6. Prevalence of various types of Renal stones
% of all stones
Ca.Oxalate and PhosphateCa.Oxalate and Phosphate 7070
Idiopathic hypercalciuria (50%)
Hypercalciuria & hypercalcemia (10%)
Hyperoxaluria (5%)
Enteric (4.5%)
Primary (0.5%)
Hyperuricosuria (20%)
Hypocitraturia
No known metabolic abnormality (15-20%)
Magnesium Ammonium Phosphate ((STRUVITE)) 15-20
Uric acidUric acid 5-105-10
Associated with hyperuricemia
Associated with hyperuricosuria
Idiopathic (50% of uric acid stones)
Cystine 1-2
Other or unknownOther or unknown +5+5
7. Calcium stones
• Most common 75%
• Pure stones of Ca oxalate 50%
• Pure stones of Ca phosphate 06%
• Mixture of Ca oxalate & Ca phosphate 45%
8. Etiology of calcium stones
• Idiopathic hypercalciuria w/o hypercalcaemia 50%
• Hypercalcaemia and hypercalciuria 10%
– Hyperparathyroidism
– Absorptive hypercalciuria
– Renal hypercalciuria
• Hyperuricosuria with normal blood uric acid level
and without any abnormality of Ca metabolism 15%
• Idiopathic Ca stone disease 25%
– Unknown, No abnormality in urinary excretion of ca, uric acid and oxalate
9. Pathogenesis
• Imbalance b/n the degree of
supersaturation of ions forming the stone
and concentration of inhibition in urine
• Nidus – crystals of Ca oxalate, Ca PO4
precipitate in tubular lining around some
fragment of debris in tubules
• The stone grow, deposition of more
crystals at nidus
10. Factors contributing stone formation
• Urinary alkaline pH
• Decreased urinary volume
• Increased excretion of oxalate and uric acid
17. Etiology of Struvite stones
• Infection of UT with urea splitting bacteria
• Proteus, Klebsiella, Enterobacter
• Infection induced stones
18. Morphology struvitie stones
• Yellow - white or grey
• Soft, friable, irregular in shape
• Stag horn stone: large solitary stone that
takes the shape of renal pelvis
19.
20. Uric acid stones. 6%- etiology
• Hyperuricaemia, hyperuricosuria
• Primary/Secondary gout
(due to myeloproliferative dis)
• Leukemia on chemotherapy
• Administration of uricosuric drugs
(Salicylates, Probenicid)
• Other factors acid pH less than 6
low urinary volume
High nucleic
acid turnover
21. Pathogenesis of uric acid stones
• Solubility of uric acid at pH 7 is 200 mg/dl
• at pH 5 is 15 mg/dl
• Urine becomes acidic, solubility UA
decreases
• Prepecipitation of uric acid crystals
favours uric acid stones.
22. Uric acid stones - 6%
• Radiolucent X-ray
• But visible on US or CT
Radiolucent stones
Uric acid
Xanthine
Triamterene
Dihydroxyadenine
23. Morphology of uric acid stones
• Smooth, yellowish , brown, hard often
multiple
• Cut surface shows laminated structure
24. Cystine stones 2 %
etiology
Cystinuria
Genetically determined
Defect in transport of cystine across
CM/renal tubules, mucosa
25. Pathogenesis of cystine stones
• Cystine is least soluble among all
aminoacids
• Under excess cystineuria- concretion and
stone formation
30. Note also that a yellowish-
brown calculus formed in
the bladder
URIC ACID
31.
32. HydronephrosisHydronephrosis
• Defn: dilatation of renal pelvis and calyces
due to partial or intermittent obstruction to
the outflow of urine.
• Develops due to one or both pelviureteric
sphincters incompetence
• In the absence of the above there will be
dilatation and hypertrophy of urinary
bladder, but not hydronephrosis
36. Unilateral hydronephrosis
Ureteral obstruction at the level of
pelviureteric junction
1. Intraluminal- calculi in ureter/renal pelvis
2. Intramural- cong PUJ obstruction
– Atresia of ureter
– Inflammatory stricture
– Trauma
– Neoplasms of ureter or bladder
3. Extramural
Obstruction of uppr part of ureter by inf renal artery/vein
Pressure on ureter from outside ex ca cx, prostate,rectum,
caecum, retroperitoneal fibrosis
40. Extra renal hydronephrosis
• Dilatation of renal pelvis medially in the
form of sac
• As the obstruction persists
-Progressive dilation of pelvis/ calyces-
pressure atrophy of renal parenchyma
• Dilated – pelvicalyceal cystem extends
deep in to renal cortex- thin rim of renal
cortex streches over calyces- lobulation
41. Microscopy –hydronehrosis.
• Wall of hydronephrotic sac-
fibrous thickening –scarring
inflammatory cell infiltrates
• Progressive atrophy of tubules, glomeruli
• Stasis of urine- infection pyonephrosis.
Sometimes a very large calculus nearly fills the calyceal system, with extensions into calyces that give the appearance of a stag's (deer) horns. Hence, the name "staghorn calculus". Seen here is a horn-like stone extending into a dilated calyx, with nearly unrecognizable overlying renal cortex from severe hydronephrosis and pyelonephritis. Nephrectomy may be performed because the kidney is non-functional and serves only as a source for infection.
Shown below are typical urinalysis findings for this condition, with evidence for "infection stones" of magnesium ammonium phosphate.
Triamterene is a potassium-sparing diuretic.
The passage of a calculus (stone) through the urinary tract is diagrammed here. Calculi form when there is increased excretion of solutes such as calcium and when urine alkalinity, acidity, stasis, and/or concentration are favorable. The most common varieties of calculi are:
The markedly enlarged prostate seen here has not only large lateral lobes, but a very large median lobe as well that obstructs the prostatic urethra and led to chronic urinary tract obstruction. As a result, the bladder became both enlarged and hypertrophied as it had to work against the obstruction with every episode of urination. That is why the surface of the bladder appears trabeculated. Note also that a yellowish-brown calculus formed in the bladder
The arrow points to the culprit in this case of hydronephrosis--a ureteral calculus at the ureteropelvic junction. This kidney demonstrates marked hydronephrosis with nearly complete loss of cortex.
There is scarring of this kidney from chronic obstruction and pyelonephritis. The renal pelvis is markedly dilated, but the ureter is not, indicating that the point of obstruction is the ureteropelvic junction.