Renal Calculi

1. Renal Calculi
Numan Shah
2nd Batch
Renal Dialysis

2. Outlines
• Defination of renal Calculi & its types
• Pathogensis
• Common sites
• Predisposing factors
• Copmlications
• Clinical features

3. Renal Stones
Urolithiasis
Renal Calculi
Nephrolithiasis
Kidney Stones

4. Urolithiasis(renal stones)
Definition:
The stone formation within the kidney or collecting system is called
Urolithiasis
OR
Urolithiasisis calculus formation at any level in the urinary collecting
system
• kidney (nephrolithiasis),
• ureter (ureterolithiasis),
• bladder (cystolithiasis),

5. Types of renal stones
Common stones:
 OXALATE (CALCIUM OXALATE)
 PHOSPHATE
 URIC ACID / URATE
 CYSTINE

6. Un-common
XANTHINE STONES – (Autosomal Recessive . Def of Xanthine
Oxidase leading to Xanthinuria)
DIHYDROXY ADENINE STONE – ( Def. of enzyme adenine phospo
ribosyl transferase )
SlLICATE STONES – Rare in humans ( excess intake of Antacid with
Mg Trisilicate. Mostly in cattle due to ingestion of Sand )
MATRIX - Infection by Proteus - Radiolucent (all calculi have some amt
( 3%) of matrix but matrix calculus has 65% Matrix content in calculi)

7. Types of stones
Calcium oxalate stones:
Most common type (70%) containing calcium oxalate or calcium
oxalate mixed with calcium phosphate
Triple phosphate stones:
(15%) composed of magnesium ammonium phosphate
Urate stones:
About (10%) copmmposed of uric acid
Cystine stones: (1-2%) made up cystine

8. Pathogenesis
Calcium oxalate stones
Hypercalcemia:
About (10%) of patients have hypercalcemia due to hyperparattyroidism,
or vitamin D intoxication etc.
Hypercalciuria:
About (55%) have hypercalciuria without hypercalcemia (idipathic
hypercalciuria). Probably it results from hyperabsorption from calcium
from intestine or impairment in renal tubular reabsorption of calcium
Idiopathic:
In about 20% patients,stone formation occurs without either
hypercalcemia or hypercalciuria

9. Pathogenesis
Triple phosphate stones:
The magnesium ammonium phosphate (struvite) stones usually follow
the infection by urea splitting bacteria(proteus and stayphlococcus)
which convert urea to ammonia,producing urine alkaline in which
magnesium ammonium phosphate salts precipitate to form stone.

10. Patogenesis
• Urate stones:
Composed by Uric acid
Caused by high intake of protein diet and gout
Cystine stones:
They are associated with genetically determined defect in the renal
transport of cystine aminoacid.

11. Common sites of stone formation
•Renal pelvis
• Calyces
•Urinary bladder

12. Predisposing factors
Metabolic factors:
• Hypercalciuria
• Hyperphosphaturia
• Oxaluria
• Uric acid excess
Dehydration:
Causing increased urinary concentration

13. Predisposing factors
Stasis:
Obstruction to urine flow encourages salt precipitation
Urinary pH:Uric acid and oxalate stones form in an acidic urine,while
the phophate stones develop in an alkaline urine
Renal disease:
Renal infections(producing urine alkaline)
Renal Tumors (producing renal stasis)

14. Copmlications
• Pyelonephritis
• Acute urinary retension
• Recurrent chances of infection
• Renal failure
• Pyonephrosis

15. Clinical features
• Gross hematuria
• Nausea and vomiting
• Frequent or painful urination
• Dull pain when stone remains in
kidney
• Episode of flank pain radiating to
the groin when small stones pass
into the ureters

16. Clinical features
Acute obstruction of ureter---
severe colic
Flank pain referred to genitalia
Nausea, vomiting
Microhematuria
Chronic stone distends to be
associated with large or multiple
stones
can be little or no pain
may have impaired renal function,
anemia, weight loss etc.
concomitant infection more likely

18. THANK YOU