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Renal Stones: A Guide For The Non-Urologist: F. A. Fried, MD University of North Carolina Division of Urology

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Renal Stones: A Guide for the

Non-Urologist

F. A. Fried, MD
University of North Carolina
Division of Urology
Pathogenesis of Renal Stones
• all urinary stones are composed of 98%
crystalline material and 2% mucoprotein
• the crystalline component(s) may be found
“pure” or in combination with each other.
• the common characteristic that all
crystalline components share, is that they
have a very limited solubility in urine
Pathogenesis of Renal Stones
(cont.)
• 99% of renal stones (in western
hemisphere) are composed of:
– calcium oxalate 75% (mono or di hydrate)
– calcium hydroxyl phosphate (15%)(apatite)
– magnesium ammonium phosphate 10%
(struvite)
– uric acid 5%
– cystine 1%
Pathogenesis of Renal Stones
(cont.)
• investigations show that the formation of a stone
is similar to the development of a crystalline mass
in vitro
• given that stone formation is an example of
crystallization one could predict:
– the necessity for a supersaturated state in urine
– the occurrence of spontaneous crystallization
– the need for the earliest polycrystalline state to be
arrested in the u.t. allowing time for growth
Spontaneous Crystallization
• normal urine has crystals (at times)
• normal urine is extremely effective in
maintaining a stable supersaturated state
• there are certain components of urine that
– enhance ability to maintain ss state
– inhibit development of crystals
Site of Stone Development
Question: Where in the UT does urine reach its
maximal concentration while still in a
microscopic sized lumen so that crystalline
particles that may form can get “stuck” in the
lumen?
Answer: The collecting duct which runs through
the renal papilla. Any part of the UT distal to this
point has a large lumen and small particles would
easily pass.
Clinical Risk Factors
• occupation
• family history
• diet
• hydration
• small bowel disease (i.b.d.)
• medical conditions causing hypercalcuria
• medical conditions causing aciduria
Clinical Features
• acute obstruction of • chronic stone dis. tends
ureter---severe colic to be associated with
• flank pain referred to large or multiple stones
genitalia • can be little or no pain
• nausea, vomiting may • may have impaired
mislead and look like renal function, anemia,
gi problem weight loss etc.
• microhematuria likely • concomitant infection
more likely
Evaluation
Exam- costovertebral angle (cva) tenderness, no
peritoneal signs
Urine analysis (expect to see hematuria)- need to know if
there is concurrent infection
KUB (expect to see a calcification but 5% of stones are
radiolucent)
IVU will show delayed function, hydronephrosis and
ureteral dilatation to point of stone
Ultrasound can show hydro will not show ureteral stones
Treatment
• small ureteral stones • large ureteral stones
with good chance of (>7mms)
passage (<7 mms) – eswl
– allow time to pass (2-4 – ureteroscopic stone
weeks) fragmentation
– lower ureter- – open surgery
ureteroscopic stone
removal
– mid-upper ureter eswl
Role of Ureteral Stents
• Ureteral stents are commonly used they
accomplish the following:
– drain obstructed kidney thereby alleviating pain
– dilate ureter perhaps facilitate passage of stone
– facilitate performance of eswl and
ureteroscopic procedures
– avoid problems from “steinstrasse” in the post
treatment period
Treatment Renal Stones
• < 2 cm. eswl
• > 2cm or multiple stones, percutaneous
ultrasonic lithotripsy (pul)
• large branched stones “staghorn” may
require pul and eswl.
• cystine stones pul or open nephrolithotomy
Metabolic Evaluation
• The first stone or infrequent (no problem for 10
years) no work up needed.
• more than one isolated stone event:
– serum Ca, P, Uric Acid (repeat 2-3 times)
– 24 hr urine for Ca. P, Uric Acid
– serum parathormone if serum Ca is high
– urine culture
• If above is normal then obtain
– urine citrate, urine oxalate
Principles of Medical
Management
• monitor stone burden with periodic kub
• instruct patient on adequate water
consumption ( enough to produce 2L of urine
in 24 hrs.)
• instruct in low oxalate and modified calcium
diet
• if hypercalcuric treat with hydrochlorothiazide
(monitor urinary Ca)
Principles of Medical
Management (2)
• if hyperuricosuric
– allopurinol if serum uric acid elevated
– alkalinize urine if serum level is normal
• if active Ca stone former not aided by diet,
hctz add K citrate
• if magnesium ammonium phosphate stone
after reduction of burden treat aggressively
with antibiotics.
Anatomic Evaluation
• necessary to decide on how to best treat
– size and location of stone
– number of stones
– anatomy of kidney, ureter
– is stone overlying bone
– “condition” of involved kidney
Principles of Stone Prevention
• prevent supersaturation
– water! water and more water enough to make 2L of
urine per day
– prevent solute overload by low oxalate and
moderate Ca intake and treatment of hypercalcuria
– replace “solubilizers” i.e... citrate
– manipulate pH in case of uric acid and cystine
• flush! forced water intake after any dehydration

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