Transcript Urinary tract obstruction & Stones

Urinary tract obstruction &
Stones
Loin pain & hematuria
Principal sites of pathology leading to loin pain
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Spinal nerve roots
Vertebral column
Paraspinal & lumbar muscles
Kidneys
Renal pelvis / ureters
Abdominal aorta
Pancreas
• Renal pain arises because of rapid
stretching or inflammation of renal capsule
• Pain from the renal pelvis / ureter is
caused by distention & excessive
peristaltic contractions
• Any back / retroperitoneal structure may
give rise to back pain
Macroscopic hematuria
• May arise from lesions anywhere within the
urinary system, kidney, renal pelvis, ureter,
bladder, urethra
• As few as 5 x 10 6 RBC/ml ; 1ul blood/ml urine
can be detected visually as red-coloured urine
• Macroscopic hematuria needs to be
distinguished from
– Red discolouration of urine caused by certain dyes &
some drugs
– Presence of Haem pigment : intravascular hemolysis
(Hb), rhabdomyolysis (myoglobin)
– Bleeding from outside the urinary tract; perineum,
vagina
• Bleeding from the bladder or above cause
uniform discoloration of urine
• Bleeding from the urethra may cause bleeding
separate from the urine or mixed with urine
• Hematuria from the renal parenchyma –
glomeruli or interstitium – tends to be
accompanied by proteinuria, casts, & dismorphic
RBC (abnormal morphology)
• Bleeding from renal tumors or from lesions in the
renal pelvis or below may be isolated or
associated with pyuria – particularly with
infections.
• Macroscopic hematuria from tumors are usually
painless, whereas that from calculi / infection is
usually associated with pain
Pyelonephritis/infections
• The formation of stone is usually the result of many
metabolic and physiologic disorders contributing to stone
formation
• Stones in the urinary tract are composed of crystals and
matrix skeleton.
• Physical factors of stone formation
– Supersaturation of the urine with respect to a particular solute,
e.g. uric acid, due to increase in excretion or decrease in urine
volume. At some point spontaneous nucleation and crystal
growth occur – homogenous nucleation.
– Urine pH, determines the solubility of ccompounds in the urine.
Uric acid & cystine are poorly soluble in acidic media, whereas
calcium salts are poorly soluble at an alkaline pH.
– Crystalization inhibitors; normal urine contain factors that inhibit
formation & growth of crystals – Mg, citrate, pyrophosphate,
TPH, glucosamine, nephrocalcin.
– Heterogenous nucleation appears to be a major mechanism in
stone formation. A small crystal, e.g. uric acid, serves as a nidus
on which another compound, e.g. ca-oxalate, precipitates
– Infection with urea splitting / urease producing microorganisms
Disorders causing stone disease
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Gastrointestinal disorders;
– Fat malabsorption, IBD, small bowel resection & bypass can cause decreased
urinery volumes, hyperoxaluria, hyperuric-aciduria, hypocitrateuria, acidic urine.
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Hyperparathyroidism / hypercalcemia
– Causes of hypercalcemia (& hypercalciuria) are #
• Cancer, immobilization, endocrinopathies, dietary, granulomatous disease, renal, drugs
• Vit D increases Ca absorption from intestine
– Idiopathic Hypercalciuria.
• 24h urine[Ca] > 300mg/24h (men), >250mg/24h (women)
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Gout & hyperuricosuria.
– May promote Ca-oxalate stones
• Epitaxy, ca-oxalate deposits on uric acid / Na-urate crystals as nidus
• Urate in urine binds glycosamineglycans, an inhibitor of stone formation
• Uric acid promotes the degree of aggregation of precipitated crystals
– Uric acid lithiasis; elevated urinary uric acid (24h urinary uric acid), acid urine;
• Gout, myeloproliferative disorders
• Treatment: alkalinization of urine to pH 6-7 , fluids, allopurinol
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Infection with urease producing bacteria urea splitting struvite stones
– Proteus in majority; Klebsiella, Pseudomonas, Providencia, Staphylococcus,
Ureaplasma urealyticum, rarely E. coli.
– More common in patients with ileal conduits, hyperchloremic metabolic acidosis,
ureteral dilatation, increased volume of residual urine, decreased renal function
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Obstruction & anatomic abnormalities
Drugs.
– Acetazolamide causes hyperchloremic metabolic acidosis, transiently elevates
urine pH, and reduces citrate excretion
– Allopurinol increases xanthine excretion and may produce xanthine stones
– Several drugs have limited urine solubility,
• May promote stone formation or are absorbed into the crystal matrix of other stone
• Triamterene, ceftriaxone, sulfonamides, bactrim, sulindac, phenazopyridine
• Other : laxatives, vit D, calcium,
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Renal tubular disorders.
– Cystinuria,
• Inherited disorder of amino acid transport,
• associated with increased urinary excretion of cystine, ornithine, lysine, & arginine
(COLA)
• Limited soloubility of cystine promotes recurrent stones, which are radioopaque,
homogeneous, may assume staghorn form
• Therapy: high fluid intake, alkalinization of urine to pH 7.5 or more; reduce cystine
excretion by low Na diet, D-penicillamine, trioponine, captopril (drugs with sulfhydryl)
– Distal RTA
• Alkaline urine, hypocitrateuria,hypercalciuria
– Hyperphosphaturia, causing hypophosphatemia & elevated 1,25-(OH)2D3,
hypercalcemia
– Idiopathic hypercalciuria; reduced tubular reabsorption of Ca
• Enzymatic defects
– Xanthinuria. Deficiency xanthine oxidase
• Radiolucent xanthine stones
– 2,8-dihydroxyadenine.
• Deficiency adeninephosphoribosyl transferase (APRT)
• Radiolucent stones, requires infrared / crystallographic analysis
• Treatment with allopurinol
– Primary hyperoxaluria,
• Idiopathic Urolithiasis
– Majority of patients
– Risk factor profile
• Abnormally high excretion of Ca (>4mg/kg/d), uric acid, oxalate, Na
• Decrease in several inhibitory solutes
• Decreased urine volume!
• Ability of urine to inhibit agglomeration improves after treatment with
alkali, which increase urinary citrate
– Excretion of citrate is decreased by systemic acidosis, depletion of
kalium & magnesium, starvation acetazolamide,
– Most patients with low urinary citate have RTA, chronic diarrhea,
hypokalemia, malabsorption, or high intake of animal protein
First stone episode
Dietary advice: meat, dairy, salt
Fluids; f/u 6-12 months
No growth
Metabolically active
Monitor 1-2 years
Urinary risk assessment
Dietary/fluid
Factors persist
hypercalciuria
hyperuricosuria
Evaluate diet
Meat, Ca, Na
hypocitric aciduria
Evaluate for
acidosis, RTA
GI
Dietary, meat
Treatment options
Repeat
Dietary advice
specific
dietary Rx & /
Reduce meat
excess
Thiazides
allopurinol
hyperoxaluria
Evaluate for
dietary excess
malabsorption
GI disorders
measure oxalate/
glycoliate
dietary fat /
oxalate
restriction
K-Citrate
B6, PO4
Asymptomatic  No Rx
Symptomatic
Calcium stones
Mg/NH4/PO4
stones
Symptomatic
obstructive
Percutaneous
extraction +
ESWL
Cystine (cannot
dissolve, or
obstructive
Small <2cm
New stones
ESWL
<2cm
>3cm
ureteric
stones
ESWL
Perc upper1/3 lower1/3
ESWL
ESWL
Extraction
laser Rx
Acute colic: analgetics, fluids
>2cm
old stones
Perc
Uric acid
(cannot dissolve/
obstructive)
ESWL
Often requires
Urography
Usg
7-dehydrocholesterol
Skin
Diet
UV
Cholecalciferol
liver
25-hydroxycholecalciferol
kidney
PTH
Hypophosphatemia
Calcitriol
Small intestine
Bone
24,25 D
Kidney
+PTH
Increase
CaHPO4
absorption
Increase
Ca & Po4
release
Decrease
Ca & PO4
excretion
Metabolic activation of vit.D
The result is an increase in
Ca & PO4 concentration
Plasma Ca
PTH
Bone
Kidney
Vit.D
Reabsorption
Phosphate
Excretion
Release of
Calcium &
phosphate
Ca
reabsorption
Calcitriol
formation
Intestinal
CaHPO4 absorption
Effect of PTH on Ca & phosphate metabolism.
Net effect is increase in plasma Ca, with no change or decrease in plasma phosphate concentration
Plasma Ca [2+]
PTH
Cacitriol
Increased Ca
From bone
increased Ca
from intestine
Plasma Ca
increase
increased phosphate
from bone & intestine
increased phosphate
excretion in urine
Plasma Phosphate
unchanged
Plasma phosphate
Calcitriol
Ca from
intestine
PTH
Decreased
Ca from bone
Plasma [Ca]
Slight increased
decrease
phosphate
excretion in
urine
increase phosphate
from intestine
Plasma [PO4]
increased
Increased = systemic disease
Serum [calcium]
normal
Normal
Hyperuricosuria
Hyperoxaluria
No abnormality
Urinary calcium
= idiopathic hypercalciuria
RTA
Laboratory investigation
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Serum electrolytes, BUN, Cr, Ca, PO4, Uric acid
Urinalysis; microscopic exam of fresh specimen
Urine culture
Nitroprusside test for cystine
Urine pH, first AM urine, under oil
Stone analysis
24h urine for Cr, Ca, PO4, uric acid, Cystine,
oxalate
• Radiologic studies, USG, BNO, IVP
• Special test as indicated; PTH, Thyroid, Cortisol,
etc