Urinary tract obstruction &

Stones

Loin pain & hematuria

Principal sites of pathology leading to loin pain

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 compounds 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

Gastrointestinal disorders;
Fat malabsorption, IBD, small bowel resection & bypass can cause decreased
urinery volumes, hyperoxaluria, hyperuric-aciduria, hypocitrateuria, acidic urine.

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)

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

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

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,

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
Hypophosphatemi
a
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

increased Ca
From bone
excretion in urine

Plasma Ca
increase

increased phosphate
increased phosphate
from intestine
from bone & intestine

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

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