1. Urinary tract obstruction & Stones

2. Loin pain & hematuria

3. Principal sites of pathology leading to loin pain
Spinal nerve roots
Vertebral column
Paraspinal & lumbar muscles
Kidneys
Renal pelvis / ureters
Abdominal aorta
Pancreas

4. 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

5. Macroscopic hematuria
May arise from lesions anywhere within the urinary system, kidney, renal pelvis, ureter, bladder, urethra
As few as 5 x 10 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 6

6. 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

7. Pyelonephritis/infections

16. Physical factors of stone formation
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

17. 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

18. 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

19. Idiopathic Urolithiasis
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

20. Urinary risk assessment
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 hypercalciuria hyperuricosuria hypocitric aciduria hyperoxaluria
Factors persist
Evaluate diet Evaluate for Evaluate for
Meat, Ca, Na acidosis, RTA dietary excess
GI malabsorption
Dietary, meat GI disorders
measure oxalate/
glycoliate
Treatment options
Repeat specific Reduce meat dietary fat /
Dietary advice dietary Rx & / excess oxalate
restriction
Thiazides allopurinol K-Citrate B6, PO4
?thiazides

21. Calcium stones Mg/NH4/PO4 Cystine (cannot Uric acid
Asymptomatic  No Rx
Symptomatic
Acute colic: analgetics, fluids
Calcium stones Mg/NH4/PO Cystine (cannot Uric acid
stones dissolve, or (cannot dissolve/
obstructive obstructive)
Symptomatic
obstructive
Percutaneous
extraction +
ESWL
Small <2cm >2cm
New stones old stones
ESWL Perc
ESWL
Often requires
Urography
Usg
<2cm >3cm ureteric
stones
ESWL Perc upper1/3 lower1/3
ESWL
ESWL Extraction
laser Rx

22. Metabolic activation of vit.D The result is an increase in
7-dehydrocholesterol Diet
Skin UV
Cholecalciferol
liver
Metabolic activation of vit.D
The result is an increase in
Ca & PO4 concentration
25-hydroxycholecalciferol
kidney
PTH
Hypophosphatemia
Calcitriol ,25 D
Small intestine Bone Kidney
+PTH
Increase Increase Decrease
CaHPO Ca & Po Ca & PO4
absorption release excretion

23. Plasma Ca
PTH
Bone Kidney
Vit.D
Reabsorption
Phosphate Ca Calcitriol
Excretion reabsorption formation
Release of
Calcium &
phosphate
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

24. Plasma Ca [2+]
PTH
Cacitriol
Increased Ca increased Ca increased phosphate increased phosphate From bone from intestine from bone & intestine excretion in urine
Plasma Ca Plasma Phosphate
increase unchanged

25. Plasma phosphate
Calcitriol
PTH
Ca from
intestine
Decreased decrease increase phosphate
Ca from bone phosphate from intestine
excretion in
urine
Plasma [Ca] Plasma [PO4]
Slight increased increased

26. Serum [calcium] Increased = systemic disease normal Normal
Hyperuricosuria
Hyperoxaluria
No abnormality
Urinary calcium
= idiopathic hypercalciuria
RTA

27. 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