renal stone disease, mbbs, 2014 lecture

8/16/2019 Renal Stone Disease, MBBS, 2014 Lecture

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Renal stone disease @ medical

outpatient clinic

Mahesh Raj Sigdel

July 4, 2014


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Why???

At least 10 per cent of the population in theindustrialized world

Recurrence

Significant pain

Loss


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What do we generally do ?

What do surgeons generally do ?


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Stone in the urinary tract:

What is this stone type ?

Why did this stone form?

Does the stone(s) require active removal and if

so, how should this procedure be carried out?What is the risk of further stone problems for

this individual patient?

What can be done to prevent recurrent stone

formation?

Are there any systemic conditions beyond

kidney that need to be addressed ?


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Stone types

Calcium containing stones

Calcium oxalate

Hydroxyapatite

Brushite

Non calcium containing

Uric acid

Struvite

Cystine

Xanthine

Ammonium acid urate

MatrixMedication related eg acyclovir,

indinavir, triamterine, ciprofloxaxin, loop

diuretics, acetazolamide, silicate etc

Stones associated with Melamine

exposure


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Radiolucent stones..

Uric acid

Xanthine

Indinavir


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How does stone form ?

Formation of stones in the urinary tract is the result of apathological crystallization

Complex cascade of events occur as the glomerular

filtrate traverses the nephron.

It begins with urine that becomes supersaturated withrespect to stone-forming salts, such that dissolved ions ormolecules precipitate out of solution and form crystals ornuclei.

Once formed, crystals are retained in the kidney atanchoring sites that promote growth and aggregation,

ultimately leading to stone formation.


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Major steps in calcium salt crystallization


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Inhibitors

MagnesiumCitrate

Pyrophosphate

Glycosaminoglycans (heparin, heparan sulfate, hyaluronicacid, and chondroitin sulfate)

Nephrocalcin

Tamm-Horsfall mucoprotein

Uropontin

Bikunin

Other factorsUrine volume

Urinary pH


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Calcium Stones

Hypercalciuria

Hyperoxaluria

HypocitraturiaHyperuricosuria


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Hypocitraturia

Excessive protein intake

Hypokalemia

Metabolic acidosis

ExerciseHypomagnesemia

Infections

Androgens

Starvation

Acetazolamide


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Uric acid stone

Three major factors influence uric acid stoneformation:

low urine pH,

low urine volume, andelevated urinary uric acid levels


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Infection Stones

Struvite stone (magnesium ammonium phosphate) mainly

Infection with urease producing bacteria

Alkaline pH of urine

Predispositions to infection


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Cystine Stones

Cystinuria is an autosomal recessive or

dominant

Tubular defect in dibasic amino acid transport

The main contributor to cystine crystallizationis supersaturation because there is no specific

inhibitor of cystine crystallization in the urine


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Presentation

Asymptomatic/incidental

Pain

Hematuria

Lithuria

Infection/pyelonephritis

Obstruction

CKD


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Clinical Evaluation of Stone Formers

All stone formers should have basic evaluation

All patients with recurrent nephrolithiasismerit metabolic evaluation

Complete evaluation of patients with a singlestone is controversial because of theundetermined cost-benefit ratio


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Basic evaluation

RBS KFT, Na, K

Uric acid

Ca, Phosphate, ALP, iPTH

Blood Bicarbonate, Chloride (ABG) Urine R/M, Urine pH

Urine C/S

Stool analysis

USG abdomen

X-ray KUB (+/- IVU)

Helical CT plain


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History

History serves to uncover a systemic etiology for nephrolithiasis: – Any disease that can lead to hypercalcemia

– Malabsorptive gastrointestinal disorders, GI bypass surgery

– Growth, bone health

– Gout, insulin resistance, metabolic syndrome

Stone history: – Number and frequency of stones formed

– Age of the patient at occurrence of the first stone

– Size of stones

–Stone type

– whether the patient required surgical removal of the calculi

– stone response to intervention

– whether stones recur frequently in a single kidney


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History ..

Dietary history: protein, purine, oxalate, calciumrestriction

Occupation: drinking water, perspiration, avoidinggoing to toilet, ambient temperature

Family history

Medications- eg loop diuretics, salicylates, aciclovir,

sulphadiazene, indinavir, acetazolamide, topiramate,steroids, calcium, vitamin D, allopurinol, vitamin C

Exposure to melamine


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Uric acid crystals


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Calcium oxalate crystals


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Cystine crystals


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Triple phosphate crystal


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Management...


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Medical management…

Generic:

Fluids to make urine >2.5 liters/day

Low protein ( 0.8 to 1 gm/kg/day)

Low salt < 2 gm/day

Normal calcium

Treatment of primary disorder egsarcoidosis, hyperparathyroidism


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Specific..

Calcium stones

Thiazides

Potassium citrate

Orthophosphate sts


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Hyperoxaluria

Dietary and Enteric Hyperoxaluria

Dietary oxalate restriction

Calcium carbonate (1 to 1.5 g) may be added at each mealand snack

Primary Hyperoxaluria

Pyridoxine

Potassium citrate and magnesium supplementation

Orthophosphate

Oxalobacter formigenes


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Uric acid stones

Potassium citrate

Low purine diet

Allopurinol /Febuxosatat


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Infection stones

Antibiotic

Surgical

Acetohydroxamic acid (Lithostat)


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Cystine stones

d-Penicillamine

Tioproninα mercaptopropyonyl glycine (thiola)

Captopril


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Surgical management

ESWL

PCNL

Endourologic procedures

Surgeries- open/laparoscopic


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Stones less amenable to ESWLCystine

BrushiteCalcium oxalate monohydrate

M t


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Management


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What should we generally do ?

What only should not be done by surgeons?


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Thank you !!!

renal stone disease, mbbs, 2014 lecture

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