing permanent damage to the kidneys even with complete obstruction.

ESWL best for proximal ureteral stones while endoscopic technics / ureterenoscopy better for lower ureteral stones.

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ECONOLITH 3000ECONOLITH 3000

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The major indications for surgical interventionof urolithiasis are relief of pain, uncontrolledInfection, persistent gross hematuria or relief of significant obstruction that will destroyrenal function.

The best studies to determine significantobstruction is the intravenous urogram / IVP to demonstrate calyceal clubbing and dilatation as well as renal function.Ultrasound can only define the anatomyand not functional impairment.

A meta-analysis of four studies including 296 patients concluded that non-contrast helical CT is significantly better at diagnosing and ruling out stones than IVP. Thus, the new gold standard is now the use of Non-contrast helical CT or “stonogram” with a 98% sensitivity and 100% specificity.

IVP

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TREATMENT INDICATION EFFICACY

Ureteroscopic Stone in distal ureter not removal of stone progressing downward 98%

Pushing back stone Stone in proximal ureter 96-100% with ESWL not progressing downward

In situ ESWL Stone in distal ureter not 78% if w/o stent progressing downward 89% w/ stent

Kidney stones 0.5 - < 2 cm 77-80% (20% add’l procedure)

Kidney stones > 2 cm 35-40% Kidney stones in lower pole >1cm 54% (60% add’l)

PerCutaneous Stone in proximal ureter 90% NephroLithotomy not progressing downward or (PCNL) failed push-back ESWL in 1-2% cases

Kidney stones not best treated with ESWL alone 80-85% (30% add’l)

Dissolution agents:Alkali uric acid stones variable; poor if stone

coated w/ oxalate or struvite

Water + penicillamine cystine stones variable; poor if stone or tiopronin coated w/ oxalate or struvite

• Pathogenesis & Treatment of Kidney Stones- Coe and Parks; NEJM. Oct 92

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Empiric Antibiotic Regimens for Complicated UTIEmpiric Antibiotic Regimens for Complicated UTI

Antibiotics should be modified according to urine CS result.Antibiotics should be modified according to urine CS result.

Oral switch therapy done once afebrile or clinically improved after 48hrsOral switch therapy done once afebrile or clinically improved after 48hrs

Oral regimen (mild cases):Oral regimen (mild cases):Ciprofloxacin 500 mg BIDCiprofloxacin 500 mg BIDNorfloxacin 400 mg BIDNorfloxacin 400 mg BIDOfloxacin 400 mg BIDOfloxacin 400 mg BIDCotrimoxazole 800 mg BIDCotrimoxazole 800 mg BID

Parenteral regimen (mod.-severe cases) :Parenteral regimen (mod.-severe cases) :Ampicillin 1 gm q 6h IV + Genta 3-5 mkd IVAmpicillin 1 gm q 6h IV + Genta 3-5 mkd IVCeftazidime 1-2 gm q 8h IVCeftazidime 1-2 gm q 8h IVCeftriaxone 1-2 gm OD IVCeftriaxone 1-2 gm OD IVImipenem 250-500 mg q 6-8h IVImipenem 250-500 mg q 6-8h IVCiprofloxacin 200-400 mg q 12h IVCiprofloxacin 200-400 mg q 12h IVOfloxacin 200-400mg q 12h IVOfloxacin 200-400mg q 12h IV

Choice of Antibiotics: 14 day regimenChoice of Antibiotics: 14 day regimen

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PATHOPHYSIOLOGYActivity product ratio =

= measure of degree of saturation< 1 = undersaturation; > 1 = oversaturation

Formation product = APR at which solid phase begins stone

Urine of stone formers is supersaturated than normal.

APR at the limit of metastability (FP) is lower in stone formers, suggesting facilitation of crystallization.

Homogenous nucleation = spontaneous formation of new crystal nuclei in oversaturated urine.

Heterogenous nucleation = any surface that serves as substrate for ions in solution to organize.

Epitaxis = similarity of spacing of charged sites on preformed surface and on the lattice of crystal crystal growth

Ex: monosodium urate or uric acid for Ca oxalate/phosphate

free ion activity product

equilibrium solubility product

UNSTABLE

METASTABLE

STABLE

FP = upper limit of metastability

Equilibrium solubility. product= free ionized Ca x oxalate conc.

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4 MAIN TYPES OF STONES:

1. Calcium 75%

oxalate ( monohydrate/ whewellite or dihydrate/ weddellite ) 50%hydroxyapatite (CaPO4)Brushite (CaHPO4)Oxalate + Uric acid 20%Others (CO3 ; Orthophosphate)

2. Uric Acid 8%3. Cystine 1%4. Struvite (MgNH4PO4 amd CaCO3) 15%

WEDDELLITEWEDDELLITEBRUSHITEBRUSHITE

WHEWELLITEWHEWELLITE

STRUVITESTRUVITE

CYSTINECYSTINE

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STONE DENSITY BASED ON DEGREE OF RADIOOPACITY Density Degree of Opacity

Calcium phosphate 22.0 Very opaqueCalcium oxalate 10.8 OpaqueMg-Ammonium phosphate 4.1 Moderately opaqueCystine 3.7 Slightly opaqueUric Acid 1.4 Nonopaque*Xanthine 1.4 Nonopaque

* 60% or more in composition

Limits of Normal for Excreted Materials in Urine: mg/24h

Material Male Female Mg/kg/24hrCalcium 300 250 4Uric Acid 800 750 -Oxalate 50 50 0.73Citrate 500 750 -

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Calcium Stones:

Idiopathic Hypercalciuria - said to be most impt determinant for stone form.- autosomal dom. pattern; 50% of stone formers

Calcium reabsorption at the tubules is altered by high Na and protein diets.Hypercalciuria - oversat. and complexing of Ca oxalate and phosphates.

MECHANISMS:1. Idiopathic a. Renal Leak - defect in tub. Ca reabsorption with modest fall in serum Ca++

patients have high urine Ca levels despite Ca-restriction b. Absorptive Hypercalciuria - increased intestinal Ca reabsorption due to

either duodenal absorptive defect, inc. Vit D3 action or passive absorption with inc. carbohydrate intake

2. Hyperuricosuria - high purine diets or highly acidic urine; acts as nidus3. Primary Hyper PTH - 5% of stone formers; hypercalcemia and hypophos.4. Hyperoxaluria - intestinal diseases, gut bypass, Vit C excess, dietary

oxalate excess, or rarely,primary.- childhood onset and severity suggests primary type. - may be reduced with vit.B6 supplements >50mg/day

5. Hypocitraturia - 2nd most impt determinant of stone formation- 15 to 83% incidence; 61% in frequent stone formers (>2 per 3yrs)

6. Other rare causes (<5% of total): cystinuria, triamterene stones, RTA,xanthinuria, hypomagnesiuria

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Inhibitors of growth and nucleation:Citrate = provides 50% of inhibitory action for stone formation. 1. forms soluble complexes with Ca, reducing free ionic Ca++

2. inhibits agglomeration of Ca++ oxalate 3. also impairs the urate-induced crystallization of Ca++ oxalate

Magnesium= also potent inhibitor; 20% of urine’s total CaPO4crystallization inhibitory activity.

Pyrophosphate = increases formation product and adsorbs calcium on its surface. Less potent at 7% of urineinhibitory action.

Nephrocalcin = urine glycoprotein inhibitorTamm Horsfall proteinAcid mucopolysaccharide (AMPS) , acid peptides

Schema for Metabolic Classification: U Ca Uca/GFR Uca/Ucr U Ua

mg/24h mg% mg/24hRenal Leak ______> 200 > 0.11 > 0.2 < 700Absorptive Hc > 200 < 0.11 > 0.2 < 700Hyperuricosuria < 200 < 0.11 < 0.2 > 700Normal < 200 < 0.11 < 0.2 < 700

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INDICATION TREATMENT EFFICACY

Idiopathic Hypercal, Thiazides/diuretics new stones 11-22% vs 40% controls;up to 50% decreased risk

Oral phosphates new stones 9-25%

Low Ca++ diet (no bone dse) new stones in 29-38%Sodium cellulose phosphate new stones in 27%

Primary PTH parathyroid surgery 100%Hypocitraturia Potassium alkali salts new stones in 12%RTA type 1 Potassium alkali salts no dataIleostomy or small bowel malabs. Potassium alkali salts no data

Hyperoxaluria ,all kinds Potassium alkali salts no data

Enteric hyperoxal. oral Ca supplements, chole- styramine, or low fat diet no data

Hyperuricosuria w/ oxalate stones allopurinol new stones 14% vs 35% controlsUric stones, all Potassium alkali salts new stones 12% men, 0% women

Diet

Struvite ESWL or PCNL 30-40% stone free if < 2cm Acetohydroxamic acid stone growth 0% vs 95% controls

in 15-19 mos; 15% DeepVeinThrCystinuria Penicillamine

Tiopronin, Potassium alkali salts no data

SPECIFIC TREATMENT TO PREVENT OR DISSOLVE STONES

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Foods high in Oxalate

• Cocoa• Chocolate• Black Tea• Green beans• Beets• Celery• Green onions• Leeks

• Leafy greens• Berries• Orange and lemon peel• Dried figs• Summer squash• Nuts• Peanut butter

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Foods high in Purine

• Innards: liver, kidney, brains, heart

• Shell fish• Meat: beef, pork, poultry,

lamb• Fish: anchovies, sardines,

mackerel, herring, tuna, carp, halibut, cod

• Meat extracts: bouillon, broth, stock

• Gravies• Vegetables: asparagus,

cauliflower, spinach, peas, lentils

• Mushrooms• Kidney beans

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Beverage Use and Risk for Kidney Stones in Women*• 81,093 women 40-65 y.o.• Prospective cohort study with 8 year follow-up• Self-administered food-frequency questionnaires to assess

diet in 1986 and 1990• Outcome measure: incident symptomatic kidney stones

• 719 cases of kidney stones documented• Relative Risk for Stone formation

fluid 0.62 (95% CI 0.48-0.80)• Multivariate analysis for beverages

Water 0.98 (95%CI 0.94-1.02)Skim milk 0.98 (95%CI 0.86-1.12)Apple juice 0.67 (95%CI 0.36-1.25)Orange juice 1.00 (95%CI 0.80-1.26)Grapefruit juice 1.44 (95%CI 1.09-1.92)Coffee 0.90 (95%CI 0.85-0.95)Tea 0.92 (95%CI 0.85-0.99)Beer 0.88 (95%CI 0.71-1.08)Wine 0.41 (95%CI 0.25-0.68)Soda (sugared) 1.05 (95%CI 0.95-1.17)Soda (diet) 0.98 (95%CI 0.92-1.04)

* Ann Int Med 126:534-540, 1998

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Comparison of Dietary Calcium with Supplemental Calcium and Other Nutrients as Risk for Kidney Stone Disease in Women*

• 91,731 women 34-59 y.o.• Prospective cohort study with 12 year follow-up (1980-1992)• Self-administered food-frequency questionnaires to assess

diet in 1980, 1984, 1986 and 1990• Outcome measure: incident symptomatic kidney stones

* Ann Int Med 126:497-504, 1997

• 864 cases of kidney stones documented• Relative Risk for Stone formation

fluid 0.61 (95% CI 0.48-0.78)dietary Ca intake 0.65 (95% CI 0.50-0.83)potassium 0.65 (95% CI 0.51-0.84)supplemental Ca 1.20 (95% CI 1.02-1.41)sodium 1.30 (95% CI 1.05-1.62)sucrose 1.52 (95% CI 1.18-1.96)

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Stone Formers’ Diet

• Limit protein intake to < 1 gm/kg/day

• Limit sodium intake to < 100-130 meq/day

• Increase fluid intake to increase urine output to > 2 Liters/day

• Avoid calcium restriction NORMAL calcium diet, preferably using natural sources AND taken with meals

• Encourage potassium intake

• Low oxalate bran consumption of 15 gm/day

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